Neuro Physiology - Spec Senses ENG NOTES_Dr E Marais.ppt

PHYSIOLOGY OF THE SPECIAL SENSES Dr Erna Marais Division Medical Physiology e-mail: [email protected] About Chapter 10 (Silverthorn, 8th edition, 2019) Special senses: - Chemoreception: smell and taste - The ear: hearing - The ear: equilibr...

PHYSIOLOGY OF THE SPECIAL SENSES Dr Erna Marais Division Medical Physiology e-mail: [email protected] About Chapter 10 (Silverthorn, 8th edition, 2019) Special senses: - Chemoreception: smell and taste - The ear: hearing - The ear: equilibrium - The eye: vision Chemoreception: Smell and Taste Smell (Olfaction; “olfacere”, to sniff) is one of the oldest senses Taste (Gustation) is a combination of five basic sensations Smell and Taste transduction Olfactory Pathways Link between smell, memory, and emotion Vomeronasal organ (VNO) in rodents Response to sex pheromones Olfactory cells Olfactory epithelium in nasal cavity project to the Nasal cavity olfactory bulb Figure 10-15 Anatomy Summary: The Olfactory System Olfactory bulb Secondary sensory neurons Bone Primary sensory neurons (olfactory Olfactory cells) epithelium (b) The olfactory cells synapse with secondary sensory neurons in the olfactory bulb. Figure 10-14b Anatomy Summary: The Olfactory System Olfactory receptor cell axons (cranial nerve I) carry information to olfactory bulb. Lamina propria Basal cell layer includes stem cells that replace olfactory receptor cells. Developing olfactory cell Olfactory cell Olfactory (sensory neuron) epithelium Supporting cell Olfactory cilia (dendrites) contain odorant receptors. Mucus layer: Odorant molecules must (c) Olfactory cells in the olfactory epithelium live only dissolve in this layer. about two months. They are replaced by new cells whose axons must find their way to the olfactory bulb. Figure 10-14c Olfaction Odorants bind to odorant receptors, G-protein-cAMP-linked membrane receptors Activates Golf  increases cAMP  opens cAMP-gated cation channels Depolarizing the cell  triggering a signal along axon to bulb Taste Buds Gustation (sense of taste) Sweet, sour, salty, bitter and umani Sour → triggered by H+ → ion concentration in body fluid closely regulated Salty → triggered by Na+ → ion concentration in body fluid closely regulated Sweet (ass. with glucose) → nutritious food Umani (ass. with amino acid, glutamate) → nutritious food Bitter → WARNING of toxic components Figure 10-16a–b Taste Buds Taste receptors scattered in oral cavity (i.e. palate), but primarily in taste buds on tongue Taste buds composed of taste cells and support cells One taste bud = 50-150 taste cells Taste cells - non-neural polarized epithelial cells - apical membrane – microvilli - apical protein receptor or channel - each taste cell sense only one taste Figure 10-16a–b Taste Buds Sweet Umami Bitter Salty (Na+) or Sour (H+) Tight junction Two types of Taste cells: (limit movement of molecules between cells) Type II or receptor cells Support cell (Type I) – release ATP Type III or presynaptic cells – release serotonin Presynaptic cell (type III) ATP Serotonin Receptor cells (Type II) Primary gustatory neurons Taste ligands create Ca2+ signals that release Serotonin or ATP (neurotransmitter). Figure 10-16c Summary of Taste Transduction Type II taste cell: Salt Sour Type III taste cell: Sweet, umami, or bitter ligand Na+ H+ G-protein 1 1 1 1 Ligands activate the taste (Gustducin) GPCR cell. 2 Na+ 2 H+ 2 2 Various intracellular Signal pathways are activated. transduction Cell ? ? depolarizes Ca2+ Ca2+ 3 3 Ca2+ signal in the cytoplasm Ca2+ Ca2+ 3 Ca2+ 3 triggers exocytosis or ATP formation. Ca2+ ? ATP Serotonin 4 4 4 Neurotransmitter or ATP is 4 released. Primary gustatory neurons 5 Primary sensory neuron fires and action potentials are 5 5 5 sent to the brain. GPCR = G protein coupled receptor Figure 10-17 Taste neural pathways Primary gustatory neurons → cranial nerves VII, IX, X → synapse in medulla → thalamus → gustatory cortex Gustatory cortex Eye 2 Thalamus Brain stem Tongue Taste – other… “Sixth” taste sense – fat receptor? “Spicy” receptors (via somatosensory paths) i.e. capsaicin from chili peppers Specific hunger such as salt appetite (represents a lack of Na+) Cravings – reflect complex mixture of physical, psychological, environmental and cultural influences About Chapter 10 The ear: hearing The ear: equilibrium The Ear: Hearing Perception of sound Sound transduction The cochlea Auditory pathways Hearing loss Sound Waves Hearing is our perception of energy carried by sound waves Figure 10-19a Properties of Stimulus: Location Auditory information: No receptive field, but Sensitive to different frequencies The brain uses timing differences rather than neurons to localize sound Figure 10-5 Sound Waves Frequency or Pitch = waves per sec, hertz (Hz) (Avg human=20-20,000Hz; Acute hearing=1000-3000Hz) Amplitudes or Loudness (intensity of wave, decibels (dB) 60 (Avg human=60 dB; Damage > 80dB; Rock concert=120 dB!!) 5 Auditory Transduction (6:43min): https://www.youtube.com/watch?v=46aNGGNPm7s Figure 10-19b Sound Transduction Sound waves Hearing = complex Mechanical sense that involves vibrations multiple transductions Fluid waves Sensory receptors Electrical signals Cochlea of inner ear Chemical signals Action potentials Anatomy Summary: The Ear EXTERNAL EAR MIDDLE EAR INNER EAR The pinna The oval window and the round window separate directs sound the fluid-filled inner ear from the air-filled middle ear. waves into the ear Semicircular Oval Malleus Incus canals window Vestibulocochlear Nerve Stapes Vestibular Cochlea Ear appartus canal Tympanic Round membrane window To pharynx Internal jugular Eustachian vein tube (normally collapsed) Figure 10-18 Sound Transmission Through the Ear 1 Sound waves strike 2 The sound wave 3 The stapes is attached to the the tympanic energy is transferred membrane of the oval window. membrane and to the three bones Vibrations of the oval window create become vibrations. of the middle ear, fluid waves within the cochlea. which vibrate (amplification). Cochlear nerve Incus Oval Ear canal Malleus Stapes window 5 Vestibular duct 3 (perilymph) Cochlear duct 2 (endolymph) 6 4 1 Tympanic duct (perilymph) Tympanic Round membrane window 4 The fluid waves push on the 5 Neurotransmitter release 6 Energy from the waves flexible membranes of the onto sensory neurons transfers across the cochlear duct. Hair cells bend creates action potentials cochlear duct into the and ion channels open, that travel through the tympanic duct and is creating an electrical signal cochlear nerve to dissipated back into that the brain. the middle ear at the alters neurotransmitter release. round window. Figure 10-20 Anatomy: The Cochlea Vestibular apparatus Oval Vestibular Cochlear Tympanic window Saccule duct duct duct Cochlea Uncoiled Helicotrema Round Organ of Basilar window Corti membrane (hair cell receptors) Figure 10-21 (1 of 3) Anatomy: The Cochlea Perilymph in vestibular and tympanic duct Similar to plasma Endolymph in cochlear duct Secreted by epithelial cells Similar to intracellular fluid High [K+] Body Fluid Compartments: Capillary wall Cell membrane Blood cells Blood vessel ECF = Extracellular fluid compartment (Interstitial fluid and Plasma) Plasma Interstitial fluid Intracellular fluid ICF = Intracellular fluid compartment ECF ICF Cell membrane Figure 3-2 Anatomy: The Cochlea Bony cochlear wall Vestibular duct Cochlear duct Tectorial membrane Organ of Corti Tympanic duct Cochlear nerve transmits action potentials from Basilar the hair cells to the membrane auditory cortex. Figure 10-21 (2 of 3) Anatomy: The Cochlea The movement of the tectorial membrane moves the cilia on the hair cells. Fluid wave Cochlear Tectorial duct membrane Hair cell Tympanic Nerve fibers of duct Basilar membrane cochlear nerve Figure 10-21 (3 of 3) Sensory Receptors Special senses receptors: Stimulus Specialized receptor cell (hair cell) Synaptic vesicles Synapse Myelinated axon Cell body of sensory neuron (c) Figure 10-1c Signal Transduction in Hair Cells Kinocilium = longest cilium; (a) At rest: embedded in (b) Excitation: (c) Inhibition hair cells bend overlying tectorial hair cells bend away from toward membrane kinocilium kinocilium Tip link = protein bridges, act as Tip link “springs”, connected to 10% of ion Tip links pull Tip links relax. Stereocilium gates of ion channels Channels closed. more channels channels open Less cation entry open. Hair cell Cation (K+, Ca2+) hyperpolarizes cell. entry depolarizes cell. Voltage-gated Ca2+ No neurotransmitter channels open, release Primary neurotransmitter sensory release increase neuron tonic signal sent by neuron Action potentials Action potentials increase No action potentials Action potentials in primary sensory neuron: mV Special Senses Time 0 | Cochlea | Membrane potential mV of hair cell: Spiral Organ of depolarize –30 Corti (41min) hyperpolarize https:// www.youtube.com Release Release /watch?v=x4ouSb- Excitation opens Inhibition closes 10C8 ion channels ion channels Figure 10-22 Sensory Coding for Pitch Basilar membrane:  Coding for Pitch  Variable sensitivity to sound wave frequency along its length (i.e. location of key on piano = pitch) Low High Stiff region near oval window Figure 10-23a Sensory Coding for Pitch High Low Sound wave frequency determines displacement of Basilar membrane Location of active Hair cells creates a code that the brains translates as information about the pitch Figure 10-23b Sensory Coding for Pitch Spatial coding of the Basilar membrane is preserved in the Auditory cortex as neurons project from hair cells to corresponding regions in the brain Sensory Coding for Loudness Loudness of Sound wave is coded in the same way that signal strength/intensity is coded in somatic receptors. The louder the noise, more receptors/hair cells are activated, more rapidly action potentials fire in the sensory neuron. Auditory Pathways Sound Waves Electrical signals in cochlea Sound waves Primary sensory neurons to cochlear nuclei in Electrical signals medulla oblongata 1st Secondary sensory Nuclei in neurons to two nuclei in medulla pons, ipsilateral (same 2nd side) and contralateral Nuclei in pons Nuclei in pons (opposite side) Main pathway synapses in Nuclei in midbrain and thalamus nuclei in midbrain and thalamus Auditory cortex Auditory cortex Auditory Pathways Right auditory cortex Left auditory cortex Right Left thalamus thalamus Midbrain Pons Right cochlea Left cochlea Medulla Cochlear branch of right Cochlear branch of left vestibulocochlear nerve (VIII) vestibulocochlear nerve (VIII) Figure 10-24 Hearing Loss Conductive EXTERNAL EAR MIDDLE EAR INNER EAR No transmission through either external or middle Vestibulocochlear ear Nerve Central Damage to neural pathway between ear and cerebral cortex or to Cochlea cortex itself Ear canal Sensorineural Damage to structures of inner ear Need Cochlear implant Figure 10-18 The Ear: Equilibrium Equilibrium = state of balance Equilibrium components: - dynamic = tells about our movement in space - static = tells whether our head is in normal upright position Vestibular apparatus (membranous labyrinth) - Semicircular canals (three canals) - Otolith organs (two saclike organs) Equilibrium pathways (project primarily to cerebellum) The Vestibular Apparatus: Anatomy Vestibular Posterior/lateral canal Superior canal apparatus (head tilt) (nod for “yes”) Left right Horizontal canal (shake head for “no”) Vestibular apparatus: A series of interconnected fluid-filled chambers filled with high K+, low Na+ endolymph (like cochlear duct) Provides information about movement and position in space Figure 10-25b The Vestibular Apparatus: Anatomy SEMICIRCULAR CANALS: Superior Horizontal Posterior/Lateral Ampulla enlarged chamber at one end of each canal Cochlea Cristae sensory receptors for Utricle Saccule rotational acceleration little bag little sac Maculae sensory receptors for linear acceleration and head position OTOLITH ORGANS: Figure 10-25a The Vestibular Apparatus – Otolith organs (d) Macula = sensory structure in otolith organs Hair cells Otolith membrane (Gelatinous mass) Otoliths are crystals (calcium carbonate and protein particles) that move in response to gravitational forces. Nerve fibers Figure 10-25d The Vestibular Apparatus – Otolith organs Otoliths Move in Response to Gravity or Acceleration Otolith Organs sense Linear Acceleration and Head Position Figure 10-27a The Vestibular Apparatus - Semicircular canals (c) Crista = sensory structure in ampulla at base of semicircular canals Endolymph Cupula (gelatinous mass) Hair cells Supporting cells Nerve Figure 10-25c The Vestibular Apparatus - Semicircular canals Semicircular canals sense rotational acceleration Transduction of Rotational Forces in the Cristae: When the head turns right, “inertia” keeps endolymph in ampulla from moving as rapidly as the surrounding cranium. Endolymph pushes the cupula to the left. Bristles Cupula Bone bend left Stationary board Endolymph (“inertia”) “Inertia” = the Hair cells Bone resistance of any physical Brush moves object to a right change in its state of Direction of motion or rest Figure 10-26 rotation of the head The Vestibular Apparatus - Semicircular canals To sense kinocilium (hair cells bend toward (hair cells bend away from kinocilium; kinocilium; increases firing rate of decreases firing rate of action potentials) action potentials) Central Nervous System Pathways for Equilibrium Cerebral Primary site cortex for equilibrium processing Thalamus Vestibular branch of Reticular vestibulocochlear formation nerve (VIII) Cerebellum Somatic motor neurons Vestibular apparatus Vestibular controlling eye nuclei of movements Medulla These descending pathways help keep eyes locked on an object as head turns Figure 10-28 Nystagmus Physiologic nystagmus = a form of involuntary eye movement that is part of the vestibulo-ocular reflex (VOR). Nystagmus Nystagmus = the repeated back- and-forth movement of the eyes, moderately slowly in the one direction followed by a flick back in the opposite direction Nystagmus Optokinetic reflex: allows the eye to follow objects in motion when the head remains stationary Optokinetic nystagmus = caused by movement of a large part of the visual field across the retina, (as when watching the scenery along the railway line from a moving train) The purpose of nystagmus = to fixate the gaze on an object for as long as it remains in front of the eyes, and then flicking the eyes forwards to fix on a new part of the scenery as it moves by. In this way vision consists of a series of relatively stationary scenes, instead of a smear across the retina Nystagmus Otokinetic nystagmus = caused by rotation of the head, as when performing a pirouette, or spinning on a rotating stool. the result of stimulation of the vestibular apparatus (the sensors in the semicircular canals). accompanied by the subjective feeling of vertigo/dizziness Fixation inhibits the nystagmus The Vestibular Apparatus Dancer performs “pirouettes”, try to keep vision fixed on a single point (“spotting”). How does spotting keep dancer from getting dizzy? When dancer spots, endolymph in the ampulla moves with each head rotation but then stops as the dancer holds the head still. This results in less inertia than if the head were continuously turning. The Eye and Vision Light enters the eye Light Focused on retina by the lens Photoreceptors Photoreceptors Electrical signals transduce light energy Electrical signal Neural pathways Electrical signal Visual cortex Processed through neural pathways External Anatomy of the Eye Muscles attached to Lacrimal gland external surface of eye secretes tears. control eye movement. Upper eyelid Sclera Pupil Iris Lower eyelid The orbit is a bony Nasolacrimal duct cavity that protects drains tears into the eye. nasal cavity. Figure 10-29 Anatomy: The Eye Optic disk (blind spot) Central retinal artery and vein Fovea: (only cones) Macula: the centre of the visual field (b) View of the rear wall of the eye as seen through the pupil with an ophthalmoscope Figure 10-30b Anatomy: The Eye Zonules: Lens: bends light to focus it on the retina ligaments attach lens to muscle Optic disk (blind spot): region where optical nerve Aqueous humor: and blood vessels leave eye plasma-like fluid, supports cornea Central retinal Cornea: artery and vein transparent disk Pupil: Optic nerve changes amount of Fovea: light entering the region of sharpest vision eye Iris Macula: center of the visual field Vitreous chamber: gelatinous matrix, maintain shape of eyeball Retina: photoreceptors Ciliary muscle: contraction alters curvature of lens Sclera: connective tissue, continuation of the cornea (a) Sagittal section of the eye Figure 10-30a Neural Pathways for Vision (a) Dorsal view Optic tract Eye Optic chiasm Optic nerve Figure 10-31a  Neural Pathways for Vision b) Neural pathway for vision, lateral view Eye Optic Optic Optic Lateral geniculate body Visual cortex nerve chiasm tract (thalamus) (occipital lobe) Figure 10-31b The Pupil: regulates the amount of light Neural Pathways for Vision and the Pupillary Reflex The sensory (afferent) pathway from ONE eye leave the thalamus, diverges in midbrain to activate motor (efferent) pathways and control constriction of BOTH pupils Optic Optic Optic Lateral geniculate Visual cortex nerve chiasm tract body (thalamus) (occipital lobe) Shining a light into ONE eye Eye cause Light pupillary constriction in BOTH eyes Midbrain Parasympathetic fibres via Cranial nerve III (oculomotor nerve ) controls pupillary constriction. Figure 10-31c Refraction of Light Figure 10-32a Refraction of Light Figure 10-32b Optics Far objects Parallel light rays Flattened lens Focal point falls on retina Figure 10-33a Optics Close objects Light rays not parallel Lens unchanged Focal point not on retina Object unclear Figure 10-33b Optics Close objects Light rays no parallel Lens becomes rounded Focal length shortens Focal point on retina Object clear Figure 10-33c Accommodation Accommodation is the process by which the eye adjusts the shape of the lens to keep objects in focus Ciliary muscle Cornea Lens Ligaments Iris (a) The lens is attached to the ciliary muscle by inelastic ligaments (zonules). Figure 10-34a Accommodation Ciliary muscle relaxed Cornea Lens flattened Ligaments pulled tight (b) When ciliary muscle is relaxed, the ligaments pull on and flatten the lens. Figure 10-34b Accommodation Ciliary muscle contracted Lens rounded Ligaments slacken (c) When ciliary muscle contracts, it releases tension on the ligaments and the lens becomes more rounded. Figure 10-34c Common Visual Defects Presbyopia: Loss of accommodation - lens lost flexibility and remains in flatter shape for distance vision Myopia: (Near-sightedness) – increased curvature of cornea or too long eyeball Hyperopia: (Far-sightedness) – flatter cornea or too short eyeball Astigmatism: Cornea not perfectly shaped dome Figure 10-35a Common Visual Defects Figure 10-35a Common Visual Defects Figure 10-35b Phototransduction at the Retina The Electromagnetic Spectrum: Visible light: = Electromagnetic energy (photons) with wave frequency of 4.0-7.5x1014 cycles/sec (Hz) = Wave length of 400-750 nanometers Figure 10-36 Light Absorption of Visual Pigments Visual pigments of cones are excited by different wavelengths of light allowing us to see in Figure 10-40 Anatomy: The Retina Neurons that provide lateral Horizontal transmission lines that produce cell center-surround receptive fields Amacrine of ganglion cells cell Light Neurons that provide major Ganglion line of transmission of info. cell Cone (color vision) Photoreceptors from receptors to brain Bipolar cell Rod (monochromatic vision) (neurons) The Five types of neurons in Retina are organized into layers. Figure 10-37d Processing of light signals Outer edges of retina, ratio = 15 to 45 :1 In Fovea photoreceptors to bipolar neurons = 1:1 Outer edges of retina, ratio = 15 to 45 :1 Photoreceptors: Rods and Cones PIGMENT EPITHELIUM Old disks at tip are (absorbs extra light) phagocytized by pigment epithelial cells. Melanin granules OUTER SEGMENT Light transduction Disks Visual pigments in Disks membrane disks Connecting stalks INNER SEGMENT Mitochondria Location of major Changes in membrane organelles and metabolic potential operations such as photopigment synthesis Rhodopsin and ATP production molecule Retinal Cone Rods (from vit A, Opsin abs. light) (membr. prot.) Alter neurotransmitter SYNAPTIC TERMINAL (glutamate) release onto Synapses with bipolar cells bipolar cells Bipolar cell LIGHT day night Figure 10-39 Phototransduction in Rods: No Light (a) NO light, rhodopsin is inactive, cGMP is high, and channels are open (cyclic nucleotide- gated (CNG) , K+ and Voltage-gated Ca2+ channel). Pigment epithelium cell Na+ and Ca2+ ion influx greater than K+ efflux, rods Disk stay depolarized at membr. potential of -40mV Transducin (G protein) (instead of usual -70mV) Inactive rhodopsin (opsin and retinal bound) cGMP levels high - Random opening or CNG channel Ca2+ Na+ closing of channels will not open affect the membrane K+ potential of the cell; - Only the closing of a large Membrane potential number of channels, in dark = –40mV through absorption of a photon, will affect it and signal that light is in the Voltage-gated Ca2+ channel open visual field. - System is noiseless. Rod (neuronal noise limits the Ca2+ capacity of information processing by the brain) Ca2+ triggers exocytosis Tonic (continuous) release of neurotransmitter (glutamate) cGMP=cyclic Guanosine monophosphate onto bipolar neurons Figure 10-41a Phototransduction in Rods (b) Light bleaches rhodopsin. Opsin decreases cGMP, closes CNG channels, and hyperpolarizes the cell. Activated Opsin (bleached Activates retinal pigment) Transducin When light activates rhodopsin, a second- messenger cascade is initiated through G protein Transducin Cascade One photon light Decreased cGMP activates Retinal and Ca2+ Na+ its released from CNG channel One photon light Opsin = process closes activates called Bleaching K+ one Rhodopsin, that Membrane activates hyperpolarizes to –70 mV 800 Transducin (a lot of amplification!) Light Neurotransmitter release decreases in proportion to amount of light. (In Rods: Dimmer light more release, while bright light stops release) Figure 10-41b Phototransduction in Rods (c) Recovery phase, retinal recombines with opsin. (c) In the recovery phase, retinal recombines with opsin. Retinal converted to inactive form Recovery phase of rhodopsin takes some time, therefore dark adaptation (when moving from bright light into the dark) is slow. Retinal recombines with opsin to form rhodopsin. Figure 10-41c Processing of light signals LIGHT What determines signal to brain? Two types of bipolar cells, light-on and light-off. (In the light, photoreceptors hyperpolarize - decreased release of neurotransmitter, glutamate.) Inhibitory Hyperpolarized glutamate receptor 1) LIGHT-ON bipolar cells has inhibitory glutamate receptors, On- -in the light - receptors are activated and Bipolar cell ON bipolars depolarize Depolarized - in the dark - receptors are inhibited and ON bipolars hyperpolarize On- centre ganglion cell Increase rate of firing of action potentials Processing of light signals DARK What determines signal to brain? Two types of bipolar cells, light-on and light-off. (In the dark: photoreceptors depolarized - continuously release their Excitator Depolarized neurotransmitter, glutamate.) y glutamate receptor 2) LIGHT-OFF bipolar cells has excitatory Off- glutamate receptors: Bipolar cell - in the dark receptors are activated and Depolarized OFF bipolars depolarize - in the light - receptors are inhibited and OFF bipolars hyperpolarize. Off- centre ganglion cell Thus it is the excitatory or inhibitory nature Increase rate of firing of action potentials of the glutamate receptors that determines the type of bipolar cell. Processing of light signals Processing of light signals Horizontal cell Rod (photoreceptors) Pigment epithelium Ganglion cell Bipolar cell To optic nerve A group of adjacent photoreceptors form the visual field for one ganglion cell. This illustration shows an on- center, off-surround field. Ganglion cells respond most strongly when there is Bipolar cells are either good contrast of light activated or inhibited intensity between the center and the by light, depending on Visual fields have surround. their type. centers (yellow) and outer surrounds (gray). Figure 10.33 Multiple photoreceptors converge on one ganglion cell. Processing of light signals GANGLION CELLS LIGHT BIPOLAR CELLS RECEPTORS Processing of light signals ACTION POTENTIALS TO THE BRAIN GANGLION CELLS BIPOLAR CELLS RECEPTORS Processing of light signals FEWER AP’s MORE AP’s FEWER AP’s STIMULATED INHIBITED INHIBITED HORIZONTAL CELLS: Inhibit signals of nearby bipolar cells (lateral ____ ____ inhibition) Render on-centre, off-surround To enhance contrast On-center Off-surround Ganglion Cell Visual/Receptive Fields Visual/Receptive fields = On-center/Off-surround Field: Each ganglion cell receives input from particular area of retina Inputs from many photoreceptors Receptive field regions Circular areas on retina Central disk, “centre” Off-center/On-surround Field: Concentric ring, “surround” Each respond opposite to light Way of detecting contrast For detecting object’s edges Prevents overload of signals to Brain Receptive field favors Ganglion fields: Video Movement http://www.sumanasinc.com/web content/animations/content/recep Contours tivefields.html Rather than absolute light intensity Ganglion Cell Visual/Receptive Fields On-center/Off-surround Field: All dark All light Light on center Light on surround only only + + + + Bipolar cells (active or inhibited): Ganglion cell action potentials: Baseline activity Baseline activity Increased firing rate Decreased firing rate Weak signal Weak signal Strong signal No signal Ganglion Cell Visual/Receptive Fields Off-center/On-surround Field: - - - - Bipolar cells (active or inhibited): Ganglion cell action potentials: Baseline activity Baseline activity Decreased firing rate Increased firing rate Weak signal Weak signal No signal Strong signal Edge/contrast detection: At the boundary excitation and inhibition are not balanced and In regions of equal luminance thus increase the (in the middle of dark or relative difference, bright regions) excitation and 'sharpen' the transition inhibition cancel each other between dark and bright Ganglion Cell Visual/Receptive Fields Color opponent ganglion cells can have centers and surrounds each with separate color opponent/antagonist properties. Thus can not see red-green Ganglion Cell Visual/Receptive Fields Afterimages: Stare at the RED X in the middle of the green figure on the left for 15-30 seconds. Then move your gaze to the white square. Did the colors reverse themselves? Ganglion Cell Visual/Receptive Fields This can be explained by adaptation (i.e. red cones stop firing when stimulated too long) and the opponent-color theory (i.e. exposed to subsequent white light, green cones send unopposed message through red-green channel) Colorblindness: Genes for red and green are both on X chromosome; because men have only one X, they most likely to miss one gene. A test for red-green colorblindness: People with normal color vision should see an 8 on the left and a 5 on the right. People with red-green color blindness may see 3 on the left and 2 on the right. (Ishihara, S., 1954. Tests for colour-blindness. Tokyo: Kanehara Shuppan.) Visual Fields and Binocular Vision Visual Fields and Binocular Vision Visual field Binocular Visual field zone One side of visual Left Right visual visual field is processed field field Binocular zone on opposite side of brain Monocular zone Portion of visual Optic chiasm field associated Optic nerve with only one eye 2D Optic tract Binocular zone where both eye’s Lateral geniculate body visual fields (thalamus) overlap 3D Visual cortex Figure 10-43 Visual Fields and Binocular Vision  Neural Pathways for Vision b) Neural pathway for vision, lateral view Eye Optic Optic Optic Lateral geniculate body Visual cortex nerve chiasm tract (thalamus) (occipital lobe) Figure 10-31b Visual cortex Lateral geniculate body is organized in layers that correspond to different parts of visual field, thus info of adjacent objects is processed together Visual cortex From From This topographical Left Eye Right Eye organization is R L R maintained in the R visual cortex, with six layers of neurons Layers of Cortex grouped into vertical columns Within each portion of the visual field, info is sorted by form, color (“blobs”) and movement Watch video on Physiology of vision: https://www.youtube.com/watch?v=AuLR0kzfwBU