Chapter 31

Sensory Function of the Nervous System

Contents

• Sensory receptors and sensory organs• Pain• The visual system• The Auditory Systems

Section 1

Sensory Receptor and Sensory Organ

Part 1 Sensory Receptors

• specialized nerve cells that transduce energy into neural signals

• “mode” specific– “Law of Specific Nerve Energies（神经特殊能量定律）” : sensory messages are carried on separate channels to different areas of the brain

• detect a small range of energy levels– Eye: 400-700 nM– Ear: 20-20,000 Hz– Taste buds: specific chemicals

Spectrum of the Electromagnetic Wave

Somatic Sensory Nerve Endings

Free Nerve Endings

• dendrites interspersed among other cells/tissues

• pain, temperature, touch

Encapsulated Nerve Endings

• dendrites with special supporting structures

• mechanoreceptors and proprioceptors

Classification of Receptors: Location

• Exteroceptors– Located on the body surface or specialized to detect external stimuli

– Pressure, pain, temp, touch, etc.

• Visceroceptor– within internal organs, detect internal stimuli

– Blood pressure, pain, fullness.

• Proprioceptors– Limb and body position and movement.

– in the joints and muscles

– in the vestibular structures and the semicircular canals of the inner ear.

Classification of Receptors: Modalities

• Mechanoceptive – Detects stimuli which mechanically deform the receptor;– Pressure, vibration, touch, sound.

• Thermoceptive– Detects changes in temperature;– hot/cold

• Nociceptive (pain)– Detects damage to the structures

• Photoreceptors– Detect light; vision, – retinal of the eye

• Chemoceptive– Detect chemical stimuli– CO2 and O2 in the blood, glucose, smell, taste

Classification of Receptors: Complexity

• Simple receptors– Usually a single modified dendrite

– General sense

– Touch, pressure, pain, vibration, temperature

• Complexity– High modified dendrites, organized into complex structures

• ear, eye.

– Special senses

– Vision, hearing, smell, taste

Which receptor?

Sequence of Events in a ReceptorStimulus

Receptor Protein Activated

Enzyme Cascade (in some cases)

Receptor Ion Channels opened (or closed)

Receptor Current

Receptor Potential

Modulated Impulse Frequency in Second

Order Neuron

Basic Function

Reception

Amplification

Transduction

TransmissionModulated Impulse

Frequency in Receptor Cell Axon

Modulated Transmitter Release from Receptor Cell

Part 2 Properties of the Receptors

• Adequate Stimulus• Transduction• Adaptation• Encoding

1. Adequate Stimulus

• The type of stimulus the receptor is highly sensitive

• Receptor: specially designed for one kind of stimulus– The lowest threshold– Insensitive to other stimulation

2. Transduction

– A process by which an environmental stimulus becomes encoded as a sequence of nerve impulses in an afferent nerve fiber

• Transduce sensory energy into neural (bioelectrical) energy

– Receptor potentials: Changes in the transmembrane potential of a receptor caused by the stimulus.

– Generator Potential: A receptor potential that is strong enough (reaches threshold) to generate an action potential

• The stronger the sitmulus (above threshold) the more APs are fired over a given time period;

• translated by the CNS as a strong sensation

Receptor Potential and Generator Potential

3. Adaptation

The sensory receptor adapt to any

constant stimulus after a period of

time

Phasic receptors quickly adapt.

Most exteroceptors

Tonic receptors adapt

slowly or not at all.

Most visceroceptors

Phasic and Tonic Receptors

• Phasic Receptor– alert us to changes

in sensory stimuli – cease paying

attention to constant stimuli

• Tonic Receptor– useful in situations

requiring maintained information about a stimulus.

4. Encoding

• The quality of the stimulus is encoded in the frequency of the action potentials.

Stretch Receptors:

Weak stretch causes low impulse frequency on neuron leaving receptor.

Strong stretch causes high impulse frequency on neuron leaving receptor.

Time

Membrane potential

Frequency Code

Summary• The external & internal environments are monitored

by sensory receptors.

• Each type of receptor is excited most effectively by only one modality of stimulus known as the adequate stimulus.

• The stimulus is converted into an electrical potential.

• Stimuli are detected as either static or dynamic events.

• The intensity & duration of the stimulus is frequency coded as bursts of action potentials in the primary afferent nerve.

Section 2. Pain

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”

International Association for the Study of Pain

Why feel pain?

• Gives conscious awareness of tissue damage

• Protection:– Remove body from danger– Promote healing by preventing further damage– Avoid noxious stimuli

• Elicits behavioural and emotional responses

1. Nociceptors• special receptors that respond only to noxious

stimuli and generate nerve impulses which the brain interprets as "pain".

Adequate Stimulation

–Temperature

–Mechanical damage

–Chemicals (released from damaged tissue)

Bradykinin, serotonin, histamine, K+, acids, acetylcholine, proteolytic enzymes can excite the chemical type of pain.

Prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them.

Nociopectors

Hyperalgesia

The skin, joints, or muscles that have already been damaged are unusually sensitive.

A light touch to a damaged area may elicit excruciating pain

Primary hyperalgesia occurs within the area of damaged tissue

Secondary hyperalgesia occurs within the tissues surrounding a damaged area

2. Localization of Pain

• Superficial somatic pain arises from skin areas

• Deep somatic pain arises from muscle, joints, tendons （肌间） & fascia (筋膜）

• Visceral Pain arises from receptors in visceral organs

• Most pain sensation is a combination of the two types of message. – sharp pain conducted by the A fibres– dull pain conveyed along C fibres

3. Fast and Slow Pain

• Fast pain (acute)– occurs rapidly after stimuli (.1 second)– sharp pain like needle puncture or cut– not felt in deeper tissues– larger A nerve fibers

• Slow pain (chronic)– begins more slowly & increases in intensity– in both superficial and deeper tissues– smaller C nerve fibers

Impulses transmitted to spinal cord by– Myelinated Aδ nerves: fast pain (80 m/s)– Unmyelinated C nerves: slow pain (0.4 m/s)

nociceptor

nociceptor

Aδ nerve C nerve

spinothalamicpathway

to reticularformation

Impulses ascend to somatosensory cortex via:– Spinothalamic pathway (fast pain)– Reticular formation (slow pain)

reticular formation

spinothalamicpathway

thalamus

somato-sensory

cortex

4. Notable Features of Visceral pain

• Caused by

• distension of hollow organs

• ischemia

• inflammation

• localized mechanical trauma may be painless

• Poorly localized

• may be “referred”

• Often accompanied by strong autonomic and/or somatic reflexes

Afferent innervation of the viscera.

• anatomical separation – nociceptive innervation in sympathetic nerves

– non-nociceptive predominantly in vagus

• Many visceral afferents are specialized nociceptors, – small (Aδ and C) fibers involved.

• Large numbers of silent/sleeping nociceptors, awakened by inflammation.

• Nociceptor sensitization (hyperalgesia) well developed

Referred pain

• Pain originating from organs perceived as coming from skin

• Site of pain may be distant from organ

The convergence of nociceptor input from the viscera and the skin.

Convergence theory of Referred pain

1. both visceral and somatic afferents converge on the same interneurons in the pain pathways.

2. Excitation of the somatic afferent fibers is the more usual source of afferent discharge

3. the location of visceral receptor activation was “referred” to the somatic source.

4. The perception is incorrect.

5. “Pain Gate” Theory

Melzack & Wall (1965)

A gate, where pain impulses can be “gated”

The synaptic junctions between the peripheral nociceptor fiber and the dorsal horn cells in the spinal cord are the sites of considerable plasticity.

A “gate” can stop pain signals arriving at the spinal cord from being passed to the brain

– Reduced pain sensation– Natural pain relief (analgesia)

descending nerve fibers from brain

axons from touch receptors

axons from nociceptors

“THE PAIN GATE”opioid-releasing interneuron

pain pathways

How does “pain gate” work?

The gate = spinal cord interneurons that release opioids.

The gate can be activated by:– Simultaneous activity in other sensory (touch)

neurons– Descending nerve fibers from brain

Applications of pain gate

Stimulation of touch fibres for pain relief– TENS (transcutaneous electrical nerve stimulation)– Acupuncture– Massage

Release of natural opioids– Hypnosis– Natural childbirth techniques

6. Pain Relief

• Aspirin and ibuprofen (布洛芬） block formation of prostaglandins that stimulate nociceptors

• Novocain （普鲁卡因） blocks conduction of nerve impulses along pain fibers

• Morphine lessen the perception of pain in the brain.

Section 3

The Visual System

Part 1. Structure of the Eyeball

Part2 Focusing on the Retina

The images of objects in the environment are focused on the retina.

1. Principle of Optics

• Light rays are bent (refracted) when they pass from one medium into a medium of a different density.

• Parallel light rays striking a biconvex lens are refracted to a point (principal focus) behind the lens.

• The principle focus is on a line passing through the centers of a curvature of the lens, at the principal focal distance.

Light rays from an object that strike a lens more than 20 ft (6 m) away are considered to be parallel.

The rays from an object closer than 20 ft are diverging and are brought to a focus farther back than the principal focus.

Biconcave lenses cause light rays to diverge.

2. Emmertropia• The refractive system of the human eye

– cornea, aqueous humor, crystalline lens, and vitreous humor.

• When light coming from an object is brought to a focus, an image is formed.

• Emmertropia:– parallel rays of light are focused to an image on the

retina. – normal human eye

3. Accommodation• Emmertropia: ciliary muscle relax during seeing

object farther than 6 m.• objects closer than 6 m are brought to a focus behind

the retina, – the objects appear blurred.

• Problem solved by accommodation– near objects are brought to a sharp focus on the retina

(1) Accommodation of lens– Increase bulging (refraction) of lens

• Via contraction of ciliary muscle, relaxes the suspensory ligaments (parasympathetic fibers)

Focusing

Muscles working

Lens more spherical

Focus near

Muscles relaxed

Lens less spherical

Focus far

Near Point

• The power of accommodation is limited• The nearest distance of the eye at which an

object can seen distinctly– the visual accommodation is at a maximum

• Decline in the amplitude of accommodation in human with advancing age

Diopter:屈光度

(2) Pupillary reflex• Reduces the amount of light entering the eye• Restricts the light to the central part of the lens for more accurate vision

– Increase the depth of focus （景深）– Decrease the spherical aberration and chromatic aberration

(3) Convergence of eyeballs

• Viewing near object causes both eyes to move inward• Move the images on the corresponding

position on the retina of the two eyes

4. Error of Refraction

• Caused by – shape of eye

– power of lens

Farsightedness

• less common

• eye too short and/or lens too weak

• light focuses behind retinal

• correct with “convex” lens to add power

FARSIGHTEDNESS (HYPEROPIA)

UNCORRECTED

CORRECTED

Nearsightedness

• more common

• eye is too long and/or lens is too powerful

• light focuses in front of retina

• correct with “concave” lens to reduce power

NEARSIGHTEDNESS (MYOPIA)

UNCORRECTED

CORRECTED

•Astigmatism:

–abnormal curvature of the cornea

–Light from vertical and horizontal direction do not focuses in the same point

Oldsightedness (Presbyopia)

• The crystalline lens tends to harden and the capsule itself becomes less elastic with age

• The near point of distinct vision moves further and further away from the eye with age.

• The far point is normal• May be compensated by placing a

converging lens in front of the eye.

The loss in power of accommodation is most significant and dramatic between the ages of 40 and 50

Part 3 Function of the Retina

I. Rod system and cone system

• rod system – rods and subsequent bipolar cells and ganglion cells

• cone system – cones and subsequent bipolar cells and ganglion cells.

Distribution of the cones and rods on the retina.

RodsRods• located mainly in periphery of retinalocated mainly in periphery of retina

• responsible for night visionresponsible for night vision

• detail not detecteddetail not detected

• see black, white, and gray (no color)see black, white, and gray (no color)

• several rods share 1 bipolar and 1 several rods share 1 bipolar and 1 ganglion cellganglion cell

• rod vision lacks detail, but see in low rod vision lacks detail, but see in low lightlight

ConesCones• located mainly in fovealocated mainly in fovea

• work best in bright lightwork best in bright light

• enable us to see fine detailenable us to see fine detail

• responsible for color visionresponsible for color vision

• each cone has its own bipolar each cone has its own bipolar and ganglion celland ganglion cell

• this allows us to see detail but this allows us to see detail but bright light is neededbright light is needed

Cones see detail but require bright light

Rods see in low light but lack detail

Evidence of Two Photoreceptor System

• the nocturnal and diurnal animals – nocturnal animals have a preponderance of rods– diurnal animals have a preponderance of cones

• visual pigment– one classes (rhodopsin) in the rods – three classes in the cones

II Transduction of Light Energy by Rod Cell

1. Photochemical Reaction and Metabolism of Rhodopsin

Rhodopsin: the visual pigment (light-sensitive pigment).

combination of

a protein part, scotopsin (opsin)

a carotenoid pigment, 11-cis retinal

Rhodopsin: cis form of the retinal bind with scotopsin.

11-cis retinal

Retinal – Light Sensitive Pigment11-cis-Retinal - All-trans-Retinal

Light

Dark

11-cis retinal (bent shape form)

all-trans retinal (straight chain form)

Light

Dark

Converting the All-trans Retinal into 11-cis Retinal

• Occurs under the dark environment• Requires metabolic energy • Catalyzed by the retinal isomerase. • Under the dim light, the 11-cis and 11-trans

keep dynamic balance

rhodopsin 11-cis retinal + opsin

all-trans retinal+ opsin

isomerase

11-cisretinal

All-transretinal

opsin opsin

Vitamin A and Retinal （视黄醛）• All-trans retinol is one form of vitamin A• Vitamin A is present both

– in the cytoplasm of the rods – in the pigment layer of the retina

• Vitamin A is always available to form new retinal when needed.

• Severe vitamin A deficiency - Night blindness.

2. Receptor Potential of Rods： Hyperpolarization

III Color Vision

Photochemistry of Color Vision by Cones

• Three kinds of proteins on the photopigments

• Sensitive to three kinds of light– Trichromatic Theory

Visible spectrum: 380-760 nm (nm is a billionth of a meter)

Trichromatic Theory of Color Vision

– Occurs at the receptor level

– Each cone is coated by one of 3 photopigments

• Short-wave (blue)

• Medium-wave (green)

• Long-wave (red)

– Ratio of activated cones = color differentiation

Color Sensitivity of Different Cones

Primary Colors

• Red, Green and Blue

• can be mixed to produce any other color

Color Blindness

• Sex-linked conditions: Genes on X chromosome, so more common in men.– Protanopia, missing red photopigment– Deuteranopia, missing green photopigment

• Non-sex-linked condition– Tritanopia, missing blue photopigment o

– monochromats: people who are totally colorblind, more severe

Color Vision Systems

Tritanopia deuteranopia protanopia

IV Dark Adaptation and Light Adaptation

Range of luminance to which the human eye respond

Millilambert，毫朗伯

Dark Adaptation

• The decline in visual threshold in a dimly lighted environment

• First phase:• Neural adaptation

• Second phase: – chemical adaptation

– depleted of rhodopsin in bright light

– replenish their rhodopsin in dim light

Light Adaptation:

When one passes suddenly from a dim to a brightly lighted environment, the light seems intensely and even uncomfortably bright until the eyes adapt to the increased illumination and the visual threshold rises.

Mechanism?…

Section IV The Auditory System

Fig. 15.23

Part I Structure of the Ear

– Auditory Canal: conducts sound to the eardrum– Tympanic membrane (Eardrum): thin membrane

that vibrates in response to sound, transfers sound energy to bones of the middle ear

•1. Outer Ear:–Pinna (auricle): directs sound waves into the auditory canal

• 2. Middle Ear: three tiny bones “amplify sound” and transfer sound energy to the inner ear

A: MalleusB: IncusC: Stapes

–Ossicles are smallest bones in the body–Act as a lever system–Footplate of stapes enters oval window of the cochlea

• 3. InnerWhere Sound Energy is Transduced– Cochlea: snail shaped fluid-filled structure– Oval window: thin membrane, transfers vibrations from

stapes to fluid of cochlea

–Basilar membrane: runs the length of the cochlea

–Organ of Corti: rests on basilar membrane, contains “receptor” cells

–Round window: absorbs energy and equalizes pressure in the cochlea

4. Pathway Transmitting Sound Wave from External Environment to Inner EarAir Conduction

Sound wave

Auditory Canal Auditory Canal

Tympanic membraneAir in tympanic cavity

Ossicular chain Round window

Oval window Inner ear

Bone ConductionSound wave

Vibration of skull

Sound wave

Part 2. Properties of Sound

Sound travels in waves as does light• 1. Pitch: determined by “frequency,” the number of

cycles per second of a sound wave, measured in hertz (Hz)

• 2. Loudness: determined by “amplitude” (height) of the sound wave, measured in decibels (dB)

• 3. Timbre: determined by “complexity and shape” of the sound wave, gives each sound its unique quality

Loudness of Sound

• 0 dB = hearing threshold

• 50 dB = normal conversation

• 90 dB = danger zone

• 120 dB = Rock concert

• 130 dB = Pain threshold

Part 3 Role of Middle Ear in Sound Transmission

Mechanisms Involved in Transformer Mechanisms Involved in Transformer ProcessProcess

Size difference between Tympanic Tympanic MembraneMembrane and Stapes Footplate

Lever action

First Component of Middle Ear First Component of Middle Ear Transformer ActionTransformer Action

Size Difference– Tympanic membrane

.59 cm2

– Stapes footplate .032 cm2

– Pressure formula Pressure = force/area

Impact on sound transmission

Pressure gain: 0.59/0.032 = 18.4 (times)

Transformer Action of Middle EarTransformer Action of Middle EarLever ActionLever Action

Fulcrum Effect pressure gain: 1.3 times

TRANSFORMER ACTION TRANSFORMER ACTION AMOUNT OFAMOUNT OF AMPLIFICATIONAMPLIFICATION

Pressure Gain Contribution from:

18.4 TM (Tympanic Membrane)Tympanic Membrane) to stapes footplate

1.3 Lever action

23.9 Total pressure gain

(18.6 x 1.3)

Part 4 Function of Organ of Part 4 Function of Organ of CortiCorti

a structure rests atop the basilar membrane along its length

contains approx. 16,000 cochlear hair cells

1. How to discriminate the frequency of the sound? ---

Traveling Wave Theory

Vibration of Basilar Membrane and the Traveling Wave Theory

• Sound wave entering at the oval window cause the basilar membrane to vibrate

• different frequencies cause vibrations at different locations (places) along basilar membrane

• higher frequencies at base, lower frequencies at top

2. Electrical Potentials2. Electrical Potentials

DC vs. AC– Direct Current (DC) = stimulus doesn’t

change with time, constant; i.e. battery– Alternating Current (AC) = always

changing over time, looks like a sine wave

CochleaCochlea

Perilymph-similar in composition to extracellular

fluid. High in Na+ and low in K+.

Endolymph-found in the scala media. Similar to intracellular fluid. High in K+

and low in Na+

Two DC Potentials (EP)Two DC Potentials (EP)

Endocochlear Potential (EP)– +80 mV potential with respect to a neutral point on

the body– due to the Stria Vascularis (耳蜗外侧壁血管纹）

-80 mV

Reticular Lamina

+80 mV

Intracellular Potential (IP) or organ of corti potential (resting potential)

–Recorded -80 mV inside cells of organ of corti

Two DC Potentials (IP)Two DC Potentials (IP)

Hair Cell in the Organ of Corti

When the basilar membrane moves, a shearing action between the tectorial membrane and the organ of Corti causes hair cells to bend

K+ comes into the hair cell and depolarizes the hair cell.

There are mechanical gates on each hair cell that open when they are bent.

Two AC PotentialsTwo AC Potentials

Cochlear Microphonic Potential– Reproduces frequency and waveform of a

sinusoid perfectly– Generated from hair cell

Action Potential (AP)– Electrical activity from the VIII Nerve– Can be measured from anywhere in the cochlea

or in the auditory nerve

Part 5 Deafness– Conduction deafness -

• possible causes include: perforated eardrum, inflammation, otosclerosis

– Sensineural deafness - nerve damage