Psychology Article 101

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Journal of Comparative an d Physiological Psychology1969,Vol. 67, No. 4,407-414INHIBITION OF FOOD INTAKE BY A HUMORALFACTOR1

JOHN D. DAVIS,2 ROBERT J. GALLAGHER, ROBERT F. LADOVE, ANDANDREW J. TURAUSKYUniversity o f Illinois at Chicago Circle

Intake of milk by fasted rats was reduced 50 % below normal after theirblood ha d been transfused with that ofsatiated rats. Bar pressing contin-uously reinforced by dry-food pellets wasreduced to approximately 60%of normal following similar transfusion. Milk intake and bar pressing wasnot reduced when transfusionwasbetweenapair offastedrats.B ar pressingreinforced on avariable intervalschedulewasunaffected by transfusion be-tweenfasted-trained rats andsatiatedrats. In no casewas food intake bysatiated rats elevatedfollowingtransfusion with fasted rats.

Most theories of hunger assume thatchemicals circulating in the blood play acentral role in the control of food intake.The glucostat (Bulatao & Carlson, 1924a,1924b), the lipostat (Kennedy, 1952), andthe aminostat (Ugolev & Kassil, 1961)theories assume monitoring by the centralnervous system of glucose, lipid, or pro-tein reserves of the body, respectively.When these reserves are low,quantitiesofthese substances or products of theirmetabolism are assumed to below, leadingto activation of a feeding center. Yet inspite of a number of attempts to demon-strate such control (Alexeseva, 1958; Her-vey, 1959; Janowitz, Hanson, & Bross-man , 1949; Miller, 1961; Siegal & Taub,1952) the authors are aware of no directdemonstration of a humoral regulatorymechanism that controls the ingestion offood. In the absence of such informationsomeimportant questions about the controlof foodintake remain unanswered.Is food intake regulated by a hungerhormone which activates feeding centerswhen it reaches threshold levels, or is itregulated by a satiety hormone whichterminates feeding when it reaches athreshold level? Is feeding regulated bythe interaction of both a hunger and asatiety hormone (or humoral factor) act-ing through central nervous system regu-latory centers in an algebraically summa-tive fashion? Or is food intake regulated

' Supported in part by National Institute ofMenta lHealth Grant MH-12107.2Requests fo r reprints should be sent to JohnD. Davis, Department of Psychology, Box 4348,UniversityofChicago, Chicago, Illinois 60680.

principally through the joint interactionof olfactory, gustatory, gastric, and otherextrahumoral mechanisms?Answers to these and other relatedquestions can best be provided by bloodt ransfusion experiments in whichthe bloodof a hungry and a satiated animal iscrossed. If the bloodofhungry andsatiatedanimals differ with respect to hunger orsatiety factors, crossing blood betweensuch animals should affect their subsequentfood intake. Following crossing a satietyfactor in theblood should causethe hungryanimal to eat less, and a hunger factorshould cause a satiated animal to eatmore.Previous blood-crossing techniques usingparabiotic preparations or blood transfu-sions under anesthesia are unsuitable fo ran investigation of this sort. The parabi-otic preparation, while permitting thedemonstration ofhumoral control, does notpermit an easy quantification of resultingeffects because of the difficulty of deter-mining the rateorquantity of exchangeofspecific humoral factors. Furthermore, it isnot possible, with this technique, to inde-pendently control the blood compositionofthe two members of the pair prior to anexperimental evaluation of differences inblood composition. Blood transfusion un-der anesthesia does not permit behavioralevaluation of the transfusion until theeffects of anesthesia have worn off, atwhich time all effects of the transfusionmay have disappeared aswell.To circumvent these problems, a tech-nique was developed in collaboration withNeal Miller to directly investigate the

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Copyright 1969by theAmerican Psychological Association, Inc.


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408 DAVIS, GALLAGHER, LADOVE, AND TURAUSKYrole humoral factors play in the controlof food intake (Davis & Miller, 1966).By means of this technique it is possibleto cross the blood of a pair of unanesthe-tizedratsand immediately followingtrans-fusion determine th e effect of the trans-fusion on the behavior of the animal. Theexperiments described below utilizing thistechnique suggestthat food intakeisregu-lated in part by humoral satiety ratherthanhunger factors.

METHODSubjects

Male albino Sprague-Dawley strain rats, 90-150days old at the beginning of the experiment, wereused throughout.Procedure

Since the transfusion technique is described indetail elsewhere (Davis & Miller, 1966) only abrief accou nt is given here.Tw o days prior to blood tr ans fus ion, siliconerubber cannulas were implanted under pentobarbi-tal anesthesia. The cannulas (.025 in. OD X .047in .ID, Dow Corning Silastic medical grade tubingNo. 602-155) entered the right extern al jug ula rvein 2-3 mm. anterior to the point whereit passesbeneath the pectoral muscle. The cannulas ex-tended 32-38 mm. into th e vein (length adjustedto the size of the animal), terminating in or nearthe hear t . The distal portion of the cannula wasthreaded subcutaneously along the ventral mid-line, up along the right side of the animal, an demerged through an incision on the back. Thecannula was filled with normal saline before im-plantingand wassealed with a plug at thecomple-tionof the operation.During the course of these exper iments tw omodifications were introduced that greatly in-creased the ease of construction of the cannulasand extended their useful life considerably. Neitherof these modifications would be expected to, norappeared to have any effect on the outcome ofthe experiments. The first improvement was amodification in the technique of constructing thecannulas.Theywereconstructedby joininga4-cm.lengthof the No. 602-155 Silastic tubing (.025in. ID) toa 20-cm. length of polyethylene (Intramedic P.E.60) tubing. To assure a firm connection,the poly-ethylene tubingwas flaredslightly at one endwithheat and the silicone tubing was worked over theflared end. This ca n only be done if the siliconetubing is softened first by soaking it in trichloro-ethelene for a minute or so. In this softened stateit can easily be slipped over the flared end of thepolyethylene. Afterthesolventhas evaporated thesilicone tubing returns to its original state and

forms a tight seal around the polyethylene. A Uis then formed in the polyethylene and anchorthreads are attached as previously described(Weeks Davis,1964).The second improvement, suggested by AntonSteffans,8 considerably extended the useful lifeof th e cannulas by preventing blood-clot forma-tion in the lumen and at the tip of the cannula.This was achieved by filling the cannula, afterimplantation, with a solution consisting of 10-ml.heparin (1,000 unitsper ml.) and 8-gm. polyvinyl-pyrrolidone.This viscous solution keeps blood from clottingwithinthe venous portion of the cannula, is viscousenough not to be pumped into the blood streamwhen the distal end of the cannula is open, andcan be withdrawn easily prior to transfusion. Afterthe cannula was filledwith thissolution the distalend of the cannula was sealed by m elting it withth e heat of a match and then clamping it withforceps. Prior to transfusion this seal was cuto f f and the polyvinylpyrrolidone-heparin solutionwaswithdrawn.Immediately prior to transfusion bothratswereinjected via the cannulas with heparin (.15 ml.,1,000 units per ml.) . The rats were then insertedhead first into round cardboard restraining holdersmounted side by side. The distal ends of thecannulas were attached to a silicone rubber-valvesystem which in turn was connected to a pair ofplastic syringes. The valve system permitted th eblood of each animal to be drawn into a syringeand then injec ted into the opposite animal withoutexposingit to air.Blood was withdrawn from each animal 2 ml.at a time and wasthen injected into th e oppositeanimal at the ra te of 1-2 ml. per minute. A totalof 26 ml. of blood was mixed in this way, enoughto assure complete mixing of the blood of the twoanimals.At the end of transfusion approximately50% of the blood of each animal was its own and50% was its partner's. Immediately followingtrans-fusion each animal was given access to food for30 min.

These procedures were followed in all of theexperiments to be described below. The individualexperiments differed with respect to the depriva-tion and satiation conditions, the nature of thefood ingested, and the means by which the animalobtained thefood.EXPEEIMENT 1

This experiments (previously publishedby Davis, Gallagher, & Ladove, 1967)was designed to determine if a satietyfactor could be demonstrated to exist inth e blood of rats maintained on ad-libfeeding conditions, and if a hunger fac torexisted in the blood of rats maintained ona 23i/2-hr. feeding schedule. Sixteen pairs

3Personal com mu nication, 1967.


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HUMORAL FACTORS IN FOOD INTAKE 409of rats were adapted to a feeding schedulefor 10days. One member of eachpair wasgiven ad-lib access to diluted condensedmilk (two parts milk to onepartwater);the other had access to this diet for 30min. in each 24 hr. Continuous access towater was available at all times. Duringthis adaptation period the intake of bothgroups of animals was recorded. By thefifth day the daily and 30-min. intakeshad stabil ized.On the experimental day the blood of apa ir ofrats, onedeprived and onesatiated,was mixed 30 min. beforethe deprived ratwas usually fed. Immediately followingtransfu sion both animals w ere given accessto the diluted condensed milk for 30 min.,and the amount ingestedwasrecorded.The mean intake and SD of the distri-bution of intakes of the 16 deprived ani-mals in the 30-min. feeding period on theday prior to blood mixingwas 15.8 ml. and5.2ml., respectively.The mean intake andSD of these same animals in the 30 min.immediately following blood mixing was8.0 ml. and 5.9 ml., respectively. The dif-ference in the mean intake on these twosuccessive days representing a 50% reduc-tion is statistically significant (t 4.01,p


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410 DAVIS, GALLAGHER, LADOVE, AND TTJRAUSKY

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N O R M A L A F T E RM I X I N G

N O R M A L A F T E RM I X I N G

FIG. 1. Mean intake in 30min. by the deprivedanimals. (On the left, a, the mean intake on theday prior to transfusion, normal, is compared withthe mean intake of the same animals immediatelyfollowing the mixing of theirblood with satiateddonors, after mixing. On the right, b, the samecomparison is made for animals where blood wasmixed with the blood of 24-hr, deprived donors.This figure was previously published in Davis,Gallagher, and Ladone, 1967. Copyr igh t 1967 bythe American Association for the AdvancementofScience.)schedule and deprived rats trained to ac-quire their daily food ration in30-min.con-tinuous-reinforcement operant bar-pressingsessions with food-pellet reinforcement.Eleven pairs of rats were used. Onemember of each pair ha d continuous freeaccess to Purina Mouse Breeder Chow,the other wastrained to bar pressfor P. J.Noyes standard 45-mg. reinforcement pel-lets on a continuous-reinforcement sched-ule. No food other than that obtained inthe operant box was given these animals.Magazine training and shaping required2-3days.Thereafter, theanimals wererunin daily 30-min. sessions until daily bar-pressing rates had stabilized. Ten dayswere usually sufficient fo r this training.Twodaysafter cannulaimplantationtrans-fusions were carried out in the usual man-ner between a satiated rat and a trained-hungry rat 30 min. before the latter wasnormally run in the operant box. Im-mediately after transfusion the deprived

rat was run for 30 min. in the operantbox and the total number of responsesemittedwas recorded.The mean number of responses madebytheseanimals on the daypriortotrans-fusion was 135 (SD = 40.0). The meanresponse rate of these same animals im -mediately following transfusion was 80(SD = 37.0). The difference in responserate, which represents a 59% reduction inbar-pressing rate, is statistically signifi-cant (t - 2.82,p .10).The results obtained with bar pressingand dry food replicate those obtainedwith drinking diluted condensed milk, al-though the effect obtained using bar press-ing was smaller than that obtained withdrinking (59% reduction in bar pressingcompared with 50% reduction in milk in-take following transfusion). Nevertheless,these results indicate that the satiety ef-fect produced by mixing the blood ofsatiated and hungry rats is not unique toeither the type of food or response meas-ureusedinExperiments 1 and 2.

E X P E R I M E N T 4Miller (1957) has shown that measuresof hunger depending principally on theamount of food consumed do not always

agree with other measures of hunger.Miller's quinine aversion test and rateof bar pressing on a variable intervalschedule of reinforcement both showedan increasing relation to hours of depriva-


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HUMORAL FACTORSIN FOOD INTAKE 411tion over the range 0-54 hr. deprivation,whereas volume of milk consumed becameasymptotic at about 6 hr. of food depriva-tion. Thus, the quinine aversion test andoperant responding on a variable intervalre inforcement schedule appear to be moresensitive measures of hunger asdenned byhours of food deprivation than does totalamount consumed in a limited period oftime. This greater sensitivity to food dep-rivation of intermittently reinforced barpressing suggests that such a responsemeasure might also be more sensitive toblood transfusion effects than the volumeof food ingested.

Thirteen pairs of rats were used. Onemember of each pair had continuous freeaccess to Purina Mouse Breeder Chow.The other wastrained to bar press in anoperant box for P. J. Noyes standard 45-mg. food pellets. Following 1 day ofmagazine training, each animal was given2 days of training on a continuous-rein-forcement schedule followed by eight daily30-min. training sessions on a VI 30-sec.re inforcement schedule. Cannulas wereimplanted 2 days before transfusion w asto becarried out, and the transfusion wasbegun 30min. before th e animal was usu-allyrun in theoperant box.The mean 30-min. response rate of thetrained animals immediately followingt ransfusion was 237(SD =81.2) responses.The mean number made on the previousday, 48 hr. after operation, was 218(SD =108.6). The animals were run on the dayfollowing transfusion in order to providean additional estimate of their normalbar-pressing rate. The mean rate of re-sponse onthat day was 267 (SD = 99.7)responses. Statistical comparison of theposttransfusion rates with both of theseestimates of normal response rates wasnot significant (t = 1.27, p > .10; t 2.10,p > .05).Intermittently reinforced bar-pressingrate which appears to be a sensitive in-dex of motivational level in some situa-tions appears to be quite insensitive to ablood transfusion procedure that produceslarge reductions in continuously reinforcedbar-pressing rate. This result suggeststhat

the blood factors responsible fo r reducingintakedo not behave asmotivational vari-ables in the sense that they modify theeffort expendedinobtaining food.DISCUSSION

For many years a hunger hormonehasbeen assumed to exist and has frequentlybeen linked with carbohydrate metabolism.Luckhardt and Carlson (1915) demon-strated the existence of a stomach motilityactivating factor present in the blood of afasted dog,and Bash (1939) later reportedthat th e normalactivity of the stomachofa fasted dog could be inhibited by bloodtransfusions from a satiated dog. In otherstudies it wasshownthat intravenous glu-cose infusions inhibited the gastric ac-tivity of a fas ted dog, and that insulininfusions decreased this activity (Bulatao& Carlson, 1924a, 1924b). These studiescombined with the theory of hunger whichheld that the activity of the stomachwasresponsible for the sensations of hunger,and thus presumably food intake (Cannon& Washburn, 1912),provided the basis forthe postulation of a hunger hormone. Theargument w as straightforward. Stomachmotility is an index of hunger. Stomachmotility is under the control of humoralfactors , therefore these factors are respon-siblefor the controlofhunger.Cannon's theory (Cannon &Washburn,1912) has now been rejected largely be-cause of accumulated evidence showingthat animals with denervated stomachs(Grossman, Cummins, &Ivy, 1947), or nostomachs at all (Ingelfinger, 1944; Mac-Donald, Ingelfinger, &Belding, 1947), canregulate food intake in such a way thatnutritional requirements are met. Clearlyfeedback from gastric activity is not theessential controlling element of food in-take. Whether or not the humoral fac-torsthat regulate stomachactivityactalsoon CNS centers to control food intake isa matter on which the evidence providedby Carlson and his students (Bulatao &Carlson, 1924a, 1924b; Luckhardt &Carl-son, 1915) shedsnolight,sincetheir experi-mental animals were anesthetized and food


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412 DAVIS, GALLAGHER, LADOVE,AND TUKAUSKYintake following transfusions could not bemeasured .It thus seems clear that prior evidencefor a hunger hormonerests on the tenuousfoundat ion of a discredited theory ofhunger. More recently, views about theconcept of hunger have changed and few,if any, todayarewilling to identify hungersolely as the activity of a gastrointestinalorgan, the verbal expression of a sub-jective state, or any other single responseof an organism to astateof food depriva-tion. Hunger now has a broader descrip-tive base. It implies not only the activityof the internal organs of the bodythat haveevolved to process food, but also the be-havior of the organism that is involved inidentifying, selecting, and ingesting food.The demonstration of a hunger hormonemust thereforebe based on evidence show-ing control of ingestion, in addition to con-trol of the mechanisms that process theingested food.The results of the studies reported hereprovide direct evidence for the existenceofa humoral factor (or factors) that playsan inhibitory role in the regulationof foodintake. These results show consistentlythat food intake can be inhibited byhumoral factors that appea r to be gener-ated by states of satiety. They also showthat food intake by satiated rats is notelevated when their blood is t ransfusedwith that of deprived rats. These latterresults were quite unexpected.There are a number of reasons for ex-pecting an elevation of intake by satiatedrats following a blood transfusion with de-prived ones. If food intake is regulated bya hu mora l excitatory factor , then it shouldbe t r ans fe r r ed from the deprived animalduring the transfusion and initiate feed-ing in the satiated animal. If, on the otherhand , food intake is regulated by humoralinhibitory factors these factors should havebeen diluted by the transfusion. In eithercase the satiated partners would be ex-pected to eat more than they did in thepost t ransfusion period.Although the control studies reportedabove in which transfusions were carriedout between pairs of 23i/2-hr. deprived ani-mals seem to indicate that the t ransfusion

procedure itself does not lead to a de-pression of food intake, it is still possiblethat thereis an artifact present which onlyappears in the intake measures of less-hungry animals. If the strength of eatingbehavior is relatively weak, as it is insatiated animals, then manipulation of theblood by itself might have further reducedthis tendency to eat, an ar t i fac t that isoverwhelmed by the much stronger feed-in g behavior of the 23i/2-hr.food-deprivedanimals. The technique is a new one, andfurther research with it should provide abasisfor evaluating this possibility.Onthe other hand,the fai lure to elevatethe food intake of the satiated membersof th e pairs of animals may not be arti-fac tua l , but may be a real effect that canprovide information about the way thatthe feeding mechanism works.One view that is consistent with thepresent results is that the feeding mecha-nism is controlled principally by inhibitoryfeedback from satiety signals. It is sug-gested that in the absence of inhibitoryinput to the feeding centers environmentalstimuliactivatethe feedingsystem and theanimal eats. During th e course of eating,oral, gastric, and humoral satiety signalsaccumula te and when the sum of these in -fluences reaches a critical threshold levelfeeding is terminated. If feeding cannot be-gin again until the sum of all the inhibitorysignals acting on the feeding center fallsbelow the critical threshold level, thenlowering the level of one of these satietysignals by itself may not be sufficient initself to release the feeding center to per-m it feeding. Although the humora l satietyfactor in the satiated par tners was pre-sumably diluted by approximately 50% asa result of the transfusion, it is conceivablethat some other satiety signal, such asfeedback from the partially full stomachsof these animals, exerted sufficient inhibi-torycontrol overthe feeding center to pre-vent feeding.

Another possible explanation for theseresults isthat in an animal main ta ined onan ad-lib feed ing schedule, there may be aconstant elaboration of humoral sat ietyfac tors that are replaced by the organismas they are removed during th e courseo f


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HUMORAL FACTORS IN FOOD INTAKE 413a transfusion. Indeed, it seems quite un-likely that humoral satiety factors elabo-rated endogenously and removed artifi-cially would not be replaced by theirsource as along as the animal remains innutri t ional balance. It may have beenthatthesatiatedpartnerm aintained arela-tively constant levelof thesatiety fac torinspite of the fact that it was being re-moved by the transfusion. Even if itweren ' t maintained at a constant level itmay have been maintained at a level suf-ficiently high to inhibit the initiation offeeding.An example of such a mechanism and apossible explanation of the results reportedhere is suggested by studies recently re-ported by Schally, Kedding, Lucien, &Meyer (1967). They showed that entero-gasterone, a hormone released by theduodenum in response to fats and sugars,when injected into fasted mice signifi-cantly reduced their food .intake. It ispossible that enterogastrone, releasedphysiologically during the course of diges-tion, was t ransfer red from the satiatedanimal to the deprived one and was re-sponsible for the inhibition of food intakeinthelatter. It isalso possiblethat entero-gastrone removed from the satiated ani-mal by the transfusion was replaced byits duodenum and thus continued to in-hibititsfeeding.These interpretations are admittedlyspeculative. There is no direct evidence atpresent to substantiate them. They areoffered as plausible explanations of thefai lure to activate feeding in the satiatedanimals and are consistent with the veiwthat humoral feeding factors exist prin-cipally as inhibitory rather than excitatoryfeeding signals.Another question raised by these stud-ie s concerns the fa i lu re to observe a re-duction in the response rate reinforced onan intermittent schedule. The different re-sults obtained with the continuous andvar iable schedules may be due to the fac tthat with the continuous-reinforcementschedule the animals becomesatiated dur-in g the experimental period, whereas onthe VI schedule they could obtain atmost 60 45-mg. food pellets during the

session, a little more than the amoun tusually obtained on continuous reinforce-ment. If the humoral satiety factor actedto set an upper limit on the amount offood ingested, and if that upper limit isgreater than 3.6 gm. ( the maximumamount of food that can be ingested on aVI 30-sec. schedule with 45-mg. pelletsduring a 30-min. experimental session),then blood transfusion would not be ex-pected to reduce bar-pressing rate. Theamount of food ingested never got closeto the newlowered limitset by thehumora lsatiety factor. Further research will benecessary to evaluate this interpretation.These results, however, suggest that thehumoral satiety factor does not operate onthe motivational state of the organism inthe same w ay that amount of deprivation(Clark, 1958) or magni tude of re inforce-ment (Hutt,1954) does.The demonstrat ion of a hu m o ra lsatietyfactor raises the question of the natureof such a factor, a question on whichthere has been much speculat ion. Theseresults do not provide an answer to thisquestion. The factor couldbe a direct prod-uct of absorption from the small intes-tine, it could be a hormone such as gluca-gon (Penick & Smith, 1964) or en-terogastrone (Schallyet al., 1967), it maybe some link in the intermediate metabo-lism of carbohydra tes , fa ts , or proteins,or, as suggested by TJgolev and Kassil(1961), some link in the final commonmetabolic pa thway of these substances, th eKrebs oxidation cycle. Nevertheless, thesuccessful demonstrat ion of a satiety f a c -tor through direct blood transfusion be-tween hungry and satiated animals pro-vides a first step in the direction ofult imately identifying such a factor. Rela-tively simple modification of this tech-nique combined with established bloodf ract ionat ion procedures m ay provide theanswertothislong-debated question.

REFERENCESA L E X E S E V A T. T. Nervous and humora lfactors inthe maintenance of alimentary excitability inconjoined twins. Sechenov Physiology: Jour-nal of the USSR,1958, 44, 259-304.BASH, K. W. An investigation into a possible or-


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414 DAVIS, GALLAGHER, LADOVE, AND TURAUSKYganio basis for the hunger drive. Journal o fComparative Psychology 1939, 28, 109-134.

B U L A T A O E., & C A E L S O N A. J. The relation ofbloodsugarto thegastrichunger contraction. Ameri-can Journal ofPhysiology 1924,68, 148. (a)B U L A T A O E., & C A R L S O N A. J. Contributions toth e physiology of the stomach: Influence ofexperimental changesin blood sugar level onthe gastric hunger contraction. American Jour-nal o f Physiology 1924,69, 107-115. (b)C A N N O N W. B., & W A S H B U R N A. L. An explana-tion of hunger. American Journal o f Physiol-o g y 1912,29 444-454.C L A R K F. C. The effect of deprivation and fre-quency of reinforcement on variable intervalresponding.Journal o f th eExperimental Analy-sis of Behavior 1958, 1, 221-228.DAVIS, J. D., G A L L A G H E R R.J., & L A D O V E R. Foodintake controlled by a blood factor . Science1 9 6 7 156, 1247-1248.DAVIS, J. D., & MILLBH, N. E. A technique formixing the blood ofunanesthetized rats. Jour-na l of Applied Physiology 1966, 21, 1873-

1 8 7 4 .G R O S S M A N M. I., C U M M IN S G. M., IVY,A. C.The effect of insulin on food intake aftervagotomy and sympathectomy. AmericanJournal of Physiology, 1947, 149, 100-102.H E R V E Y G. R. The effects of lesions in the hypo-thalamus in parabiotic rats.Journal o f Physi-

ology,London, 1959, 145, 336-352.HUTT, P. J. Rate of bar pressing as a functionofquality and quantity of food reward.Journalo f Comparative and Physiological Psychology1 9 5 4 47, 235-239.

I N G B L F I N G E R F. J. Late effects of total and sub-total gastrectomy. New England Journal ofMedicine 1944, 231, 321.JANOWITZ, H. D., H A N S O N M. E., & G R O S S M A N

M. I. Effect ofintravenously administered glu-cose on food intake in the dog. AmericanJournal ofPhysiology 1949, 156, 87-91.K E N N E D Y G. C. The role ofdepot fat in the hypo-thalamic control of food intake in the rat.Proceedings of the Royal Society of London,SeriesB,1952, 140, 578-592.L U C K H A R D T A. B., C A R L S O N A. J. Contributionsto the physiology of the stomach: XVII: Onth e chemical control of the gastric hungermechanism. American Journal of Physiology1915,36, 37-46.M A C D O N A L D R. M., IN G E L F IN G E R F. J., & B E L D I N GH. W. Late effects of total gastrectomy inman. New England Journal of Medicine 1947,237, 887-896.MILLER,N. E.Experiments onmotivation.Science

1 9 5 7 126, 1271-1278.MILLER, N. E. Analytical studies of drive and re-ward . American Psychologist 1961, 16, 739-7 5 4 .PENICK, S. B., & SMITH, G. P. The effect of glu-cagon on food intakeandbody weightinman.Journal of Obesity 1964,1, 1-15.S C H A L L Y A. V., K E D D I N G T. N., L T J C I E N H. W., &MEYER, J. Enterogastrone inhibits eating byfastedmice.Science 1967, 157, 210-211.S I B G B L P. S., &TAUB,D. V. Ahunger hormone?Journal of Comparative andPhysiological Psy-chology,1952,45,250-253.U G O L E V A. M., & KASSIL, V. G. Physiology ofappetite. (Trans, by Library Branch Divisionof Research Services, Upekhi SouremennioBiologii 1961, 51, 352. National InstitutesofHealth,No.9-23-63.)WEEKS, J., & DAVIS, J. D. Chronic intravenouscannulas fo r rats. Journal o f Applied Physiol-o g y 1964,19 540-541.

(Received April 17,1968)

Psychology Article 101

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