AN OPPONENT-PROCESS THEORY OF MOTIVATION: I ...

1'sychological Review1974, Vol. 81, No. 2, 119-145

AN OPPONENT-PROCESS THEORY OF MOTIVATION:

I. TEMPORAL DYNAMICS OF AFFECT 1

RICHARD L. SOLOMON *

University of Pennsylvania

JOHN D. CORBIT

Brown University

A new theory of motivation is described along with its applications toaddiction and aversion. The theory assumes that many hedonic, affective,or emotional states are automatically opposed by central nervous systemmechanisms which reduce the intensity of hedonic feelings, both pleasantand aversive. The opponent processes for most hedonic states are strength-ened by use and are weakened by disuse. These simple assumptions leadto deductions of many known facts about acquired motivation. In addition,the theory suggests several new lines of research on motivation. It arguesthat the establishment of some types of acquired motivation does not de-pend on conditioning and is nonassociative in nature. The relationshipsbetween conditioning processes and postulated opponent processes are dis-cussed. Finally, it is argued that the data on several types of acquiredmotivation, arising from either pleasurable or aversive stimulation, can befruitfully reorganized and understood within the framework provided bythe opponent-process model.

First, we describe the kind of phenome-non which has caught our attention. Twofictitious examples will suffice. In the first,a woman at work discovers a lump in herbreast and immediately is terrified. Shesits still, intermittently weeping, or shepaces the floor. After a few hours, sheslowly regains her composure, stops cry-ing, and begins to work. At this point, sheis still tense and disturbed, but no longerterrified and distracted. She manifests thesymptoms usually associated with intenseanxiety. While in this state she calls herdoctor for an appointment. A few hourslater she is in his office, still tense, stillfrightened: She is obviously a very unhappywoman. The doctor makes his examination.

1 This research was supported by U. S. PublicHealth Service Grant MH-04202 to the first au-thor and Grant MH-16608 to the second author.We are grateful to Burton S. Rosner, Francis W.Irwin, and Martin E. P. Seligman for their pains-taking and helpful editing of an earlier draft ofthis paper. Finally, we are indebted to DorotheaJameson Hurvich and Leo M. Hurvich, whosedevelopment of the Hering theory into their co-herent, opponent-process color vision theory firstsuggested to us a new way of thinking about af-fect and hedonic process.

2 Requests for reprints should be sent to RichardL. Solomon, Department of Psychology, Univer-sity of Pennsylvania, Philadelphia, Pennsylvania19104.

He then informs her that there is no possi-bility of cancer, that there is nothing toworry about, and that her problem is justa clogged sebaceous gland requiring nomedical attention.

A few minutes later, the woman leavesthe doctor's office, smiling, greeting strang-ers, and walking with an unusually buoyantstride. Her euphoric mood permeates allher activities as she resumes her normalduties. She exudes joy, which is not incharacter for her. A few hours later, how-ever, she is working in her normal, per-functory way. Her emotional expression isback to normal. She once more has thepersonality immediately recognizable by allof her friends. Gone is the euphoria, andthere is no hint of the earlier terrifying ex-perience of that day.

In the second example, a couple have justbegun sexual foreplay, and it is quite plea-surable. After a few moments of a constantlevel of mutual stimulation, the pleasure de-creases somewhat. Normally, this declinewould elicit behavior calculated to increasethe intensity of mutual stimulation and tomaintain the high level of pleasure. Un-fortunately, at that moment a telephonerings. One partner leaves and goes intoanother room to answer it, and the otherpartner lies alone in the bed. The aban-

119

120 RJCJJARIJ L. SOLOMON AND J O H N D. COKBIT

+100INTENSITY OF

PRIMARYAFFECT

INTENSITY OFAFFECTIVE

AFTER-REACTION

+100

PEAK OF PRIMARYAFFECTIVE REACTION

ADAPTATION PHASE

^STEADY LEVEL

DECAY OF"AFTER-RE ACTION

PEAK OF AFFECTIVEAFTER-REACTION

ON

TIME

Standard Pattern of AffectiveDynamics

FIGURE 1. The standard pattern of affectivedynamics, showing the five distinctive features:the peak of the primary affective reaction, theadaptation phase, the steady level, the peak of theaffective after-reaction, and, finally, the decay ofthe after-reaction. (The heavy black bar repre-sents the time during which the affect-arousingstimulus is present. The ordinate represents twohedonic scales, each departing from neutrality, onefor the primary affect, the other for the affectiveafter-reaction.)

cloned partner experiences a quick declineof the pleasure, then becomes tense and ir-ritated, and strongly craves a resumption ofthe sexual stimulation. Time goes by, how-ever, and the other partner does not return.Finally, the abandoned partner gets out ofbed, absentmindedly turns on the televisionset, and becomes absorbed in a news broad-cast. Gone is the irritability and intensecraving. There is no hint, in overt beha-vior, of the pleasurable sexual experienceof a few minutes ago. A type of dispas-sionate normality now pervades.

We can distill from these two examplessome important empirical features commonto many hedonic, emotional, or affective ex-periences. First, following the sudden in-troduction of either a pleasurable or aversivestimulus, an affective or hedonic reactionbegins and quickly rises to a peak. It thenslowly declines to a steady level where itremains if the stimulus quality and intensityis maintained. Then, at the sudden termi-nation of the stimulus, the affective reactionquickly disappears and gives way to a quali-tatively very different type of affective re-action which reaches its own peak of inten-sity and then slowly disappears with time.

Figure 1 diagrams these changes in he-donic or affective state and illustrates what

we call the standard pattern of affective dy-namics. The pattern has five distinctivefeatures: (a) the peak of the primary he-donic process or state, precipitated by stim-ulus onset; (6) a period of hedonic or affec-tive adaptation during which the intensityof the hedonic state declines, even thoughstimulus intensity is maintained; (c) asteady level of the hedonic process whichcontinues as long as stimulus intensity ismaintained; (d) a peak of affective after-reaction, which quickly follows stimulus ter-mination, and whose quality is hedonicallyvery different from that of the primary he-donic state; and ( e ) finally, the afterstatedecays and subsequently disappears.

This standard pattern describes both fic-titious examples. In the first, the initial,primary hedonic or affective process was un-pleasant and the after-reaction was pleasant.In the second, the primary process waspleasant and the after-reaction was unpleas-ant. The data of psychology contain liter-ally dozens of examples of this kind. Forbrevity we will first describe some of themore interesting or important cases chosenfrom very different areas of psychologicalresearch. We can therefore demonstratethe great generality of the standard patternof affective dynamics. Then we will de-scribe a theoretical model for the underlyingmechanism.

EXAMPLES OF EMPIRICAL PHENOMENATo BE EXPLAINED

Table 1 presents seven examples of emo-tional, affective, hedonic, or motivationalphenomena. Some are "behavioral," some"experiential." Some are experimental,others are observational, derived from com-mon everyday experiences. Finally, someare precipitated by pleasant, and some byunpleasant stimuli.

Example 1 describes behavior changesseen in a dog subjected to intense aversivestimulation. The example draws on selectedparts of studies reported by Katcher, Solo-mon, Turner, LoLordo, Overmier, and Res-corla (1969) and Church, LoLordo, Over-mier, Solomon, and Turner (1966). A dogin a Pavlov harness was stimulated by sev-

OPPONENT-PROCESS THEORY OF MOTIVATION 121

TABLE 1

SELECTED EXAMPLES OF HEDONIC-AFFECTIVE PHENOMENA

Example

Dogs in Pavlovharness, 10-secondshocks, grossbehavior

Dogs in Pavlovharness, 10-secondshocks, electro-cardiograph re-sponses

Epstein's para-chutists, free fall ,gross behavior,physiology

Opiate users, intra-venous injection,moods and feelings

Dogs and M & Ms,gross behavior

Love, interpersonalstimulation, moods,feelings

Imprinting, the at-tachment ofcreatures to their"mothers"

First few stimulations

State A(input present)

terror, panic

large cardiacacceleration

terror, autonomicnervous systemarousal

euphoria, rush,pleasure

pleasure, tail wag-ging, chewing

ecstasy, excite-ment, happiness

pleasure, cessationof fear, nodistress

State B(input gone)

stealth (subdued,cautious, inac-tive, hesitant)

slow deceleration,small overshoot

stunned, stony-faced

craving, aversivewithdrawalsigns, shortduration

tenseness, motion-less

loneliness

loneliness, distresscries, shortduration

After many stimulations

State A'(input present)

unhappy (an-noyed, anxious,afraid)

small accelerationor none

tense, eager,expectant

loss of euphoria,normal feeling,relief

—

normal, comfort-able, content

pleasure, no cries

State B'(input gone)

joy (euphoric,active, social),happy

quick deceleration,large overshoot

exhilaration,jubilation

intense craving,abstinenceagony, longduration

—

grief, separationsyndrome, longduration

loneliness, intensecries, longduration

eral 10-second shocks. The dog appearedto be terrified during the first few shocks.It screeched and thrashed about, its pupilsdilated, its eyes bulged, its hair stood onend, its ears lay back, its tail curled betweenits legs. Expulsive defecation and urina-tion, along with many other symptoms ofintense autonomic nervous system activity,were seen. At this point, the dog was freedfrom the harness, it moved slowly about(l ie room, appeared to be stealthy, hesitant,and unfr iendly. Its "state" had suddenlychanged from terror to stealthiness.

We now arbitrarily label the state duringshock (the terror state or the peak of theprimary reaction to shock) State "A." Thestealthy state, right after shocks were ter-

minated (the after-reaction), will be calledState "B." In that way, we can temporarilyignore whether we have correctly labeledthe states. We know that State A was notState B. Indeed, State A was very differ-ent from State B, judging by the many be-havioral changes observed when the dog wassuddenly released. Furthermore, State Bgradually disappeared. In a few minutes,the clog appeared to he normal, like its pre-vious, preshock, natural, self: active, alert,and socially responsive. When this hap-pened, it was impossible to tell by lookingat the dog that either State A or B had justtranspired. The evidence was gone. Thedog had progressed from "normalcy" to Ato B, and back to "normalcy." This sequen-

122 RICHARD L. SOLOMON AND JOHN D. CORBTT

250

200

150-

BASELINE

0 2.5 5.0 75 10.0

Time After Shock Onset (Sec)

100-

90-

80

BASELINESLINE 4 maP ^>,---° «>.- -™O-»Vi(

8 ma

0 10 20 30 40 50

Time After ShockTermination (Sees)

FIGURE 2. Heart rate changes as a function ofshock onset, maintenance, and termination. (Thereis a decline following the initial peak reaction toshock onset. There is a deceleratory "overshoot"following shock termination, and then the heartrate slowly returns to baseline rate. Note that theeight-milliampere shock produces a bigger heartrate increase and a bigger deceleration than doesthe four-milliampere shock.) (Adapted from anarticle by Russell M. Church, Vincent LoLordo,J. Bruce Overmier, Richard L. Solomon, and Lu-cille H. Turner appearing in the August 1966Journal of Comparative and Physiological Psy-chology. Copyrighted by the American Psycho-logical Association, Inc., 1966.)

tial pattern will be seen in all of the ex-amples given in Table 1. ft is, we believe,the basic pattern for the dynamics of affect.

However, Example 1 has not yet beenfully described. When the same dog wasbrought back for the same treatment dayafter day, its behavior gradually changed.During shocks, the signs of terror disap-

peared. Instead, the dog appeared pained,annoyed, or anxious, but not terrified. Forexample, it whined rather than shrieked, andshowed no further urination, defecation, orstruggling. Then, when released suddenlyat the end of the session, the dog rushedabout, jumped up on people, wagged its tail,in what we called at the time "a fit of joy."Finally, several minutes later, the dog wasits normal self: friendly, but not racingabout. Here again, the sequence was nor-mal —» State A —> State B —» normal, whereState A accompanied the arousing input,and State B directly followed the suddentermination of that input, and then slowlydied out.

We wish to emphasize that the qualita-tive and quantitative features of States Aand B during later shocks were not the sameas those for States A and B during the firstfew shocks. This pattern of changes, occur-ring as a consequence of repeated exposuresto the stimulus input which causes A, alsois,. we believe, typical of the basic patternof affective dynamics. Because the laterStates A and B were not identical to theearlier states, we label the later ones A' andB', respectively.

Look at Example 2 in Table 1. A dogwas in an experiment in which its heartbeatwas measured by an electrocardiograph dur-ing repeated shocks to its hind feet. Theobservations are from Church et al. (1966).During the first few shocks, there was alarge cardiac acceleration; in some dogs itwas an increase of 150 beats per minute.At shock termination, the rate suddenly de-creased, and within 5 seconds it descendedbelow the baseline rate. It often fell as lowas 20 to 30 beats per minute below baselinerate. Then, it slowly "recovered" to base-line rate, over a period of as long as 30 to60 seconds. The below-baseline excursionhas been called "vagal overshoot." It is awell-studied phenomenon. Figure 2 is takenfrom Church et al. (1966) and demonstratesthese dynamic events. The figure also sug-gests that there may be a relationship be-tween intensity of the A state and the mag-nitude and duration of the B state. Nowwe can define baseline, State A, State B,and the return to baseline using an electro-


cardiograph measurement instead of grossobservations of emotional behavior.

States A and B changed markedly afterseveral sessions. Shock onset now causedlittle, if any, increase in heart rate. Any in-crease was momentary. The rate often de-creased even while the shock was still on.However, when shock was suddenly termi-nated, the "overshoot" was much largerthan it was on early shock trials. Heartrate in some individual cases descended to50 to 60 beats per minute (sometimes morethan 50 beats per minute below baselinerate), and recovery to baseline took as longas two to five minutes. As Katcher et al.(1969) put it, "The deceleratory heart-rateovershoot produced by stimulus terminationshows shortened latencies . . . and greatermagnitude over trials [p. 172]." Thus,States A and B have changed: A' seems tobe weaker than A, B' stronger than B, andB' longer lasting than B. But, as in theprevious examples, we can still identify thesequence: baseline —> A —> B —» baseline.

Example 3 comes from Epstein's (1967)report of physiological, emotional-expres-sive, and social reactions of parachutists.When parachutists make their first jump,they are often terrified, judging by tele-metered autonomic responses and photo-graphed facial expressions. When they landsafely, they look stony-faced or stunned forseveral minutes, then gradually resume nor-mal composure. After the parachutists havemade several jumps and are experts, theirresponses are different. When jumping,they are no longer terrified. They may beanxious, tense, or even eager. After theyland safely, they feel exuberant, exhilarated,and good. They like the feeling, and themood lasts sometimes for hours. Suchparachutists love to jump because of thisafter-feeling. Again, we see that the quali-tative and quantitative attributes of StatesA and B have changed with the repetitionof eliciting conditions. However, two verydifferent states are still observable, and witheach stimulation input, we can identify thesequence: baseline —> A —» B —» baseline.

Example 4 represents states in opiate use(Jaffa, 1965; Maurer & Vogel, 1967).Early in a history of opiate use, the user

experiences the "rush" (an intensely plea-surable feeling) directly after the opiate in-jection, followed by a period of less intenseeuphoria. Then, with further passage oftime, the user suffers aversive, painful, andfrightening somatic withdrawal symptoms,together with a feeling of craving. Hereagain, we see a baseline —> A —> B —> base-line sequence. However, with opiates, Bmay last a long time, sometimes for severaldays.

After repeated dosages of opiates overseveral weeks, State A begins to weaken,and at the same time State B begins to in-tensify and takes longer to return to base-line. State A' is called "normal" ratherthan euphoric. The rush is no longer ex-perienced. Yet, State B' is more physio-logically disturbing than B was, and lastsmuch longer than did State B. The cravingaspect of State B' is now extremely intense,aversive, and enduring. It is called absti-nence agony. It can be months before B'returns to baseline. Perhaps it never reallydoes. It is a ghastly experience.

The repeated use of some drugs resultsin the behavioral phenomenon of addiction.People find themselves craving a substancein which they previously had little interest.It is the most vivid instance of acquiredmotivation, because of its intensity andduration. It also provides a fruitful, em-pirical model for analyzing many kinds ofacquired motivation. Indeed, we later show,with examples taken from love and affection,social attachment, and imprinting in birds,that addiction does not differ in principlefrom any acquired motivational system. Wecan easily describe opiate, alcohol, barbi-turate, amphetamine, or cigarette addiction(see Solomon & Corbit, 1973) within theempirical framework of the analysis we haveproposed. They all have four attributes:(a) The B' state lasts a long time; (&) theB' state is intensely aversive; (e) the elici-tation of State A or A' is effective in caus-ing immediate removal of State B or B';and (rf) the user learns to employ the drugwhich elicits States A and A' in order toget rid of State B or B'.

A lasting cycle of addiction will not arise,even though A and B are repeatedly experi-

124 RICHARD L. SOLOMON AND J O H N D. COKUIT

enced, if the properties of affective responseto a drug are such that B fades out to base-line very quickly. This is true because an-other dosage of the drug is never needed inorder to get rid of the aversive B state. Itquickly gets rid of itself. This is the case inExample 5, a common type of pleasurablesituation. A laboratory dog is sitting de-jectedly in a cage. It is suddenly handedone M & M candy. It wags its tail, movesabout, chews, and swallows. This reflectsState A. It smacks its lips a few times,curls its tongue across its lips, then becomesmotionless and tense. It orients toward theexperimenter and focuses its eyes on the ex-perimenter's hand (the one which held thesingle M & M). Assume this to reflectState B. Then, if another M & M is notforthcoming, the B state dies out afterabout 15 to 30 seconds. The clog movesaway, walks around the cage, sniffs here andthere, begins to "ignore" the experimenter,then sits again. It has returned to its origi-nal state. Here again, termination of onehedonic event has precipitated another statenot present prior to the onset of stimula-tion, and the second state disappeared byitself merely with the passage of time. Inthis case, A is pleasant, so we infer B to bequalitatively different, and probably cravingis the best term for it. The so-called "pea-nut phenomenon" in humans is comparable.Once you start eating peanuts, it is hard tostop unless the cycle is interrupted for aperiod longer than the time required for thepeanut craving, or B state, to die out. Thishas been called a mini-addiction.3 Indeed,the case of the couple interrupted duringmutual sexual stimulation, described in theIntroduction, is certainly similar.

In Example 6, the pleasurable input gen-erates a condition in which the B state typi-cally lasts a lot longer than that for anM & M or a peanut, and so the favorableconditions for addiction are present. A boyand girl "fall in love." This State A ischaracterized by pleasurable excitement, fre-quent sexual feelings, a prevailing mood ofecstasy, happiness, and good feelings. Whenthe lovers, whose multimodal mutual stimu-

3 This term was first suggested by Eliot Stellarat a cocktail party.

lation will cause State A, are separated fromeach other, they will feel lonely, sad, and de-pressed (State B). Even with anticipationsof reunion (symbolic, conditioned arousersof State A) loneliness may prevail. Actualreunion will simultaneously erase B and re-instate A just as described in Attribute cof addiction to opiates.

After several years of repeated mutualstimulation, the qualitative and quantitativechanges in A and B are a matter of publiclore. State A' is characterized (if all hasgone well) as contentment, normalcy, andcomfort. But State B' is now potentiallyof high intensity and long duration. If itshould occur, it is often called grief or, asBowlby (1952) has described it in children,the "separation syndrome." It requires alot of time for this B' state to decay. Thepartners have become addicted to one an-other, and when separated they experiencewithdrawal symptoms. As in all the pre-vious five examples, note that the suddentermination of the stimulus that arouses Aor A' leads to the occurrence of B or B'before the eventual return to emotional base-line or normalcy. In this case, the termina-tion of A', even though A' does not manifestitself as intensely as did A, is followed bya more powerful and much more protractedB' state. This is the same pattern seen inall the previous examples, whether the Astate is pleasurable or aversive.

Example 7 is one of imprinting. Ff wetake the duckling as our subject, it showsthe same patterns of affect revealed in opiateaddiction. First, right after hatching thereare very few distress cries. Indeed, theduckling may appear to be quite happy withits new environment. Then, if the ducklingis exposed to a white, moving object, itlooks intently at it. Also, if there were anydistress vocalizations, they tend to disap-pear. However, if the moving object is thenremoved from view (Hoffman, 1968; Hoff-man, Stratton, Ncwby, & Barre t t , 1970),there is a burst of distress crying whichmay last for several minutes and then dis-appear. With successive presentations andremovals of the imprinting stimulus, thefrequency and intensi ty of distress cryingwill increase.


The efficacy of the presentation of themoving stimulus in eliminating the distresscries appears to be optimal at the outset.Then the duckling can be shaped to push apole in order to present itself with the im-printing stimulus. At that point, of course,the duckling is exhibiting all criteria foraddictive behavior. It is "hooked" on theimprinting object, the presence of which isa positive reinforcer and the absence ofwhich is an aversive event.

Note that the ethological description ofimprinting as the sudden establishment of"following behavior," released by an ade-quate imprinting stimulus, is utterly inap-propriate in the light of our analysis. Themoving object releases some affective StateA, presumably an unconditioned, pleasantemotional reaction to the moving stimulus.The removal of the stimulus then precipi-tates State B, which is an aversive event.State B intensifies with repeated stimula-tions. Ducklings will then work on an avoid-ance schedule to prevent the disappearanceof the imprinting object, just as the opiateaddict will develop anticipatory behaviorwhich prevents the occurrence of at leastthe more intense withdrawal symptoms.

EMPIRICAL GENERALIZATIONS

First, in all seven empirical examples, aswell as in the fictitious ones in our Introduc-tion, the sudden onset of some new stimulusaroused an affect or hedonic state not pres-ent prior to onset. The state terminatedwhen the stimulus terminated. Then, a newstate appeared, qualitatively unlike eitherthe prestimulation state or the state pro-duced by the onset and maintenance of thestimulus. Finally, this new poststimulusstate persisted for a while and died out.The baseline state eventually returned. Innone of the examples did the subject's af-fective state return directly to baseline uponcessation of stimulation. Baseline was re-gained via some new state which becamemanifest at stimulus termination, and thenslowly died away.

Second, in some cases the states changedin their quality and intensity with successive,repeated stimulations. Whenever this oc-

curred, the A states became weaker and theB states stronger and longer lasting.

These two phenomena, the dynamic he-donic response pattern, and its modificationwith repeated experience, were seen whetherthe A state was pleasurable or aversive.

THE EXPLANATORY MODEL

In our opinion, the simplest theoreticalmodel that organizes these typical motiva-tional phenomena (and countless other phe-nomena of innate and acquired motivation)is an opponent-process system. It was bor-rowed from previously developed accountsof sensory dynamics (Hurvich & Jameson,1957). The primary a process for a givenhedonic state is aroused by its adequatestimulus. We then imagine a single oppo-nent loop generating the secondary b processand having an hedonic sign opposite to thatof the state aroused by the input. The loopgenerating the b process is activated when-ever any input evokes a sufficient hedonicconsequence. The b process is sluggish, soit has a relatively long latency, recruitsslowly, and dies out slowly. Finally, theb process is strengthened by use and weak-ened by disuse.

Because many formal properties of thepatterns of both sensory and affective phe-nomena seem so similar, we must show atthe outset that they are not identical andthat the standard pattern of affective dy-namics is not a direct consequence of thepattern of sensory dynamics. Otherwise,one could explain all hedonic or affective dy-namics in terms of sensory events. Forexample, in the case of the woman who dis-covered the lump in her breast, one mightargue that her steady-level anxiety state wasless intense than her initial peak of terrorat the discovery of the lump because ofsensory adaptation; that is, the perceivedpresence of and magnitude of the lumpdecreased. We can refute such an interpre-tation, leaning heavily on the fact that thetime course of typical sensory dynamics isof a completely different order of magnitudefrom that of the standard pattern of affec-tive dynamics reflected in Figure 1 andTable 1. Sensory changes usually occur in

126 RICHARD L. SOLOMON AND JOHN D. CORBIT

a matter of milliseconds, seconds, and min- occur in minutes, hours, days, weeks, andutes, whereas the emotional changes usually months. There is, therefore, a theoretical

Pbnel A. THE PROCESSING SYSTEM

nodoUL J L

^Environmentalstimulus:a dog

yesf

Cognitive -Perceptual

categorical,all-or-none

detectornetwork

J L

,̂Cognitive - r

Perceptualsignal;yes -nodetection

Affectiveor Hedonic

0 1

^Affectivesignal

Panel B. THE AFFECTIVE STAGE OF THE SYSTEM

1 1 FIRST nJ L COMPONENT °

^Cognitive -Perceptualsignal

Process a :affectemotionhedonic tonefeelingmood

I Is^

,

a -signal

-t-

0

>

SECONDCOMPONENT

Process b =

THIRDCOMPONENT

Summingdevicea + b, whereb is(-)

/

-1

opponent -affect

opponent -emotion

opponent -hedonic toneopponent -

feelingopponent -

mood

<^r~b- signal

0 7 1

.

Affective signalg-b

Reinforcerquality andintensity;

^ Hedonic outputstandardpattern

FIGURE 3. Panel A: The detection of an environmental stimulus by a cognitive-perceptual mecha-nism, and the arousal of an affective stage yielding an affective signal which shows the standard pat-tern of Figure 1. Panel B: An analysis of the three components of the affective mechanism. (In thefirst component the a process is aroused. The second component, the b process, is aroused via thearousal of a. Then the third component, a summing device, combines the a and /; signals to generate thestandard pattern of affective dynamics.)


necessity for a distinct opponent-processmechanism for affect and motivation in-dependent of mechanisms for sensory dy-namics.

Figure 3 illustrates the type of system thatwe have in mind. Panel A shows twostages of information processing, a cogni-tive-perceptual stage that converts the stim-ulus to an informational signal, and anaffective or hedonic stage that converts theinformational signal to an affective signal.The affective system in Figure 3 receives asquare wave input, and follows it with a dy-namic affective response of the standardpattern shown in Figure 1.

Perhaps an example will clarify the pointof Figure 3. The sight of a dog is a fear-arousing stimulus for a cat. The dog repre-sents a complex, multidimensional display,and the perception of the dog is categorical,all-or-none. The stimulus sequence is asfollows: The dog enters the cat's environ-ment, remains for a while, and then leaves.The cognitive-perceptual sequence is: Thedog is detected, continues to he detected aslong as it remains, and then ceases to bedetected when it leaves. There is no adap-tation (i.e., the dog does not become lessdoglike), nor is there any appreciable sen-sory after-reaction at stimulus removal (i.e.,no negative [antidog?] afterimage). Theaffective sequence, in contrast, will show theprimary reaction and after-reaction compo-nents : intense fear at first, subsiding to asteady level, and then, when the dog is gone,the appearance of another state, very dif-ferent from the first. The after-reaction(relief?) then gradually dies out.

Figure 3, Panel A, shows that the affec-tive system follows its square wave inputwith an output having the complex dynamicfeatures of Figure 1. How can we accountfor this behavior? The affective system inPanel A is shown as a single stage. Now,we will open the "black box" for this stageand look inside. Our proposal for themechanism responsible for affective dynam-ics is shown in Figure 3, Panel B. Here,the affective stage is analyzed into its threecomponent parts. The cognitive-perceptualstage has acted as a categorical detector.The informational signal enters the affec-

tive system as input to the first component,the a process, which has a short time con-stant. The signal from the a process acti-vates the second component or b process,which responds with a slow rise and a slowdecay. The third component is a summingdevice that adds the a and b signals, and itgenerates as its output the affective signal,which shows the sequence of the peak pri-mary reaction A, adaptation, steady level,after-reaction B, and decay of B. Thus,we see that the input from the perceptual-cognitive stage has an affective, hedonic sideeffect, Process a. When it does, the oppo-nent loop is activated, calling into play theopponent process (which has a hedonicquality in some way opposite to, and verydifferent from, that of Process a). The op-ponent process, which we call Process b,reduces the hedonic intensity of the statewhich the input initially aroused. When theperceptual-cognitive input ceases, the op-ponent process reveals itself as "pure" StateB, because the b process takes a while todecay.

The opponent process is a slave process:It is activated indirectly via the activationof the a process. Presumably, the slaveprocess has an evocation threshold, a la-tency, a recruitment or augmentation time,and a decay function, all characteristic ofa given opponent-process system. We willalso see later that the opponent process can,under proper conditions, be activated byevents in memory, as a consequence of Pav-lovian conditioning procedures.

The block diagram of the affect-controlsystem in Figure 3 yields the temporal dy-namics of affect shown in Figure 4, PanelA. There we first see a baseline state.Then the affect-arousing stimulus is pre-sented and it stays on for 10 seconds. Next,it is suddenly terminated. This simple eventsequence activates the underlying opponentprocesses. First, there is a quick rise ofProcess a to a peak intensity. Shortly after-ward, there is a slow recruitment of Processb. When the stimulus is terminated, Pro-cess a quickly goes to zero, but Process b,having a sluggish decay property, persever-ates and dies out slowly. The resultantmanifest dynamics of affect are a conse-


A

MANIFESTAFFECTIVE 0

RESPONSEB

UNDERLYING

OPPONENT

PROCESSES

STIMULUSEVENT

Panel A.

FIRST FEW STIMULATIONS

Panel B.

AFTER MANY STIMULATIONS

g-b

TIME

FIGURE 4. Panel A: The operation of the summing device for the firstfew stimulations. (The summation of the underlying opponent processes,a and b, yields the manifest affective response.) Panel B : The operationof the summing device after many repeated stimulations.

quence of subtracting the b process from thea process. The subtraction of the two quan-tities yields Manifest State A when a > band yields Manifest State B when b > a.The intensity of the manifest state is givenby the quantity |a — b\.

When we subtract the underlying pro-cesses, a and b from each other, we obtain

the manifest affective response patternshown in Figure 5. Immediately afterstimulus onset, a is large and b is zero, thusyielding a peak of State A. As b is slowlyrecruited, the quantity \a — b\ decreases,yielding a decline in the magnitude of StateA. This is the adaptation phase shown inFigure 1, the standard pattern of affective

+100

to

Neutral oca

J5to

+100

First Few Stimulations

PEAK OF A

ADAPTATION^STEADY LEVEL OF A

4 OF BPEAK OF B

ON

TIMEFIGURE 5. The manifest temporal dynamics generated by the opponent-

process system during the first few stimulations. (The five features ofthe affective response are labeled.)


dynamics. When the b process reaches anasymptote, there will be a steady level ofState A. Then, when the stimulus is ter-minated, the intensity of a goes quickly tozero, but the b process dies away slowly.At this moment, b > a, yielding the peakand subsequent decay of State B. At thispoint, State B is pure b.

The theory represented in Figures 3 and4 gives a rough, qualitative account of allof the data of Table 1, for the first few stim-ulations only. First, it explains peaks ofintensity of affect or hedonic quality at stim-ulus onset: The opponent process has notyet had enough time to get into action. Sowe see phenomena like terror, the rush,ecstasy, etc. Or, rate the painfulness of a30-second shock. The peak painfulness isat onset. For example, see the peak ofheart rate in Figure 2.

The other major event explained by thetheory is the emergence of the after-reaction,postulated to be a function of the opponentprocess, which becomes manifest after thetermination of stimulus input. This emer-gence is due to pure b perseverating in timeafter the a has quickly disappeared. TheB state slowly decays, and baseline is even-tually attained.

In each of the seven empirical examplesof Table 1, the manifest B state was, in someunspecified way, related to A, but not thesame as A. The model designates the rela-tionship as oppositeness. But in what waycan we say, for example, that loneliness isopposite to the pleasure produced by thepresence of a loved one? Surely, they arehedonically opposed. This concept is builtinto the theoretical model. If A is pleasant,then B must be unpleasant. If A is a posi-tive reinforcer, then B is a negative rein-forcer. Other affective attributes of A andB remain an empirical question. The modeltells us how to identify the attributes ofoppositeness. All one has to do, for anygiven A state, is observe the attributes ofaffect which are revealed at the peak of B.Therefore, the model puts a constraint onwhat we call oppositeness. For example,the opposite of love must be the attributesof grief. To say that, "Hate is the oppositeof love" is simply wrong, when at the death

of a loved one, one experiences grief, nothate. The kinds of oppositeness which aregenerated by each A state are still, in manycases, waiting to be studied and named.Here is a vast, neglected area of investiga-tion.

We postulated that the /; process is a slaveprocess. That means that at first it cannotbe aroused directly by ordinary sensory in-puts, but instead can arise only indirectlyvia the arousal of an a process (see Figure3) and the subsequent activation of the op-ponent loop. This fits common sense. Tryto imagine being grief-stricken without hav-ing loved someone. Try to imagine cravingand abstinence agony without drug use.Try to imagine the exhilaration of the para-chutist without any jump. On the otherhand, we will point out later that it may bepossible to arouse a b process directly byelectrical or chemical stimulation of thebrain, or to eliminate it by surgery, or tocondition it by Pavlovian procedures. In-itially, however, it is a slave process, inac-cessible to direct environmental inputs, butindirectly arousable via hedonic and affec-tive processes elicited by environmentalinputs.

STRENGTHENING OF OPPONENT PROCESSESBY REPEATED STIMULATION

We have not yet explained the changes inhedonic dynamics brought about by repeatedaffect-arousing stimulations over a relativelylong period of time. There are importantdifferences between the A and B states onthe left side of Table 1 as compared to theright side. Fortunately, one postulate bringsorder into the data: The opponent processis strengthened through use and weakenedthrough disuse, but the primary affectiveprocess is not seriously affected by use. Ab process will acquire more power if fre-quently elicited. It will show a shorterlatency of response to a, a quicker rise, ahigher asymptote, and a longer decay time.In contrast, an a process is a relativelystable, unconditioned reaction. This seemsreasonable for a system which is designedto minimize deviations from affective neu-trality. Why should an opponent processnot act like a defensive or immunization pro-


After Many Stimulations^nn+JUU

ICO

Neutral °eo

+1001

STEADY LEVEL OF A'-=^>- .- --_,-_._„ Baseline

PXEAK OF B'

ON

TIMEFIGURE 6. The manifest temporal dynamics generated by the opponent-

process system after many repeated stimulations. (The major features ofthe modified pattern are labeled.)

cess, which produces antibodies more effi-ciently and in larger numbers in the faceof repeated challenge? In the same vein,disuse should weaken a b process, and itshould slowly return to its original magni-tude whenever its a process has not occurredfor a long time.

Figure 4, Panel B, shows how the oppo-nent processes will interact after the b pro-cess has been strengthened by repeated use.A comparison of Panels A and B explainswhy the left-hand portion of Table 1, de-scribing "early stimulation," differs from theright-hand portion of Table 1, describing"later stimulations."

The effect of repeated experiences on thehedonic response is confined to strengthen-ing the b process. During later stimulationsthe b process increases at a faster rate atstimulus onset and reaches a greater asymp-totic intensity. In addition, the b processrequires a much longer time to decay afterthe later stimulus terminations. As a con-sequence of these changes in the b process,the resultant pattern of the affective reactionchanges so that the peak of A is consider-ably attenuated, and the peak of B becomesmuch greater and longer lasting. Figure 4,Panel B, shows these simple algebraic sum-

mations of the a and b processes after manyrepeated stimulations.

Figure 6 shows the pattern of emotionaldynamics after many repeated stimulationsand should be contrasted with the patternshown in Figure 5. Three phenomena arecorollaries of the use postulate. First, thepeak of A' will be less intense because thelatency of the b process is decreased and itsintensity is increased. Second, the steadylevel of A', |a — b\, during maintainedstimulation will be close to baseline and per-haps even below it in some cases. Third,the peak of B' should be intense and longlasting, compared to what it was duringearly stimulation (Figure 5).

The events in Figure 6 do not follow froma simple affective contrast model. If a prin-ciple of simple hedonic or affective contrastwere operating, then the peak of B in Figure5 should be greater in intensity than it is inFigure 6, because the intensity of A directlyprior to stimulus termination is greater inFigure 5 than it is in Figure 6. However,if we run down the descriptive adjectivesfor States A, B, A', and B' in Table 1,even as loosely defined as they are, theopponent-process model works well, and asimple contrast model fails.


More convincingly, the objective datafrom the electrocardiograph experimentswith dogs fit the opponent-process model.In Table 1 we saw the following:

A, large acceleration;B, small overshoot, short duration;A', small or absent acceleration;B', large overshoot, longer lasting.

These findings fit the postulate that repe-titions of affect-arousing stimulation, in thiscase shocks, will strengthen the opponentprocess which dampens the primary cardiacacceleration process. Furthermore, thereare many signs of qualitative changes; e.g.,signs of pleasure and euphoria appear in theperiod following termination of the shocksession, although they were absent in earliersessions. Our model cannot yet deal pre-cisely with these qualitative changes whichare produced by many repetitions of thesame stimulus. A' is less intense than A,and B' is more intense and longer lastingthan B. The model deduces these quantita-tive changes (Figure 4). In many cases,however, A' is qualitatively different fromA, even though they have the same hedonicsign. Similarly B' and B are sometimesqualitatively different, even though theyhave the same hedonic sign. When themodel is fully developed, it must contain arationale for these qualitative changes.

The observations on the right-hand sideof Table 1 also support the assumption thatmany repetitions of pleasures will strengthentheir aversive opponent processes. Aversivestates, manifesting themselves after the sud-den termination of pleasurable inputs, be-come more intense with repeated experi-ences. Mild loneliness later becomes grief.Mild craving later becomes abstinence agonyand intense craving. In addition, aftermany repetitions the steady level of plea-sure produced by the continued presence ofthe pleasurable stimulus input has decreased.The confirmed opiate user experiences a"loss of euphoria," and the rush is gone.The pleasure-affective systems seem even-tually to yield to opponent processes whichkeep departures from hedonic equilibriumrelatively small. The aversive opponentprocess, when it is manifest, is more intense

and longer lasting than it once was. So fre-quently repeated pleasure has its costs, psy-chologically, in an increased potentiality fordispleasure.

Similarly, for A' states aroused by aver-sive input, there is a "cost," but this costis an increased potentiality for pleasure.Table 1 lists in the column under B' theopponent affects for the aversive A' states.Words like "joy," "exhilaration," and "goodfeeling" appear. These are the emotionalcosts of aversiveness. The model thus re-quires that any prolonged or repeated de-partures from hedonic or affective neutrality,regardless of hedonic sign, have a cost.Any significant departure from hedonic oraffective neutrality should have correlatesin increased autonomic and central nervoussystem activity aimed at reducing that de-parture. The cost of this activity will notonly be psychological, but also will be physi-ological (metabolic, hormonal, and neural).

We are assuming that prolonged exerciseof an opponent-process system, whether itbe pleasurable or aversive, might causephysiological stress in the same sense thatSelye (1950) uses the term stress. That is,many physiological resources might be re-quired in order to keep the opponent pro-cess strong. If we follow Selye's argument,we would expect that such a constant de-mand might lead to the exhaustion of a par-ticular overworked opponent-process systemor to the debilitation of other defensivesystems.

Thus we come to a major implication ofour opponent-process model: There proba-bly are stresses caused by pleasurable stim-ulation just as there are stresses causedby aversive stimulation. Therefore, thereshould be adaptational costs as a conse-quence of both kinds of stresses. Further-more, if we look for them, we should finddiseases of adaptation jor both, due to thecorrelated, physiological side effects of long-duration often-elicited intense b processes.

In the past, psychologists have identifiedpsychological stress with aversion, pain, andunpleasantness. Theories of mental disease,psychosomatic disease, and behavior disor-ders usually emphasize that aversivenessmeans stress, stress means aversiveness, and


both cause emotional disorders, psychoso-matic illnesses, and behavioral malfunctions.Our opponent-process theory of motivationputs all this to question. From our pointof view, stresses caused by aversive stimu-lation are only one half of the story. Thereshould be emotional disorders, psychoso-matic diseases, and behavior disorders causedby long-lasting, repeated, and intense b pro-cesses in general, whether these opponentprocesses are pleasurable or aversive.

Take the case of the parachutists. Theiroperant behavior, when B' is strong, will bereinforced by the pleasurable experience ofB'. But the cost of neutralizing the innateaversiveness of a fall through space mightbe high, both physiologically and emotion-ally, just as Epstein (1967) has postulated.Even so, one might imagine, if there wereno other pleasurable sensory inputs else-where available to the individual, that hemight put himself through repeated aversivestimulation in order to experience the plea-surable B' state which would be both intenseand lasting. From our point of view, thistype of apparent masochistic behavior is nota mental disorder but is, rather, a reflectionof the normal functioning of a healthy, auto-matic, affect-control system. Thus, also,from this point of view, there is nothing ab-normal or strange about addiction. It isonly a socially vivid example of the normalhedonic and motivational functionings of anefficiently operating affect-control system.

Motivational systems involving pleasur-able A states and aversive A states are simi-lar. In both cases the onset, maintenance,and termination of the stimulus results in acertain amount of pleasure and a certainamount of displeasure. They differ mainlyin whether pleasure or displeasure comesfirst. In the case of the pleasurable Astates, we can assume that the subsequentaversive B state functions as a drive thatenergizes the performance of operants, andthat the pleasurable A states may positivelyreinforce these operants. Electrical self-stimulation of rewarding brain sites, chemi-cal self-stimulation with opiates, and loverelationships should work this way. In con-trast, when the A state is aversive, andwhen the A state stimulation is absent, noth-

ing functions as a drive to energize an oper-ant upon which the A state is contingent.So we have the problem of how to get thebehavior started. The B state for an aver-sive A state is not an energizer. Instead,it is a positive reinforcer. There is thus animportant asymmetry between motivationalsystems for pleasurable and aversive Astates. Some outside energizing influenceis needed to get behavior started when theoperant is followed by an aversive A state.Examples of such behaviors include "thrill-seeking" behaviors, such as parachute jump-ing, mountain climbing, automobile racing,etc., all of which involve an aversive com-ponent, followed by a pleasurable feeling ofexhilaration. Why should one initiate anactivity when its immediate effect is aver-sive, i.e., when a punishment contingencyexists? Some competing outside influence,such as social pressure from peers, is re-quired. However, after many repeatedstimulations, such outside influences maynot be needed. Because the aversive A stateis then weak and the subsequent, positivelyreinforcing B state is strong, the A statewill function as a positive reinforcer. Weknow that this can happen when a weakshock signals the onset of food for cats(Masserman, 1943). Note that an out-side influence is not needed when the Astate is pleasurable. These operants areenergized by the aversive B state.

RELATION OF THE THEORYTO OTHER CONCEPTS

To the reader well versed in the historyof theories of learning, two aspects of ourmodel should now be apparent. First, thephenomena of acquired motivation producedmerely by the repetition of affect-arousingstimuli are nonassociative in nature. Forexample, the person repeatedly dosed withmorphine does not have to know anythingand is not required to be subjected to Pav-lovian stimulus contingencies, nor to con-tingencies between operants and outcomes,in order to develop an increasing tendencyto suffer when the morphine is withdrawn.The model is therefore very different fromprevious theories of acquired motivation,


all of which have emphasized associationalprocesses.

Second, the model, in relating its hypo-thetical mechanism to the phenomena ofoperant conditioning, explicitly assumes thatoperants are energized only by aversivestates and that they can be reinforced eitherby the onset of pleasurable states or by thetermination of aversive states. This is thecase whether the pleasure or aversivenesscomes from A states or B states. For ex-ample, the reinforcing effects of shock ter-mination will not only be due to the elimi-nation of the aversive A state but also, andperhaps more importantly, it will be dueto the subsequent pleasurable B state.Woodworth and Schlosberg's (1954) con-cept of "safety," Mowrer's (1960) con-cept of "relief," and Denny's (1971) conceptof "relaxation" are all emphasizing this con-cept of reinforcement in aversive situations.

The assumption that operants are ener-gized only by aversive states fits most com-fortably with the theoretical position takenby Hull (1943, 1952) and elaborated byMowrer (1947), Miller (1948), Spence(1956), and Brown (1961). The assump-tion that operants can be reinforced by theonset of pleasurable states fits easily withthe position taken by Young (1955) and byPfaffman (1960). Of course, the assump-tion that operants are reinforced by thetermination of aversive states is most likethe drive-reduction position maintained es-pecially by Hull (1943) and by Mowrer(1947). These assumptions are really notat issue for us. We take all three to beaxiomatic, a point of departure, and we goon from there to spell out the dynamics ofpleasurable and aversive states.

CONDITIONABILITY OF A STATESAND B STATES

The opponent-process theory would en-compass an even larger array of data onacquired motivation if it could be safelyassumed that A states, or B states, or bothcould be brought under the control of pre-viously neutral stimuli as a consequence ofexperience. A Pavlovian conditioning pro-cedure then would result in the establish-

ment of conditioned stimuli which couldevoke either state as a conditioned response.

Assume that we have a valid measure-ment of the intensity of affect produced bythe onset and maintenance of a 10-secondshock in dogs and that we can measure theopponent process when it reveals itself di-rectly after shock termination. Now we re-peatedly pair a conditioned stimulus (tone)with shock onsets. If a Pavlovian condi-tioning process is effective, then the condi-tioned stimulus would then become an A-state elicitor. We call such a conditionedstimulus a CSA. (In the Pavlovian frame-work such a conditioned stimulus would becalled a CS+.) If we present a test trialwith CSA, with no shock presented, weshould see CSA arouse a conditioned StateA (or a weak relative). When CSA is sud-denly terminated, we should see State Bappear, peak, and then decay to baseline intime. The hedonic recovery from such atest with CSA alone should therefore ap-pear to be biphasic.

Contrast this with what should occur ifwe establish a conditioned stimulus by pair-ing a signal with the peak of State B, whichwill occur directly following shock termi-nation. That paradigm is Pavlovian back-ward conditioning: The conditioned stim-ulus always follows termination of theunconditioned stimulus closely in time. Sucha conditioned stimulus should become a Pav-lovian CS—, or in our terminology, a CSn.It should be able to elicit a conditioned statevery similar to State B. A test with CSs(without a shock preceding it) should resultin the conditioned State B appearing at theonset of CSa. Then, after CSu termination,State B should decay monotonically, andbaseline should be reestablished. In otherwords, a monophasic recovery followingCSn termination should occur, whereas abiphasic recovery ought to occur followingCSA termination. Why a monophasic re-covery for B? Because, if the b process isa slave process with respect to a, and yetthe resultant states are also conditionable,then we ought to be able to arouse the bprocess directly by onset of a CSB, but then,after CSB has terminated, all State B cando is die away. But a CSA, if successful in


20

16-

12-

8-

4-

«-CS+

+10 +15 +2'0 +2T+30,

Pos»-CSPre-CS CS

Successive 5 -Second PeriodsFIGURE 7. Data from Rescorla and LoLordo

(1965). (The solid lines and dots show the bi-phasic response following termination of the fear-arousing conditioned stimulus [CS]. In this graphthe CS+ is a CSA. The dotted lines and opencircles show the monotonic recovery following thetermination of the fear-suppressing conditionedstimulus. In this graph the CS— is a CSu.)

eliciting the conditioned a process, will alsoindirectly arouse its opponent process.Therefore, State B will be seen immediatelyafter CSA is suddenly terminated, yieldinga biphasic recovery. But a peak of State Awill never be seen after a CSB is terminated :Only a return of State B to baseline willoccur.

In comtnonsense terms, what the oppo-nent-process theory is saying for the caseof conditioned fear is peculiar. The suddentermination of a danger signal (CSA)should cause the conditioned subject to actas though it had received a safety signal.But the sudden termination of a safety sig-nal (CSn) should not cause the conditionedsubject to act as though it had received aclanger signal. An analogous asymmetryshould of course exist for appetitively con-ditioned stimuli, though we are not awareof the existence of experimental data onthis point.

Some Pavlovian conditioning data fitthese expectations very well for aversivestimulation. Rescorla and LoLordo (1965)trained dogs to avoid shocks on a Sidmannonsignalized avoidance schedule (shock-shock interval = 10 seconds, response-shock interval = 30 seconds) . The avoid-ance response rate was used as a measureof fear intensity. When the dogs' avoid-

ance response rate had stabilized, they weretested during avoidance performance with aCSA which had previously been paired withshock onsets during separate Pavlovianfear-conditioning sessions. The onset of theCSA during the shock-free tests resulted ina large increase in the avoidance responserate. This was interpreted to mean that theavoidance response was energized by the in-crement of conditioned fear caused by thepresentation of the CSA. The most inter-esting phenomenon to us is the fact thatrecovery from a CSA test was biphasic. Theavoidance response rate, when CSA was ter-minated, dropped quickly below baseline,then recovered slowly to baseline in 30 to45 seconds (see Figure 7, solid line withsolid circles).

Rescorla and LoLordo (1965) used a dis-criminative conditioning feature, with aconditioned stimulus paired with a longshock-free intertrial interval. When theconditioned stimulus was tested during theclogs' avoidance performance, it suppressedthe avoidance response rate. Then, whenthe conditioned stimulus was terminated, therate slowly returned to baseline in 30 to45 seconds (see Figure 7, dotted lines withhollow circles). The recovery from theconditioned stimulus was exactly what weshould expect if the conditioned stimulushad been conditioned to the B state. In-tuitively, one might think that the termi-nation of the conditioned stimulus, whichis, after all, a safety signal, ought to causea sudden intensification of fear above theoriginal fear baseline. This does not hap-pen, and adds strength to the theoreticalanalysis we have presented. However, thereis a serious problem in applying the modelto these data on Pavlovian differential con-ditioning. The conditioned stimulus wasalways presented following an intertrial in-terval of 1| minutes or longer. Therefore,by no stretch of the imagination could weconsider the conditioned stimulus to havebeen regularly paired with the peak of B,because the peak of B would have occurredvery shortly after the previous shock termi-nation. How, then, can we manage thisconceptual problem? If we are to staywithin the confines of our model, we must


make two assumptions. First, after manyconditioning trials during which hundredsof shocks have been sustained, the b processwould be very strong and last a long time(perhaps for many minutes, or even forhours). Second, we must assume contem-poraneous conditioning, an event—state con-ditioning process, where the conditionedstimulus is the event and the state is B.This is an assumption for which we haveno empirical support.

The findings of Moscovitch and LoLordo(1968) add more unambiguous support forthe conditioning of a B state. Using thesame experimental situation as did Rescorlaand LoLordo (1965), they employed a Pav-lovian backward-conditioning paradigm toestablish a CSB. According to our analy-sis, this should pair the CSB onset with thepeak of B and create a maximally powerfulCSB. Recovery from a short-duration testwith such a CSB should be monotonic, be-cause there is no mechanism whereby the bprocess could engender the a process. Thisis indeed what happens, as shown in Figure8. Tests with CSB caused a reduction inavoidance response rate to a level about 1/5of that during the baseline performance.Recovery to baseline after CSs terminationtook more than 30 seconds (see Moscovitch& LoLordo, 1968, p. 675, Figure 1), and itwas monotonic. Moscovitch and LoLordoreferred to the backward conditioned stimu-lus as a "safety signal"; they reported theirdogs to be relaxed; "there were no indi-cations of freezing or fright [p. 675]." Thisrelaxation occurred in spite of the fact thatthe dogs were still in the avoidance-trainingsituation, which was frightening enough tomotivate a steady rate of avoidance re-sponses (about six per minute). So theirbackward conditioned stimulus met all thecriteria for a conditioned stimulus for a Bstate.

To convince oneself that B-state condi-tioning has indeed occurred, it might notbe sufficient merely to show that the back-ward conditioned stimulus will suppress anongoing Sidman avoidance response. Thedecrease could reflect a reduction of fear, adecreased expectation of shock, or bothrather than some pleasant hedonic state with

3-

2

1-

-J5 -10 -5

Pre-CS+15 +20 +25 +30,

Post-CSFIGURE 8. Data from Moscovitch and LoLordo

(1968). (Here we see the response to a Pavlo-vian backward conditioned stimulus [CS]. Therecovery from the conditioned stimulus presenta-tion is monotonic and is a C5n.)

positive reinforcement properties. Two linesof evidence would help. First, the gross be-havior of the subjects, such as tail waggingin the presence of the backward conditionedstimulus, would suggest a qualitatively dif-ferent state from that which the avoidancesituation normally evokes. Second, thedemonstration that a backward conditionedstimulus would subsequently reinforce thedevelopment of a new operant in a non-fearful situation might strengthen the con-viction that the conditioned stimulus wasreally a CSB of a pleasurable sort.

We have seen that Pavlovian laws seemto apply well to the conditioning of bothA states and B states precipitated by aver-sive stimulation. We should then expectthe same laws to hold for A states and Bstates precipitated by pleasurable sensoryevents. First, the conditioned stimulusevents for pleasurable A states should bepositive reinforcers, should be able to rein-force operants, and finally should be ableto counter and sometimes even temporarilyeliminate the B state. Therefore, in opiateaddiction, presentation of a drug container,a syringe, a needle prick, or a room full ofsatisfied addicts should all tend to functionas CSAs which would oppose the B stateby arousing a conditioned A state. Suchconditioned opposition would of course beweaker than that produced by the opiateitself, but it should be detectable. Many


opiate addicts actually give themselves"sham" injections. Even the familiarsocial surroundings where the drugs are ob-tained and used should have CSA proper-ties. They should temporarily reduce crav-ing and abstinence panics. Clinical evidencesuggests that this is indeed the case (Mau-rer & Vogel, 1967; Wikler, 1971).

The action of €83 events should be evenmore interesting in addiction, because theyshould augment the B state and producemore intense craving. Such CSnS would bethose paired with the peak of B, the mostintense craving state. Thus, we would ex-pect a variety of social and personal eventsto become conditioned arousers of craving.In general, they should be events and placesassociated with lack of the addictive drug.A jail cell, confinement, lack of money, allof these should be able to arouse a condi-tioned B state to augment an existing un-conditioned B state. Perhaps the occur-rence of the conditioned B state mightprecede the actual emergence of the uncon-ditioned B state. This conditioning phe-nomenon should lead to increased frequencyof dosage. For someone trying to "kick ahabit," the careful avoidance of these CSnevents, which elicit B states, should be veryhelpful.

The conditioning process results in theaddict being "hemmed in" to a great extent.If we assume that the events in Figures 7and 8 occur also for the addictions, then in-creased craving would be a consequence ofconditioned stimulus events, no matterwhether a CSA or a CSu were presented.In the case of the CSA, the craving shouldoccur following the termination of the CSA(see the biphasic recovery in Figure 7). Inthe case of CSB, the craving should occurduring and after the CSs presentation (seethe monotonic recovery in Figure 8). Thus,the Pavlovian conditioning of A states andB states, during the acquisition of an ad-dictive cycle, overdetermines the craving forthe drug. The addict, even if he tries toreinforce himself symbolically, i.e., with avariety of CSA onsets, will experience anincreased aversive B state afterward.

Conditioned b processes can become verypowerful relative to a processes, just as un-

conditioned b processes can become verypowerful. Take the work of Kimmel(1971), who used the galvanic skin re-sponse as an anxiety index. In analyzingthe phenomena of galvanic skin responseconditioning with aversive unconditionedstimuli, he found that the magnitude of an-ticipatory galvanic skin responses in re-sponse to CSAS often increased on the veryearly trials of conditioning. However, onlater trials they decreased, even though thesame unconditioned stimulus reinforcer wasbeing regularly presented. Kimmel calledthis phenomenon the inhibition of emotionalbehavior, a manifestation of the organisms'adaptive adjustment. His idea is that thefear of the unconditioned stimuli has be-come manageable by the action of a fear-inhibition mechanism. Kimmel's conceptsseem to be close to our own, if we changethe inhibition concept to an hedonic oppo-nent-process concept. We do not knowexperimentally whether the phenomena dem-onstrated by Kimmel also manifest them-selves in appetitive conditioning. We sus-pect that they do.

The observations of Kimmel (1971),taken in conjunction with an opponent-process theory, suggest a variant of the ex-periment by Rescorla and LoLordo (1965)which would be a very strong test of theopponent-process theory. One would traindogs to perform a regular Sidman avoid-ance response. Then, during the condition-ing phase of the experiment, a long seriesof trials with the unconditioned stimulusalone could be presented. Theoretically,this should strengthen the b process forfear. Then the discriminative conditioningphase of the experiment could be carriedout just as Rescorla and LoLordo did.When the CSA is presented on a test trialwhile the dogs are performing this avoid-ance response, the CSA now, in contrast towhat Rescorla and LoLordo found, shouldbe relatively impotent in energizing theavoidance response. In other words, theCSA onset would be a weak fear elicitor(Kimmel, 1971). In contrast, the termi-nation of CSA as well as the presentationof the CSB, when presented during avoid-ance responding, should powerfully suppress


avoidance behavior. This suppressive ef-fect should persist for a relatively long timeafter termination of the test with CSB.These deductions stem from the assumptionthat the long series of pretreatment trialswith the unconditioned stimulus alone hasstrengthened the b process, so that when theconditioned stimuli are finally introducedin the later discriminative conditioning, CSAwill be paired with a shock which elicitsvery little fear (b is large, so a minus b issmall), but CSB will be paired with theintense peak of the B state which is theopponent of fear (joy, euphoria).

A further deduction from opponent-pro-cess theory suggests a way to reverse whathas heretofore been a strong empirical gen-eralization. In most discriminative-condi-tioning experiments the elicitation power ofthe CS+ grows quickly as a function oftrials of conditioning, but the inhibitoryproperties of the CS— require many moretrials to manifest themselves. In the vari-ant of the Rescorla and LoLordo (1965)experiment which we suggested as a strongtest of our opponent-process model, the re-verse should be true if discriminative con-ditioning is started after a long series oftrials on which the unconditioned stimulusalone has been presented. The effective-ness of the unconditioned stimulus shouldbe greatly attenuated when conditioning isstarted, and a conditioned stimulus pairedwith an ineffective unconditioned stimulusshould acquire excitatory properties veryslowly. In contrast, a conditioned stimuluscoming directly after unconditioned stimu-lus termination would be associated with anintense B state. Such a conditioned stim-ulus should quickly acquire CSB properties.

The postulates of an opponent-processtheory of affect, combined with Pavlovianlaws for the conditioning of A states and Bstates, give us a new way of looking at thephenomena of acquired motivation.

ANALYSIS OF SELECTED MOTIVATIONALPHENOMENA IN LIGHT OF THE

OPPONENT-PROCESS THEORY

There are many areas of psychologicalresearch which can be profitably reanalyzed

within the confines of the opponent-processmodel. For example, we have found themodel useful in increasing our understand-ing of addiction, childhood attachments, loveand affection, imprinting in precocial birds,rewarding and punishing electrical stimula-tion of the brain, so-called thrill-seekingbehavior, the dynamics of fear and avoidancebehavior, the pleasures and displeasures as-sociated with thermoregulatory behavior,some aspects of masochistic behavior, de-pression and euphoria, and taste cravingsand obesity, to mention a few. We haveselected only two of these phenomena forintensive and detailed analysis in order todemonstrate the applicability and use of theopponent-process model to deduce new phe-nomena and experiments. In the first, theA state is pleasurable, and in the second itis aversive.

Addiction and Stimulation of A and BStates with Drugs

We have discussed the main features ofan opponent-process theory of affect. Theseare as follows: (a) Process a; (b) Oppo-nent Process b, a slave process; (c) thestrengthening of the b process as a functionof repetitions of the a process; and (d) theconditioning of A and B states by Pavloviancontingencies.

We believe any addiction can be betterunderstood by reference to these features.First, the addictive substance must be capa-ble of giving pleasure, at least sometimeduring its early use. Actually, there maybe some aversive effects from the first fewdoses, but these are overshadowed by thepleasure effects coming either from the drugitself or from other available reinforcers.If not, the dosage will not be repeated. Ifdosage is repeated, the opponent process willbegin to strengthen. Withdrawal symp-toms and craving will intensify and becomelonger lasting. They will be aversiveenough and persistent enough so that theuser will try ways of getting rid of them.

It is here that we have to qualify thetheory with a specificity assumption. Weassume that, because the b process is theopponent of a, the quickest and most effec-


tive way of getting rid of the B state is touse the substance which directly producesthe A state. We do not know, however,why this should be so, but it is the way ad-dictive drugs work. Thus, behavior re-sulting in the obtaining and use of theA-arousing substance will be strongly re-inforced because it produces A and it simul-taneously terminates B. This will lead tofurther strengthening of the b process.Therefore, amounts of the substance willhave to be increased in order for the sum,(a— b ) , to be greater than zero, or abovebaseline. This is the drug tolerance phe-nomenon (Jaffe, 1965; Wilder, 1953). In-crease of dosage then will reinforce all thebehavior upon which it is contingent, andthe b process will be further strengthenedby more frequent use. This is the addictivecycle.

During early doses, when the quantity|a — b\ is large, previously neutral stimulishould become conditioned to A if they di-rectly precede the onset of State A. Theywill become CSA stimuli, Pavlovian elicitorsof the A state or components of it. Thesestimuli, as CSAS for a pleasurable DrugState A, will be positive secondary reinforc-ers, capable of reinforcing new operants.

As the b process becomes stronger, thePavlovian conditioning of previously neutralstimuli which directly follow a-process ter-mination, and which also directly precedethe peak of B, should readily occur. Wewill then see the emergence of strong CSBs,aversive in quality. They will be the con-ditioned stimuli for the craving and with-drawal symptoms. Thus they will be sec-ondary negative reinforcers and will energizeescape and avoidance behaviors. As theCSBs become stronger they will becomemore anticipatory, and so redosage and re-stimulation will start to occur at shorterintervals. The addict then will be usingthe drug partly to remove conditioned B-state arousals precipitated by the presenceof CSBs. Therefore, increased dosage fre-quency, until some asymptote is reached,should occur whenever: (a) The b processbecomes stronger, and (b) CSsS are estab-lished by Pavlovian conditioning contingen-cies. Increased frequency of dosage should

occur even if drug amounts per dosage donot substantially change. Finally, if the ad-dict, under the influence of other motivation,stops using the drug, the b process willweaken gradually with the passage of time.

The dynamics of behavior change whichwe have outlined are typical of most addic-tions (see Solomon & Corbit, 1973). Natu-ralistic observations appear to fit the deduc-tions from the opponent-process model.Could the opponent-process model for ac-quired motivation help us to understand bet-ter the problems of the addict who wantsto quit? Could we devise a regime to helphim quit? In a well-addicted drug user,the major behavioral engineering task wouldseem to be to weaken B'. This is the statewhich energizes the strong escape and avoid-ance behaviors which terminate craving eachtime it occurs. The well-addicted druguser is exhibiting avoidance behavior muchof the time rather than escape behavior. Hewould rather not experience the B state; heindulges so frequently that he rarely lets itoccur, and if it occurs, he quickly gets ridof it with another dosage. However, inorder to weaken B', the addict must lessenthe constant, repeated challenges to the op-ponent process. One way is to stop arous-ing A, i.e., cold turkey withdrawal, totalcessation all at once. Another way is todecrease the intensity and frequency of Ainputs. In other words, fade out A by grad-ually cutting down on drug use.

There is an analogy in color vision. Takea saturated red, and very gradually diminishthe saturation until it is gray. A greenafterimage does not occur, but the time offade-out has to be equal to, or longer than,the duration of the green afterimage whenred is suddenly terminated rather than fadedout. If the time of fade-out is shorter thanthat, there will be a green afterimage be-cause some finite quantity of the opponentprocess will still be operative due to its ownintrinsic decay time. Therefore, reasoningby analogy, in order to weaken the b processin addiction by a fade-out technique, wemust first know how long the craving wouldhave lasted had the addict gone through coldturkey withdrawal until the craving had dis-appeared. This could be a very long time,


and it must be estimated. If the fade-outtechnique involves a gradual decrease ofdrug use frequency and amount, which lastsfor a shorter period than the cold turkeyperiod, the technique is bound to fail. Thatis because, after the last small dose is takenand terminated, the B' state would still comein strongly enough to energize behaviorleading to another redosage.

The opponent-process model warns ofstill another problem for the addict whowants to quit. Even if the drug user weresuccessful in reducing the amount of B,there is still the positive reinforcing effectof A to contend with. Together with so-cial reinforcers, it was probably importantinitially in reinforcing the user's behavior.Now the a process again has a chance to re-inforce drug use, because the quantitya — b\ gets larger as b gets smaller. Thus

a strong positive reinforcer (A) for druguse will again become available for any ex-perienced user late in the cold turkey with-drawal or the fade-out regimen. Thistrade-off, deduced by the model, makes the"kicking" of an addiction very difficult.Late in addiction, the aversive craving stateenergizes the behavior more forcefully, butafter partial withdrawal, the positively rein-forcing state reinforces the self-administra-tion operants.

How does one handle the problem ofcountering a positive reinforcer? First, bythe action of punishment. To weaken thedrug-use behavior at a time when |a — b\is large, punishment is one indicated alter-native. Punishment probably should not beused early in withdrawal, or early in fade-out, because the drug-use behavior is com-posed of avoidance and escape operantsdriven by the aversive B' (the withdrawalagony and craving). Punishment at thattime might intensify the operants, as it fre-quently does for any operants controlled byaversive states (the vicious circle phenome-non). Perhaps late in withdrawal, strongrewards for abstinence might be used to-gether with punishment for drug taking.But such rewards would have to be hedoni-cally stronger than is the drug-producedreward A at the time when a is strong andb is weak.

Another technique suggested by the op-ponent-process theory of motivation is theuse of antagonistic drugs. It should be pos-sible to break the addictive cycle with adrug which antagonizes or eliminates theaversive b process. The addict medicatedwith such a b process antagonist would stillexperience the pleasurable A state, but thewithdrawal agony and craving would begone. He might, under the impetus of othermotivational influences, become a casualuser rather than a driven addict. An evenmore effective therapy could be developedif we had two drugs, an o-process antago-nist as well as a ^-process antagonist. Theformer could be relatively short acting, butthe latter would have to be long acting inorder to counteract the long-lasting aversiveb process.

The opponent-process model deduces thatthere will be great difficulty in eliminatingthe addictive cycle. Even though all theconditions for weakening the b process areoptimal, trouble can ensue. In addiction,State B is aversive. If aversive B statesare not completely specific to their A states,then other aversive states might be reactedto as though they were the B state. A per-son who has reduced his craving by meansof protracted abstinence might respond tosome types of other aversive emotional statesas though they were intense craving states,thus remotivating the drug-seeking beha-vior. We need to know a great deal moreabout the narrowness of specificity of A andB states before addiction is satisfactorilyunderstood. The cross-tolerance phenome-non tells us that specificity in many casesis not narrow. For example, the alcoholaddict develops a strong cross tolerance tobarbiturates even though he does not usebarbiturates. Therefore, he requires alarger barbiturate dose to produce a speci-fied behavioral effect than he would if hehad not already acquired alcohol tolerance.The opponent-process model suggests thatthe b process elicited by the primary affec-tive consequences of alcohol is somehowsimilar to that elicited by barbiturates. Theopponent-process model is concerned withaffective and hedonic processes. Therefore,two drugs, no matter how chemically unre-


lated they may be, if they arouse very simi-lar affective states, will be candidates forcross tolerance. Furthermore, this reason-ing deduces that drug-aided withdrawaltreatments must fail if the drug used to an-tagonize the b process is one which itselfgenerates an affect similar to that producedby the original addictive agent. Finally, anaddict should be very quickly and easily ad-dicted to such a treatment drug. Thus,there are grave problems associated with theuse of ^-process antagonists.

There is another difficulty. The actionof CSA and CSs stimuli, whose propertieswere acquired over thousands of condition-ing events usually involved in long-standingaddiction, must be considered in the processof withdrawal and "cure." The CSn stimuliwill be conditioned arousers of B, the crav-ing. The CSA stimuli will be conditionedarousers of the positive reinforcing State A.A major problem during withdrawal oughtto be CSn events, the conditioned elicitorsof craving. They would be stimuli asso-ciated with the absence of the drug: nopushers, empty pockets, new surroundings,nonusers (they cannot offer you drugs), etc.Their presence should produce some degreeof conditioned craving.

It appears possible, at first glance, to useCSA stimuli to enable an addict to endureintense craving episodes. For example, anicotine addict might take out a pack ofcigarettes, take out a match, put a cigarettein his mouth, then suck on it without light-ing it, going through all the usual acts, in-cluding inhaling, blowing out, etc. Thiswould arouse a conditioned a process, andtherefore should temporarily result in lesscraving than that felt before these acts.However, when the acts are terminated,their aftereffect should be the appearance ofa conditioned B state which would be super-imposed on the existing unconditioned one.Then, of course, the craving should tem-porarily intensify. Once again, we see thatthe behavior of the addict is tightly hemmedin by processes, both conditioned and uncon-ditioned, which overdetermine the persis-tence of the behavior leading to a redose(Solomon & Corbit, 1973).

In conclusion, nature has devised a

powerful way of maintaining behavior whichinitially produces pleasure, even thougheventually the pleasurable consequences ofthe behavior may become minimal while theaversive consequences of absence of that be-havior become more pronounced. Weshould not expect a quick cure for addic-tion, then, until we learn how to suppress orantagonize both opponent processes.

The powerful control of behavior result-ing from repeated pleasures is not limitedto drug pleasures. Any intense pleasure,the termination of which is followed by anenduring aversive state, should lead to per-sistent, recurrent behavior that is extremelyhard to eliminate. Addiction is, therefore,a possible consequence of any repeatedpleasure.

Drug addiction is not the only behavioralphenomenon simply organized by an oppo-nent-process model. We cannot examineall of these cases in detail, but we are cer-tain that the reader in each case can de-velop the explanations imposed by the op-ponent-process model. One example is thereinforcing electrical stimulation of thebrain. Assume only that the onset of suchstimulation produces a pleasurable A stateand that the sudden termination of the samestimulation reveals an aversive B statewhich is of relatively short duration (about30 seconds). Another example is imprint-ing in precocial birds. Assume only thatthe sight of a moving white object arousesan unconditioned A state which is a strongpositive reinforcer and that the removal ofthat object reveals a very aversive, long-lasting B state which intensifies rapidly withrepeated elicitation. All of the known dataon both distress calling in ducklings andfollowing behavior (as well as other oper-ants) are simply explained (Hoffman &Solomon, 1974). Indeed, most of the majorphenomena of human attachment behaviorare subsumed in this analysis.

Aversive Learning and Performance

We have previously presented evidencethat both A states and B states are condi-tionable. Stimuli directly preceding thepeak of A will become CSAs for the elicita-


tion of a conditioned A state. Stimuli di-rectly preceding the peak of B will becomeCSsS for the elicitation of a conditioned Bstate. We have been referring to hedonicor affective processes, and so our condi-tioned A states, in the case of shocks, willbe conditioned aversive states (fears). Ourconditioned B states, in the case of termina-tion of shocks, will be conditioned pleasurestates (happiness, relief, euphoria, exhilara-tion). The onset of the A state will nega-tively reinforce operants while the onsetof the B state will positively reinforceoperants.

The assumptions about the conditionabil-ity of opponent processes suggest a reinter-pretation of escape and avoidance learningand extinction. On the first few avoidancetraining trials, the aversive A state will bevery intense, and its onset will energize avariety of escape behaviors. If signalizedshocks are used, the signal will quickly be-come a conditioned A-state elicitor. If aSidman, unsignalized, training procedure isused, the responses or acts of "staying still"or "doing the incorrect thing" will becomeconditioned A-state elicitors, and so longbursts of energetic activity will ensue.Early in training, shock termination willresult in a weak b process, without muchpositively reinforcing effect, and it will fadequickly.

As shocks are repeated, two affective pro-cesses will evolve. First, the shocks willdecrease in their aversiveness as the oppo-nent b process strengthens. Second, thepositively reinforcing effect of the B statewill increase, so that successful operantswill have an opportunity to be reinforcedby two events, the termination of the aver-sive A state and the onset of the pleasurableB state. These operants will be circum-scribed, as contrasted with the wild, disor-ganized, quickly altering bursts of behavioroccurring during the first few shocks. Fur-thermore, if the b process strengthens veryquickly, some subjects will not learn. Theywill be the failures so frequently referredto in footnotes (see Turner & Solomon,1962). They will become "used to "shocksbefore B-state reinforcement can accuratelyselect the successful avoidance response for

them. Their behavior will first be chaotic.Then they will appear to "give up" and be-come unresponsive to shocks. They willact as if shocks no longer "bother" themvery much. Probably they do not.

Provided that the responses narrow downsufficiently to those successful in preventingshocks, a new stage of learning will ensue.Inactivity and other danger signals will con-trol a conditioned aversive A state. Thecorrect avoidance response will control theappearance of the peak of B, the pure Bstate. The b process will be furtherstrengthened by the repeated elicitation ofconditioned A states even when the shocksare no longer experienced. The A stateconditioning will then start to extinguishdue to the nonoccurrence of the shocks.Meanwhile, the correct avoidance responsewill continue to be reinforced, differentiated,and perfected as an automatic act, as longas it will produce the pleasant B state. Atthis point the subject's behavior will haveother attributes, too. Because the condi-tioned aversiveness of all stimuli in thetraining situation is now extinguishing, thesubject may willingly enter the experimentalroom and apparatus. He will perform hisavoidance behavior without signs of fear.Yet he will appear overjoyed when thetraining session is over. This reflects boththe weakening of conditioned A and thecontinued strength of unconditioned andconditioned B. The subject has a newsource of positive reinforcement in his en-vironment, the CSu (see Weisman & Lit-ner, 1969a). As Weisman and Litner(1969b) have shown, the CSBs have thepower to reinforce new operants. They are,then, conditioned stimuli for a B state whichis pleasurable. These stimuli must be serv-ing a function like that of the correct beha-vior of the ski-jumper which produces anexhilaration mood when the danger is over.Another example is that of the parachutists(Epstein, 1967).

The model predicts that avoidance beha-vior will eventually extinguish, but may takea long time. Extinction may, as Hulliansclaim, be motivated only by the aversivenessof effort, but the contrary aversive forcesare also great. Should the subject fail to


perform a correct avoidance response dur-ing an extinction series, he will reinstate apowerful C$A which has not been experi-enced since the early training trials. Arou-sal of the A state will then strengthen theb process further. Because no shocks oc-cur, the conditioned A state will weaken.The aversiveness of failing to perform theavoidance operant will consequently decrease.

Avoidance behavior will cease only whenall response-produced and external dangersignals no longer produce an aversive Astate strong enough to energize the avoid-ance behavior. The more effortful the be-havior, the sooner this should happen. Thesooner this happens, the more likely is thesubject to appear to be frightened by hisown inactivity even though he fails to re-spond. Toward the end of an extinctionseries, then, behavior should be variable. Along "vacation" away from the training situ-ation would weaken the b process, so (a —b) would increase and frequent "spon-taneous recoveries" should be seen, withavoidances occurring early in a new session.At the same time, the joyous behavior,which once characterized the end of a ses-sion, should disappear. Sources of positiveaffect thus dry up late in the extinction ofavoidance responding, but sources of aver-sive affect are still lurking and are rela-tively weak. There should be no suchphenomenon as extinction of avoidancebehavior with equanimity.

Most of these phenomena deduced froman opponent-process model have occurredat one time or another in avoidance-trainingexperiments, but they have tended to beoverlooked or ignored by most writers, in-cluding one of us (Solomon & Brush, 1956;Solomon & Wynne, 1953; Turner & Solo-mon, 1962).

The analysis of escape and avoidancelearning and performance in terms of op-ponent-process theory has generality be-yond the mere habituation to electricalshocks in the laboratory. The intense aver-siveness of the first free fall through space,the first exposure to the intense heat of asauna bath, the first ski jump, or the firstkilling of another man in war might initiallysuggest that escape and avoidance behavior

would occur. Instead, the subject oftenperseveres in re-exposing himself to theaversive event. He looks like the rat whichfails to learn to avoid shocks in the labora-tory and appears to be "unmoved" by thoseshocks. Why would these failures of es-cape and avoidance occur? There must besome outside motivational influence whichkeeps the subject in the aversive situationlong enough to allow the strengthening ofthe b process. Once this has occurred, thequantity (a — b) is reduced and the B stateafter stimulus termination is more pleasur-able and long lasting. There is then a rea-sonable trade-off between the immediate oc-currence of the weakened, aversive A stateand the somewhat delayed occurrence of thestrengthened, pleasurable B state. Accord-ing to our theoretical model, many seem-ingly masochistic behaviors should have theetiology we have described.

A STATES WHICH HAVE LITTLE ORNo OPPONENT PROCESS

A few hedonic disequilibriums may causevery little corrective, oppositional reactionin the nervous system. A nonopposed sys-tem would manifest no peak of the A state,no adaptation, and no appearance of a Bstate after stimulus termination. One possi-ble example is the hedonic state engenderedby marijuana. As a chemical stimulus itprecipitates a mildly pleasurable A state.However, there is no reported peak or adap-tation, nor are there aversive withdrawalsymptoms or craving. Furthermore, toler-ance often does not develop with repeateddosages. The concommitance of all theseattributes would be exactly what the oppo-nent-process model would predict for apleasure without an opponent. Nausea isan example of an aversive A state whichmay have no opponent B state. Perhapssome aesthetic pleasures have no opponentprocess.

We have already talked about the varia-tions in the intensity and duration of Bstates as a function of the particular kind ofA state elicited. For example, we men-tioned the intense and long-lasting aversiveB states in the cases of grief and opiate


withdrawal. In contrast, we mentioned therelatively short duration of B states asso-ciated with the taste of M & Ms and pea-nuts, and rewarding electrical stimulationof the brain. In addition to these inherentvariations in intensity and duration of Bstates elicited by different types of stimuli,repeated elicitation causes large changes inthe intensity and duration of B states insome cases and not in others. Therefore,differences in the initial strength of b pro-cesses must reflect a parameter of ourmodel, and the effects of repeated elicitationof A states must operate on this parameter.In the case of A states having no opponentprocess, the value of the parameter is zero.

We have been constantly amazed by thehuge variations in the strengths and dura-tions of different b processes after repeatedelicitations. Some b processes, even whenwell exercised, last but a few minutes.Some examples are taste cravings, the aver-sive b process for electrical stimulation ofthe brain, cardiac deceleration after shocktermination, the "fit of joy" when the dog isreleased from a shock box, etc. Some lasta few hours. Examples are the exhilarationfollowing dangerous or endurance-challeng-ing exercise, or distress calling in precocialbirds when the imprinting object is gone.Yet others last for months. Examples areloneliness and grief, craving following with-drawal from either opiates, alcohol, or bar-biturates.

At first glance it may appear that we havecompletely undercut our theory. We havespeculated that some A states may notarouse B states, and we have provided noprinciples by which one could designate inadvance whether or not a particular A statewould be a part of an opponent-process pair.At present, we look on this as an empiricalproblem, and we use the following argu-ment. Opponent processes defend a hedonicequilibrium. They are part of the biologi-cal defense system mediated by the brain.In the realm of foreign body reactions tobacteria, viruses, and poisons we often candetect defense systems. Indeed, the actionsof antigens and antibody formation bearmany resemblances to the opponent-processsystems we have described. However, not

all poisons and not all foreign bodies engen-der defense reactions. We can be defense-less. These substances are, therefore, calleddeadly poisons. We think the same situa-tion holds in the defense of hedonic equi-librium, and so we should not be surprisedto discover that a given A state goes rela-tively unopposed. Perhaps one day we willhave a theoretical rationale for the param-eter and operator involved here.

DISCUSSION

We have argued that there are certainsystems in the brain, the business of whichis to suppress or reduce all excursions fromhedonic neutrality, whether those excursionsbe appetitive or aversive, pleasant or un-pleasant. The systems operate to decreasethe intensity of subjective "hedonic qual-ity," "affect," "emotion," "arousal," or theobjective reinforcing properties of stimuli.The systems function independently of oper-ants or instrumental acts. They are fullyautomatic. Thus, whereas operants tend tomaximize positive reinforcement and tominimize negative reinforcement, the affect-controlling systems of the central nervoussystem minimize both. They are broughtinto play whenever significant departuresfrom affective equilibrium occur as a con-sequence of stimulation onset and mainte-nance. When such a system is effective, itwill reduce the intensity of the affective ex-perience even while the input is still there.This reduction will be manifest for bothpositive and negative reinforcers, and forpleasant and unpleasant stimuli. The theo-retical model refers to both subjective andobjective psychological phenomena.

Reduction in affective or hedonic inten-sity is postulated to be brought about bythe activation of an opponent loop, precipi-tated into action whenever affective, hedonic,or emotional states are aroused. The op-ponent loop opposes the stimulus-arousedaffective state. Furthermore, the opponentprocess is postulated to be sluggish in itslatency, recruitment, and decay (a heavilydamped circuit, an inertia-laden system).The opponent loop itself is postulated togenerate an hedonic process which is, in


some abstract sense, the opposite to thatprecipitated by the stimulus input whichhas initially aroused affect. The opponentprocess will manifest its quality and inten-sity when the stimulus is suddenly termi-nated. The persistence of the opponentprocess will be seen for some time becauseof its sluggish decay property.

Furthermore, we have postulated that theopponent process is strengthened throughuse and weakened through disuse. Thesechanges are nonassociative in nature. Thismakes the affect-control systems similar tosome immunological mechanisms in theirproperties.

Even though the model is not yet as pre-cise as some mathematical models, from it,nevertheless, one can unambiguously de-duce many of the known phenomena of ac-quired motivation. As examples of this, wehave illustrated in detail how the model or-ganizes information on aversive behaviorcontrol and the drug addictions.

The theory postulates no conditioning orlearning mechanisms responsible for the oc-currence of the acquired motivations wehave discussed. The acquisition is auto-matic, merely by virtue of the repeated oc-currence of affect-producing stimuli. How-ever, the interrelationships between theaffect-control mechanisms and Pavlovianconditioning processes, and the interrela-tions of both with operant behavior, arediscussed.

The novel feature of the opponent-pro-cess theory is that it sees the behavioralphenomenon of addiction as an empiricalmodel for all acquired motivation. Addic-tion is not viewed as an abnormality. In-stead, it is the inevitable consequence of anormally functioning system which opposesaffective or hedonic states. We assume, forexample, that love is an addiction phenome-non characterized by habituation to thepresence of the loved one and intensifiedaversion in the absence of the loved one.In the same vein, we assume that imprintingin precocial birds is an addiction phenome-non. In the case of aversive stimulation,we assume that masochistic phenomena arethe consequence of a normally functioningsystem which opposes affect. These phe-

nomena are characterized by habituation tothe presence of the feared or unpleasantevent and intensified pleasure after the ter-mination of that event.

Finally, we have pointed out some newlines of empirical research suggested by theopponent-process theory of motivation.

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(Received May 29, 1973)

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