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The Retina

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McMaster University
Laura Parker

The Retina 0. Introduction - Images from the retina are analyzed for form/movement/color. For each point in the outside world, there is a corresponding image point on the retina in each of the two eyes. These images from the two eyes are then brought together and compared at higher stations in the visual pathway for extration of information about depth. - Development of retina: The prosencephalon protrudes laterally and enlarges to form primary optic vesicles. These later invaginate to give double-walled optic cups, with a largely obliterated ventricular space between the two walls. The outer wall becomes the pigment epithelium, while the inner wall becomes the neural retina. The two are separated by the subretinal space, the residue of the ventricular cavity. I. Structure of retina - The retina is composed five main types of neurons, segregated in to three main layers: 1) Outer nuclear layer: photoreceptors, no direct blood supply. Instead, they receive nourishment from the choroidal circulation filtered thru the pigment epithelium. 2) Inner nuclear layer: bipolar (second order visual neurons), horizontal (lateral association neurons), amacrine (ditto), Mueller glial cell bodies 3) Ganglion cell layer: retinal ganglion cells (third order visual neurons, who axons constitute the optic nerve). - The outer and inner plexiform layers are sites of synapses between layers II. Photoreceptors - There are two types of photoreceptors 1) rods: most sensitive in dim light, only one type 2) cones: less sensitive to light, three types mediate color vision (peaks at blue, green and yellow). - Distribution of photoreceptors is not uniform: fovea has high density of cones and few rods, periphery has more rods. Blue sensitive cones are also absent from the center of the fovea. - The fovea has the highest visual acuity, or spatial resolution of the visual space. This is achieved by having thinner cones and more of them per unit space than elsewhere in the retina; with the layers of cells anterior to the receptors being pushed aside. This clearing minimizes light scattering which tends to degrade the quality of the image. - The structure of the photoreceptors: o Outer segment: where light is absorbed and a neural signal is generated. It contains an orderly stack of membranes in which is embedded the light sensitive visual pigment (rhodopsin in rods, and one of three cone pigments in cones). In cones these membranes are continuous with the plasma membrane to form a highly convoluted surface membrane. In rods, the membranes are completely internalized to form a stack of flattened membranous discs. The high density of pigment provides a high probability of absorption of an incident photon. o Inner segment: contains the metabolic machinery of the cell, while the synaptic terminal forms chemical synaptic connections with bipolar and horizontal cells. o Glu is the NT released by both rods and cones. - Pigment epithelial cells serve to (1) absorb light not absorbed by the rods/cones using melanin, (2) phagocytose shedded fragments of rods/cones, (3) regenerate pigment by supplying frest chromophore to the bleached pigment in the outer segment. III. Visual pigments - Pigment is composed of a chromophore covalently bound to an opsin 7TM protein that is different in different pigments. The two parts are joined together by a protonated Schiff base. - Humans have 4 pigments (1 rod, 3 cones) each maximally sensitive at different wavelengths - Upon photon absorption, the chromophore undergoes several configuration changes; the configuration that triggers vision takes several ms to reach; the ultimate result is the release of chromophore, and binding of fresh chromophore with opsin IV. Phototransduction - In darkness, rods and cones have a membrane potential of about –30 to –40 mV. - Rods/cones hyperpolarize in response to light in a graded fashion with respect to intensity. Cones require more light and their responses rise and fall more rapidly than rod responses. Their briefer responses permit cones to have a better time resolution of light stimuli. - Phototransduction mechanism: In darkness the surface membrane of the outer segment has a higher permeability to cations, as a result of which there is a steady influx of sodium (and Ca and Mg) ions into the outer segment, being driven by their inward-directed electrochemical gradients. This steady influx of + charge in darkness (the dark current) maintains the cell in a partially depolarized state and, consequently, a steady release of NT from the cell’s synaptic terminal onto second-order neurons. In light, the ionic permeability of the outer segment is reduced, thus decreasing the influx of cations and producing a membrane hyperpolarization, which spreads passively to the synaptic terminal where it reduces the rate of transmitter release from the receptor. The permeability reflects the opening of a cGMP-activated conductance, which by itself has no intrinsic light sensitivity. Light, however, closes the conductance by activating an enzyme cascade that leads to the lowering of the cGMP level in the outer segment. Metarhodopsin II, an intermediate photoproduct of rhodopsin, catalyzes the activation of GPCR (rod/cone transducin) thru GTP binding  G-prot activates cGMP phosphodiesterase  which hydrolyzes cGMP  GMP. Shut off of the cascade involves: 1) phos of the photisomerized rhodopsin, rendering less effective in activating the G-prot, followed by final capping due to binding of another protein called arrestin to the phos rhodopsin. 2) deactivation of the active G-prot thru its intrinsic GTPase activity, which converts the bound GTP to GDP. 3) turn off of the active phosphodiesterase by rebinding of an inhibitory subunit of the enzyme. Summary - In dark, cGMP keeps a nonselective cation channel open, and cell is depolarized. Rhodopsin is coupled to G-protein that activates phosphodiesterase and lowers [cGMP]. - Ca influx plays a key negative feedback function and mediates light adaptation. In dark, there is a circulation of Ca++ at the surface membrane of the outer segment, consisting of an influx thru the cGMP-gated channels and an efflux thru a transport mechanism involving an exchange of cations. In the light, the Ca++ influx stops due to closure of the channels, but the efflux continues, thus resulting in a decrease in the cytosolic Ca++ concentration. This decrease leads to 1) an increase in guanylate cyclase activity 2) a more effective phosphorylation of the photoexcited rhodopsin and 3) a higher likelihood of channel opening by cGMP. These effects all antagonize the action of illumination, and underlie the ability of photoreceptors to adapt to background lights. V. Synaptic connections in the retina (see Figure on p. 12) - The synaptic terminals of rods and cones are morphologically different with rods ending in spherules (smaller and round) and cones ending in pedicles (larger and with a flat base). These terminals form connections with horizontal cells and bipolar cells. - Throughput pathway: photoreceptor  bipolar  retinal ganglion cell  optic nerve - Lateral associations: between photoreceptors (via gap junctions), and via horizontal and amacrine cells - There are distinct synapse morphologies in the retina - Synaptic triad: photoreceptor with horiztonal-bipolar-horizontal cells, and contains a synaptic ribbon - Dyad: proximal bipolar end synapses with two cells - Primary nxt’s in the retina are Glu (excitatory) and GABA (inhibitory, released by some horizontal cells). DA is released from interplexiform cells. VI. Information processing in the retina - Only amacrine and ganglion cells give all-or-none impulses. The rest of the cells in the retina have graded responses. - The receptive field of a single photoreceptor is bigger than itself due to connections with neighboring photoreceptors; for the same reason, the receptive field of horizontal cells is bigger than the multiple photoreceptors it contacts - Since bipolar cells receive synapses from both photoreceptors and horizontal cells, their receptive field is divided into a center (dominated by photoreceptor) and surrounding antagonistic ring (dominated by horizontal cells) - In light, on-bipolars depolarize in response to light in the center of its receptive field and hyperpolarize in response to light on the surrounding ring; off-bipolars are vice versa. In terms of synaptic organization, an on-bipolar cell’s receptive field is derived from sign-inverting (i.e. hyperpolarizing) synapses from the receptors (in the field center) and sign-preserving (i.e. depolarizing) synapses from the horizontal cells (for the surround). - The above property of bipolars, propagated to on- and off-center ganglion cells, probably helps mediate contrast and edge detection - Ganglion cells have a center-surround receptive field organization like bipolar cells. In terms of synaptic connections, the on-center ganglion cell probably receives sign-preserving inputs from on-bipolars in its field center. The on-bipolar cell already has a center-surround organization, but, in addition, the on-bipolar cells in the surround probably excite amacrine cells, which in turn have an inhibitory input on the ganglion cell. They can also be classified as X (slow adapting) and Y (fast adapting) types. - Amacrine cell firing pattern is best fit to respond to moving objects. When light is shown anywhere in their receptive field, these cells usually depolarize transiently at the on and the off of the illumination. The do not have a center-surround organization. Early Vision: Retina and LGN I. Ganglion cells: - M Ganglion cells: large cells bodies with widely branching dendrites and a large myelinated axon; large, center-surround receptive fields but with no preference for wavelength; display a brisk response so long as an appropriate stim is moving, responding to both the leading and trailing edge; rapid adaptation is stimulus is held in place; projects to LGN. - P Ganglion cells: smaller cell bodies with narrow dendrites and smaller myelinated axon; small, center-surround receptive fields, with single cone projecting to center and many to surround, which are specific for wavelength (e.g. Red-ON center); will continue to dire as long as appropriate stim is present in receptive field; projects to LGN. - Small bistratified cells (SBS): fairly large receptive field that is ON to short wavelengths (blue) and OFF to both long and middle (Red and Green); center only, no surround; extremely sensitive to insult to nervous system (acquired tritanopia); projects to LGN. - Melanopsin containing ganglion cells project to the SCN in hypothalamus to entrain circadian rhythms and are capable of transducing light in the absence of rods and cones. - Ganglion cells that send axons to regions in the midbrain: Superior colliculus deals with reflexive eye movements; pretectum plays a role in controlling the size of the pupils as the level of light increases or decreases. These cells have small cell bodies but large dendritic fields and receptive fields. II. Specialization of the retina: - At the fovea, all ganglion cells, bipolar cells and their processes are swept to the side creating a pit where light can get to the outer segments of the cones without having to travel thru a bunch of junk. - Each cone in the fovea synapses directly onto 5 bipolar cells, and each of those bipolar cells synapse on a single ganglion. So you have five ganglion cells carrying separate signals to the brain from a single cone. - Ganglion cell axons penetrate thru the retina at the optic disc (blind spot) to form the optic nerve. III. Optic nerve and tract - Axons in the optic nerve cross at the optic chiasm so that each optic tract represents the contralateral visual field. Axons from nasal side of retina cross midline; temporal side axons remain ipsilateral and each hemifield info travels together in the optic tract. Information from each visual hemifield is processed by the contralateral cerebral hemisphere. - Only the extreme periphery of each hemifield is processed by a single eye (monocular crescent). - Damage in optic tract and back (caudal to chiasm) results in damage to vision in contralateral visual hemifield. - There are three major visual pathways: 1) optic tract  LGN  primary visual cortex (higher visual processing) 2) optic tract  superior colliculus (saccades) 3) optic tract  pretectum (pupillary light reflex) IV. Lateral Geniculate Nucleus (LGN) - Visuotopic map: central retina  posterior (caudal) LGN; peripheral retina  anterior (rostral) LGN; superior retina  lateral LGN; inferior retina  medial LGN. - LGN is made of 6 layers: magnocellular 1,2 and parvocellular 3-6 - There are 4 Parvo layers because there is two for each eye, with one for ON-center and one for OFF-center receptive field ganglion cells each. - Ipsilateral retina maps to layers 2,3,5 (prime!) and contralateral to 1,4,6 - LGN neurons have receptive fields that resemble on- and off-center ganglion cells - Intralaminar cells respond to blue light only, may be responsible for color V. LGN to primary visual cortex - LGN projects dorsally to V1 in the occipital lobe with inferior-superior inversion with respect to visual field (this makes the object appear right-side up to the cortex since the image was initially inverted by the lens). - Neurons in V1 are the first to respond not to spots of light, but to lines, bars and edges. - Neurons in V1 are first to respond to activity in both eyes; they have binocular receptive fields. Visual Cortex: Organization and Plasticity I. Primary visual cortex - Located in both banks of calcarine sulcus - Consists of 6 layers and the physiological properties in V1 vary from one layer to the next. - Neurons above layer 4 send their axons to other areas of cerebral cortex whereas below layer 4 send their axons to subcortical targets. - Foveal region has high cortical magnification in dorsal/caudal V1. Parts of the visual field progressively farther away from the foveal representation are mapped at progressively more rostral parts of V1. - All axons of neurons in both Magno and Parvo layers of the LGN terminate layer 4 of V1. The bigger cells in the upper half of layer 4 receive all axonal input from Magno LGN and the smaller cells in the lower half from Parvo LGN. Layer 4 amplifies imput and sends it along to layers 2 and 3. - Layer 4 is organized in alternating ocular dominance columns - Columns in LGN project to same part area of V1 (recall that layer 4 receives thalamic input) - Parvocellular  layers 4Cβ and 4A in cortex - Magnocellular  layers 4Cαand 4B in cortex - Intralaminar projects to layer 3 - Layers 2 and 3 respond preferentially to bars, edges and contours, not just spots. Moreover, the neurons respond selectively for the orientation of a bar, with responses maximum at one angle but still responds +/- 20/30 degrees. - Layers 2 and 3 communicate, in part, with layers 5 and 6. - In V1, input is sent to stellate interneurons, with output via pyramidal cells - Input and output comes from/goes to LGN, pulvinar, superior colliculus, other cortical areas II. Columns - A cortical column is a collection of neurons across all layers that are similar to one another in some functional property and that differs from neurons in adjacent columns by that same property. - Ocular dominance and orientation selectivity properties stand out dramatically in V1. o Ocular dominance:  Neurons in layer 4 are monocular: they are driven exclusively by stimuli falling on one retina. Their projections are generally vertical (radial connectivity), neurons throughout V1 create columns about 1 mm wide that display dominant responses to one eye. The columns alternate between contralateral and ipsilateral eyes. But some projections from 4 cross borders such that neurons in layers 2 and 3 are the first with binolcular receptive fields. Ocular dominance columns are the means whereby signals from the two eyes are kept separate initially and then combined in a precise manner to provide subsequent stages a strong signal about depth.  Any perturbation in the vision of one eye disrupts the normal pattern of ocular dominance organization, leading to expansion of columns dominated by the normal eye and shrinkage of columns dominated by the deprived eye. o Orientation selectivity:  Layers 2 and 3 show fairly sharp tuning for the orientation of a stimulus and their vertical projections create columns in V1 down thru layers 5 and 6 that are all tuned to the same orientation. Over the distance of 1 mm, a full coverage of all stimulus orientation is made (180 degrees). III. Early Development of visual cortex organization - Despite the diminished light level and the absence of patterned visual input in the uterus, babies are born with ocular dominance columns already established. - In both the LGN and V1, competition for trophic factors appears to be the principal means for establishing segregated inputs. Coordinated activity among adjacent cells is the means whereby neighboring cells come to terminate next to one another. - The neurotrophins are normally released in tiny amounts by cortical neurons, thereby setting up a competition among axons that innervate cortical neurons. When a super- abundance of the neurotrophins is experimentally presented into the V1 of a neonate, geniculocortical axons no longer segregate into ocular dominance columns. This failure occurs because the competition between axons driven by the ipsilateral and contralateral eye has been eliminated by excess neurotrophin. IV. Later Development and the critical period - Deprivation by lid-suture: If suturing is done early enough in the postnatal period, the result is a dramatic rearrangement of ocular dominance columns with the normal eye expanding (not abnormal retention) to take up >90% of the total cortical volume. The columns driven by the deprived eye shrink as a result of loss in synaptic sites. Moreover, the cells that are still driven by this eye are weakly active and fatigue easily with repeated presentation of stimulus (amblyopia). - Deprivation by strabismus: If one of the muscles that moves an eye is damages, that eye looks inward or outward, but it is aimed differently than the other, normal eye. The result is the same level of light and the same extent of patterned visual input reaches the two eyes, but the two see different things. As a result, connectivity and column development is normal, but all neurons are monocular (even in layers 2, 3, 5) The most likely explanation is that cells in layer 4 no longer maintain some axonal connection across ocular dominance columns. - Critical periods: first 22 weeks in rhesus monkeys, first 22 months in humans. - Reverse-Deprivation experiments ask what happens if, during the critical period, a deprived ye is returned to normal and the formerly normal eye is deprived/patched? Development of connections and columns can be normal is timed right, but cortical cells with binocular receptive fields fail to develop. Therefore, the use of stereoptic cues for depth perception is permanently lost. Extrastiate Visual Processing - Higher visual areas can be broadly divided into two parts - Dorsal pathway (where): spatial position and motion, input primarily magnocellular - Ventral pathway (what): shape, texture, color of objects, input from all layers of LGN - Secondary visual cortex can be stained to reveal a thick-pale-thin-pale stripe pattern - Color sensitive neurons in V1 CO blobs  thin stripe V2  ventral pathway, V4 - Neurons with fine spatial sensitivity in V1 layer 2/3 interblob  pale/inter stripe V2  ventral pathway, V4 - Motion sensitive neurons inV1 layer 4B (magno.)  thick stripe V2  dorsal pathway, MT I. Introduction to the ventral pathway - The ventral pathway processes shape and color - It is composed of V1, V2, V4, V8 (most color sensitive region in brain), and inferotemporal regions (ant., post., central) - Other miscellaneous regions - Lateral occipital (LO): object/shape - Fusiform face area (FFA): face stimuli or complex shape stimuli - Prospagnosia: the selective inability to recognize individual faces; a result of FFA lesion. - Parahippocampal place area (PPA): landscapes and building interiors - Extrastriate body area (EBA): bodies and body parts - As you progress in an anterior direction toward higher levels in the ventral pathway, receptive fields become larger, more bilateral, more concentrated near the fovea, and cells become increasingly sensitive to large-scale complex shape properties. - The neural mechanism underlying shape perception is not fully understood but it appears to be a parts-bases processing system in which the capacity of encode a large number of objects as combinations of parts. II. V1: simple orientation tuning - V1 cells are tuned to the orientation of lines/edges - Simple cells: tuned to orientation, position variant - Have on/off receptive fields structured to recognize edges, perhaps as a result of convergent input of multiple LGN cells whose receptive fields are aligned - Complex cells: also tuned to orientation, but position invariant - This property may be a result of convergent input of multiple simple cells - Hypercomplex cells: added property of end-stopping (tuned to short lines) - Columnar organization: each column is orientation tuned, and exact orientation shifts gradually from column to column - Color contrast is mediated by single- or double-opponent receptive fields III. V2: more complex visual processing than V1 - V2 has a thick-thin-pale-thin stripe pattern - Thick: tuned to motion, depth - Thin: tuned to color and is organized in a hue map - Pale: tuned to shape - V2 cells have property of figure ground segmentation: tuned to properties of object outside receptive field (e.g. what side is the object on?) - Unlike V1, will respond to illusionary contours IV. V4: curvature tuning - V4 cells are tuned to curvature, the start of part-based coding - Color tuning in V4 is complex V. Inferior temporal regions: highest level of ventral pathway, parts-based coding - Integrates edge and contour information to code objects as a collection of geometrical parts - Even complex objects like faces can be represented in a parts-based way I. Introduction to the dorsal pathway - The dorsal pathway processes depth and motion - Components of the dorsal pathway are V1, V2, V3, middle temporal (MT), medial superior temporal (MST), intraparietal regions (lat., vent., med., ant.), and area 7a - MT is buried in the superior temporal sulcus and receives inputs from layer 4B in V1 and the thick stipes in V2, which contain a high percentage of cells tuned for motion direction and cells tuned for position in depth. MT neurons show strong tuning for motion and depth. - Dorsal division of MST, MSTd, is specialized for processing optic flow, movement fields produced when the observer translates thru the environment. Some neurons in MST show complex interaction between motion direction and stereoscopic depth. This type of interaction is thought to relate to MST’s role in representing optic flow. If we walk while gazing off to the left, the optic flow of near objects across the retina will be leftward, while the optic flow of far objects will be rightward. - Lateral division of MST, MSTl, is specialized for smooth pursuit eye movements. - LIP is associated with eye position and saccadic eye movements. - VIP processes both visual and somatosensory information about peripersonal space. Many of these neurons are sensitive to both visual and tactile motion. - MIP is associated with arm reach movements. - AIP is associated with spatially precise grasping of objects with the hand. - The sequence LIP  MIP  AIP is responsible for grabbing objects of interest - 7a, on the surface of the inferior parietal lobe, is considered the highest stage in the dorsal pathway, and may be the site of convergence of multiple kinds of spatial information. - Parietal cortex is also thought to be critical for controlling spatial attention. - Lesions in the human parietal cortex can cause - Attentional hemineglect: neglect of contralateral space, also manifested in memory - Constructional apraxia: inability to reproduce complex objects - Lesions to MT and MST (MT+) can cause akinetopsia, the inability to perceive motion. II. V1, V2: lower level processing of stereoscopic vision - 3D depth perception is achieved by stereopsis: there is a slight disparity between the images on the two retinas - Both V1 and V2 are tuned to binocular image disparity and motion direction III. MT: intermediate level processing - MT cells respond to motion direction and speed, as well as to binocular disparity. V1 and V2 cells (especially in the thick CO stripes) tuned for binocular disparity project preferentially to area MT. - MT receptive fields are larger than in lower levels - MT columns are organized in smooth gradients of direction preference and stereoscopic depth - Microstimulation of MT cells can bias perception of motion direction and depth IV. Note on visuospatial coordinate systems - Visual system must deal with information coded in various coordinate systems (e.g. retinotopic, head-centered, body-centered, etc.) - How coordinates systems are dealt with - Sequential transformation from one system to another as one progresses along the visual pathway, so any given level uses only one coord sys: evidence for this in lower levels - Integration of info in multiple coordinate systems, resulting in a mix of spatial sensitivity: most cells in higher areas do this The Auditory Periphery I. Introduction to hearing - Sound is a pressure wave, and pure tones can be characterized by amplitude (measured indirectly as dB) and frequency - Dynamic range of hearing in human is about 0-100 dB (whisper to pain) and 20-20K Hz - Types of damage to ear - Chronic severely loud sound exposure kills hair cells - Ototoxic antibiotics, e.g. streptomycin or gentamicin, kills hair cells - Hearing loss of high frequencies with age, aka presbycusis I. Anatomy of the ear A) Outer ear - Pinna: collects and funnels sound toward the opening to the auditory canal, thus amplifying sound; sound shadows from sounds coming from different positions in space provide resolution of sound origin - External auditory canal: acts as resonant tube for 4 kHz tones B) Middle ear - Impedance matching of air to water sound transmission by three mechanisms (1) Area of tympanic membrane is 20x that of stapes footplate (2) Lever advantage of ossicles (malleus, incus, stapes) (3) Oval window of stapes is smaller than eardrum - Middle ear muscles (tensor tympani, stapedius): restrict ossicle movement in response to loud sound to prevent damage. The tensor tympani reduces the area of the flexible membrane in the eardrum; the stapedius restricts the amplitude of stapes motion. - Damage in the middle ear is called “conductive.” A common cause is otosclerosis in which bony growth impedes the movement of the middle ear ossicles. C) Inner ear (more on cochlea below) - Damage in the inner ear is called “sensorineural” - One can distinguish between conductive and sensorineural hearing loss by comparing the audibility of a tuning fork held in the air, or pressed against the skull. In conductive hearing loss, the latter position is effective at presenting sound by bone conduction, thus overcoming the conductive loss that pertains to air-borne sound. III. The Cochlea - Memorize cochlear structure (e.g. figure on p. 5) - The stapes footplate moving in and out if the oval window sets up a fluid wave within the scala vestibule. The motion of this wave causes the cochlear partition to move alternatively up and down within the cochlear duct. The cochlear partition of the basilar membrane and the hair cells, supporting cells and extracellular structures lying upon it, and the overlying tectorial membrane. These all lie just under the scala media, the central membraneous tube flanked on top and bottom by the scala vestibule and scala tympani, respectively. The scala media is bounded by Reisnner’s membrane on the top and is actually delimited by the apical surface of the hair cell epithelium on the bottom, not by the basilar membrane. This distinction is important because the scala media is filled with endolymph (high K, low Na), which is produced by a secreting epithelium called the stria vascularis that lines the outer wall of scala media. The s. vestibule and tympani contain perilymph (low K, high Na). Since the basilar membrane itself does not present a diffusion barrier, the basal surface of the hair cells is bathed by low K perilymph while their apical, hair-bearing surface faces high K endolymph. This disposition of ionic media is important for hair cell function. Since endolymph is 80 mV positive to perilymph, this endolymphic potential provides additional driving force for K+ ions to flow into hair cells. - Meniere’s disease arises under conditions in which the normal circulation of endolymp is blocked or altered resulting in sensorineural hearing loss. - There are two classes, inner and outer, of hair cells. In a cochlear cross section one can see the single row of flask-shaped inner hair cells, and three rows of columnar outer hair cells. - Stereocilia of hair cells are arranged in rows of increasing height and are embedded in the tectorial membrane; shear of basilar membrane with respect to tectorial membrane causes displacement of hair bundle - Tip links join nonselective cation channels on one stereocilium to the next tallest one  tilting of the stereocilia causes channel to open or close  open channel allows K, the primary cation of endolymph to travel down steep electrical gradient into hair cell and depolarize it  if depolarized, hair cell opens voltage gated Ca channels, allows Ca in, and releases Glu onto the nerve ending (see also p. 9) - Hair cell adaptation may occur through two suggested negative feedback mechanisms (1) end of tip link is attached to myosin-like motor (myosin 1C) on stereocilia, movement up or down changes the set point of system. Myosin 1C exerts steady force on the transduction channel. (2) Ca entry feeds back to regulate the mechanotransduction channel - Synaptic transmission: At its basal end the hair cell is contacted by afferent fibers whose cell bodies are located in the spiral ganglion and which send an axon centrally to end on the cochlear nucleus of the brainstem. When the hair cell is depolarized by opening of the transducer channel, voltage dependant calcium channels in the basolateral membrane are opened and synaptic vesicles fuse with plasma membrane to release Glu, which binds to AMPA receptors causing excitation of the afferent axon. This depolarizing effect of v-gated Ca+ influs is counterbalanced by v-gated K+ channels that dominate the basolateral conductance of the hair cell and allow outward flow of K into low K perilymph. - Individual afferent neurons makes only a single contact with a single inner hair cell. At the point of contact, the hair cell places a synaptic ribbon, an electron-dense body to which a number of transmitter-containing vesicles are tethered. It is thought the ribbon serves to motivate vesicles for release during stimulation by sound and during the ongoing spontaneous activity that occurs in silence. - Nearly all afferent nerves end on inner hair cells, whereas efferents end on outer hair cells. The crossed olivo-cochlear bundle arises from the contralateral superior olivary complex and synapses massively on outerhair cells. This pathway is inhibitory and when activated, causes a loss of sensitivity and freq selectivity in afferent fiber response. - Outer hair cells exhibit electromotility (contract on depolarization and vice versa) to regulate distance of tectorial membrane to inner hair cells and adjust their sensitivity; this mechanism depends on a motor protein called prestin. Targeted disruption of prestin in mice causes deafness. - OHCs express a Ca channel opened by ACh from efferent nerves; the Ca causes K channels to open and results in hyperpolarization, which ultimately results in loss of sensitivity - Otoacoustic emissions: active movement of basilar membrane can generate sound. - Active motions of OHCs are driven by the sound-evoked change in membrane potential. These active motions enhance the overall vibration pattern of the cochlear partition, thereby causing larger deflections of the IHC bundle. Cochlear signaling is enhanced by OHC electromotility. If OHCs are damaged, the cochle becomes much less sensitve. Thus, the efferent innervation of the cochlea, which causes a suppression of cochlear sensitivity, must do so by inhibiting OHCs. This occurs via cholinergic inhibition of cochlear hair cells from olivocochlear efferent activity. Hair cells are depolarized by nicotinic AChR, but only briefly. Ca++ enters the cell thru the receptor and causes the opening of Ca++ dependant K+ channels, of which there are many, causing a net hyperpolarization of the hair cell’s membrane. The Peripheral Auditory System – Auditory I I. Human perceive the frequency and loudness of sound - The dynamic range of human perception is about 100-16,000 Hz and 0-120 dB - The dynamic range of conversational speech is a small subset of total perception - One way to measure a tuning curve is to measure the loudness needed to mask a probe of single tone as a function of frequency; obviously, minimum loudness is needed when mask frequency is same as probe II. Speech consists of a mixture of tones of different frequencies - Different vowel sounds are the result of the shape of the vocal tract and how it modifies the tone produced by the vocal folds - The information needed to recognize vowel sounds is encoded as peaks of energy at certain frequencies; these peaks are called formants - The precise value of formants can vary from person to person (e.g. due to size of vocal tract), but are still recognized because vowel sounds cluster in formant-space III. Basilar membrane (BM) is responsible for tuning: the separation of sound into its component frequencies - The most important aspect of BM motion is that it is tuned, meaning that points on the BM are differentially sensitive to different frequencies in the sound stimulus. - Sound results in a traveling waveform in the BM, and the position of maximum displacement depends on frequency (high freq near stapes, low freq near apex) - Since hair cells sense motion of the BM at one point only, each hair cell inherits from the BM a selectivity for frequency, in which the hair cell is most sensitive to the freq that causes maximum BM motion at the point of the hair cell’s innervation. Likewise, since auditory nerve fibers are distributed down length of cochlea, each ANF has a different best frequency, giving rise to a tonotopic representation of sound - Outer hair cells are responsible for sound sensitivity: they amplify BM movement in response to soft sounds and partially damp BM movement in response to loud sounds; loss of OHCs (e.g. due to kanamycin) results in loss of sensitivity and broadened tuning IV. Auditory nerve fiber is phase-locked (there is a close relationship between the stimulus waveform (produced by the back-and-forth motion of hair cell flexion) and the acti
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