50-55.pptx

UNIT 10 Chapter 50: The Eye: I. Optics of Vision Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Physiological Anatomy of the Eye Suspensory fibers that connect ciliary muscle with lens White outer layer. Continuous with cornea at front. Transparent, jellylike tissue. Contains photosensitive cells. 2/3 of refractive power of eye. Resculptured in LASEKS/LASIKS surgery Visual acuity is highest. Cones only. Optic disc Aka, Optic nerve head or blind spot. Exit point for axons. Entry point for retinal blood vessels. Nasal to fovea. Free flowing, watery fluid. Fills anterior and posterior chambers Needed for Vascular layer between accommodation retina and sclera. Feeds . outer layers of retina, ciliary body, and iris. CN II. Contains retinal ganglion cell axons and glial cells. About 1.5 million axons. Refractive Index • Speed of light in air 300,000 km/sec. • Light speed decreases when it passes through a transparent substance. • The refractive index is the ratio of speed in air to speed in the substance. – For example, if speed in a substance = 200,000 km/sec, R.I. = 300,000/200,000 = 1.5. • Light rays bend when passing through an angulated interface with a different refractive index. • The degree of refraction increases as the difference in R.I. increases and the degree of angulation increases. • Structures of the eye have different R.I. and cause light rays to bend. • These light rays are eventually focused on retina. Polycarbonate RI: 1.58 Figure 50-1 Refractive Principles of a Lens Convex lens focuses light rays Concave lens diverges light rays. TMP14, Figure 50-2 TMP14, Figure 50-3 Note that a point source of light has a longer focal length compared to light from a distant source; this is why an object comes into focus as it moves closer to the eye in a person with myopia (nearsightedness, long eyeball). Refractive Power of the eye - Diopter • • 2/3 of refractive power of eye resides in anterior surface of cornea. This refraction is virtually eliminated when swimming under water since water has refractive index close to that of cornea; hence, you get a blurry image underwater. Lens has less refractive power, but it’s adjustable. – a diopter is a measure of the power of a lens. – 1 diopter is the ability to focus parallel light rays at 1 meter. – the retina is about 17 mm behind refractive center of eye. – hence, the eye has a total refractive power of 59 diopters (1000/17). 1000/17 = 59 diopters 17 mm TMP14, Figure 50-8 TMP14, Figure 50-9 Accommodation • Refractive power of lens is 20 diopters. • Refractive power can be increased to 34 diopters by making lens thicker; this is called accommodation. • Accommodation is necessary to focus image on retina. • An untethered lens is almost spherical in shape. • Lens is held in place by suspensory ligaments (zonule fibers) which under normal resting conditions causes the lens to be almost flat. • Contraction of ciliary muscle decreases tension in the suspensory ligaments, allowing the lens to become more spherical (thicker); this increases the refractive power of lens. • Under control of parasympathetic nervous system. Presbyopia: Also called age-related farsightedness. It’s the inability to accommodate. The lens gets harder and less flexible with age because of decreased levels of Power of accommodation α-crystallin. decreases with age: Child, 14 diopters (34-20) 50 years old, 2 diopters 70 years old, 0 diopters TMP14, Figure 50-8 TMP14, Figure 50-10 Errors of Refraction Normal vision corrected with convex lens Far sightedness Near sightedness Guyton, Figure 50-12 Astigmatism: unequal focusing of light rays due to an oblong shape of the cornea. corrected with concave lens Hyperopia and Myopia ciliary muscle relaxed “farsightedness” Ciliary muscle relaxed Ciliary muscle contracted HYPEROPIA (farsightness) • caused by a short eyeball or sometimes a weak lens. • contraction of ciliary muscle increases strength of lens (i.e., reduces focal distance). • So, a farsighted person can focus distant objects on retina because of accommodation. • If there is sufficient accommodation left, a farsighted person can also focus close objects on retina. MYOPIA (nearsightness) • caused by a long eyeball or sometimes too much refractive power in lens system. Genetic and ciliary muscle relaxed environmental factors contribute to myopia – too much close work can promote myopia. No mechanism to focus distant objects on retina (contraction of ciliary muscle would make distant “nearsightedness” objects even more out of focus). • Objects come into focus as they move closer to As an object moves toward the eye. eye, the rate of parasympathetic stimulation increases, causing the ciliary muscle to contract. What happens to the lens? Cataracts leading cause of blindness worldwide • Cataracts – cloudy or opaque area of the lens caused by coagulation of lens proteins – Accounts for about half the cases of blindness in the world. – UV solar radiation is major factor in production of cataracts Surgical implantation of plastic lens can usually restore vision. ~6 million per year. Visual Acuity • • • • 20/20 – ability to see letters of a given size at 20 feet (normal vision) 20/40 – what a normal person can see at 40 feet, this person must be at 20 feet to see. 20/200 – what a normal person can see at 200 feet, this person must be at 20 feet to see. 20/15 – Means what? Ans. can see at 20 feet what a person with 20/20 vision could only see at 15 feet Snellen chart Fluid System of the Eye • Intraocular fluid keeps eyeball round and distended. • 2 fluid chambers. • aqueous humor, in front of lens. (freely flowing fluid). • vitreous humor, behind lens (gelatinous mass with little fluid flow). • Produced by ciliary body at rate of 23 microliters/min. (~3-4 mL/day) • Flows through pupil into anterior chamber; then between cornea and iris, through meshwork of trabeculae to enter the canal of schlemm which empties into extraocular veins . TMP14, Figure 50-19 Intraocular Pressure •Normally 15 mm Hg (range: 2-20 mm Hg). •Level of pressure is determined by resistance to outflow of aqueous humor in canal of Schlemm. •Rate of production of aqueous humor is constant under normal conditions (can be increased in systemic hypertension). •Increased pressure can cause blindness due to compression of axons of optic nerve as well as blood vessels. Long-term hypertension is a risk factor for glaucoma. Hall, Figure 5021 Glaucoma 2nd leading cause of blindness worldwide (after cataracts) • Usually caused by high intraocular pressure (IOP). Increased IOP compresses blood vessels and axons of optic nerve at optic disc; this leads to poor nutrition of nerve fibers. Two main types of glaucoma • Open angle and closed angle (angle refers to area between iris and cornea). Open angle glaucoma (also called Chronic glaucoma) • 90% of cases in U.S. • Insidious – no pain initially • reduced flow through trabecular meshwork (tissue debris, WBC, deposition of fibrous material, etc). Types of Glaucoma Eye Drops Closed angle glaucoma Prostaglandin analogs - increase outflow of fluid • 10% of cases in U.S. – sudden closure of from eye. iridocorneal angle with sudden ocular pain. A Beta blockers – decrease production of intraocular fluid. medical emergency. Alpha agonists - decrease fluid production and • Treatment: Laser peripheral iridotomy (LPI), increase drainage. where an opening in the iris is made using a Carbonic anhydrase inhibitors (CAIs) – decrease UNIT 10 Chapter 51: The Eye: II. Receptor and Neural Function of the Retina Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Retina • Light sensitive portion of eye. • Contains cones for color vision. • Contains rods for night vision. • Contains neural architecture. • Light must pass through neural elements to activate light sensitive rods and cones. But this is not so bad since neural elements are virtually transparent in vivo. • Each retina has 100 million rods; 3 million cones; and 1.6 million ganglion cells. TMP14, Figure 51-1 The Fovea • It’s a small area at center of retina ~1 mm2. • center of fovea, called “central fovea” or “fovea centralis” contains only cones. • these cones have special structure. • aid in detecting detail. • In central fovea, neuronal cells and blood vessels are displaced to each side so light can strike cones with less obstruction. • This is area of greatest visual acuity. • At central fovea: no rods, and ratio of cones to ganglion cells is 1:1; this explains high degree of visual acuity in central retina. Figure 51-2 Figure 51-2 Distribution of rods and cones Structure of Rods and Cones Pigment layer Guyton, Figure 51-4 Guyton, Figure 51-3 Rods and Cones RODS • high sensitivity; specialized for night vision (scotopic vision) • more photopigment • high amplification; single photon detection • saturate in daylight • slow response, long integration time • more sensitive to scattered light • low acuity; highly convergent retinal pathways, not present in central fovea • Achromatic; one type of rod pigment (rhodopsin) •More common in the periphery CONES • lower sensitivity; specialized for day vision (photopic vision) • less photopigment • less amplification • saturate only with intense light • fast response, short integration time • more sensitive to direct axial rays • high acuity; less convergent retinal pathways, concentrated in central fovea • Trichromatic; three types of cones, each with a different pigment (photopsin) that is sensitive to a different part of visible spectrum • More common in the fovea and macula Pigment Layer of Retina • • • • • Contains black pigment called melanin. Prevents light reflection in globe of eye. Without pigment, light would scatter diffusely; normal contrast between dark and light would be diminished. Albinos lack pigment layer – poor visual acuity because of scattering of light. – Even with corrective lenses, vision is rarely better than 20/200. Pigment epithelium/choroid contains high levels of vitamin A (needed for phototransduction). TMP14, Figure 51-1 Visual Phototransduction Rhodopsin resides in disk membrane of outer segment of rod and encloses light sensitive 11cis retinal molecule. Absorption of a photon of light by retinal leads to a change in configuration from 11-cis to all-trans retinal. The retinal then breaks away from rhodopsin, causing rhodopsin to be activated. The activated rhodopsin (aka, Metarhodopsin II) then begins the 2nd messenger cascade which leads to Conversion of light into electrical signals ROD Rhodopsin 11-cis retinal light 11-cis retinal All-trans retinal • Occurs in rods, cones and photosensitive ganglion cells. • The pigment protein in rods is called rhodopsin; • The pigment protein in cones is called photopsin, a close analog of rhodopsin (there are 3 types of photopsin: types I (red), II (green), and III) (blue). • The pigment portion of photosensitive retinal ganglion cells is called melanopsin. • The transduction mechanism is similar for • The rods, cones, and probably light sensitive all-trans retinal is then reduced ganglion cells. retinol, which then to all-trans travels back to the retinal pigment epithelium layer to be “recharged” to become 11-cis retinal. • The 11-cis retinal travels back to the rod where it is conjugated to an opsin to form new rhodopsin or a new photopsin. Vitamin A1 is required for Phototransduction Vitamin A1 (aka, all-trans retinal) is converted into 11-cis retinal within the retinal pigment epithelium. Food source: two types found in diet. • Preformed vitamin A: animal products such as meat, fish, poultry and dairy foods. • Pro-vitamin A: plant-based foods such as fruits and vegetables. The most common type of provitamin A is beta-carotene. Pro-vitamin A is a Vitamin A deficiency precursor of vitamin A. • the leading cause of preventable childhood blindness worldwide in developing countries • Prolonged and severe vitamin A deficiency can produce total and irreversible blindness. • ~250,000–500,000 children become blind each year (with the highest prevalence in Southeast Asia and Africa). (nyctalopia): Lack of vitamin • Night blindness A1 causes a decrease in retinal, which results in decreased production of rhodopsin; and a lower sensitivity of retina to light. Night blindness can occur in patients with GI absorption problem, e.g., celiac disease, cholestasis. Why? Br J Ophthalmol. 2006 Aug; 90(8): 955–956. http://medical-dictionary.thefreedictionary.com/vitamin+A+deficiency TMP14, Figure 51-5 Rod Receptor Potential • • • • • Normally about -40 mV (in dark). Normally, outer segment of rod is permeable to Na+ and Ca++ ions. Dark In the dark, an inward current (the current dark current) carried by Na+ and Ca + + ions flows into outer segment of rod. An outward current carried by K+ ions occurs in inner segment of rod. When rhodopsin decomposes, it causes hyperpolarization of rod by decreasing Na+ and Ca++ permeability of outer segment. Greater amounts of light produce So, photoreceptor cells greater electronegativity. depolarize in scotopic conditions (low light or no Ca light) and hyperpolarize in photopic conditions (well-lit conditions). Na+ Ca++ TMP14, Figure 51-6 -40 mV -70 mV ++ Ca++ Phototransduction – Closure of cGMP-gated Na+ and Ca++ channels with subsequent hyperpolarization (1) Light activated rhodopsin (metarhodopsin II) activates transducin. (2) Transducin activates cGMP phospho- diesterase, which destroys cGMP. (3) cGMP levels decrease, (4) causing sodium channels to close. (5) Closure of sodium channels causes photoreceptors to hyperpolarize Metarhodopsin II is deactivated rapidly after activating transducin by rhodopsin kinase and arrestin. 1 2 4 3 5. -40 mV mV →-70 Na+, Ca++ channel TMP14, Figure 51-7 Duration and Sensitivity of Receptor Potential • Rods: a single pulse of light activates receptor potential for more than 1 s. • Cones: occurs 4 X faster. • Receptor potential is proportional to logarithm of light intensity. Information within the neural elements of the retina is conveyed by electrotonic potentials, not action potentials. – very important for discrimination of light intensity. Color Vision • Color vision results from activation of cones. • The pigment protein in cones is called photopsin, a close analog of rhodopsin (there are 3 types of photopsin: types I (red), II (green), and III) (blue). • The retinal portion of the photopsins is the same as in rods. • Each cone is receptive to a particular wavelength of light. Figure 51-8 Color Blindness • • • • • Lack of a particular type of cone. Genetic disorder mostly passed along on X chromosome. Hence, occurs almost exclusively in males. Blue color blindness affects both men and women equally, because it is carried on a non-sex chromosome. Most color blindness results from lack of red or green cones. – lack of a red cone, protanope – lack of a green cone, deuteranope – Lack of a blue cone, tritanopia What happens in hereditary color deficiency? – Red or green cone peak sensitivity is shifted. – Red or green cones absent. Normal cone sensitivity curves (TRICHROMAT) 437 nm B 533 nm 564 nm G R Deuteranomaly (green shifted toward red) 5% of Males 437 nm B 564 nm G R Deutan Dichromat (no green cones; only red and blue) 437 nm 1% of Males (there is no green curve) B 564 nm R Deuteranope Vision Normal Color Deuteranope, shades of orange, no yellow or green Protanomalous (red shifted toward green) 1% of Males 533 nm 437 nm B G R Protan Dichromat (no red cones; only green and blue) 1% of Males (there is no red curve) 533 nm 437 nm B G Protanomaly Normal Protanomaly Protanope Vision Normal Vision Protanope, red-green colors are difficult to distinguish Neural Organization of Retina Direction of light Figure 51-12 Signal Transmission in the Retina • • • Neural elements in retina use electrotonic potentials (aka, graded potentials) to move current along their membranes instead of action potentials (exceptions include ganglion cells and some of the amacrine cells). The electrotonic potentials allow graded conduction of signal strength proportional to light intensity. Ganglion cells have action potentials. – send signals to brain via optic nerve (CN 2). – spontaneously active with continuous action potentials. – visual signals are superimposed on this background. – many excited by changes in light intensity. – respond to contrast borders, this is the way the pattern of the scene is transmitted to the brain. Figure 51-12 Lateral Inhibition Processing the visual image begins in the retina. One example is lateral • inhibition. • • • Enhances visual contrast. Horizontal cells provide inhibitory feedback to rods and cones and bipolar cells. Output of horizontal cells is always inhibitory. Prevents lateral spread of light excitation on retina. Contrast is enhanced with excitatory center and inhibitory surround. TMP14, Figure 51-12 TMP14, Figure 51-13 Lateral Inhibition (cont.) APs from ganglion cell 1. Area excited by spot of light. 2. Area adjacent to excited spot. Figure 51-14 Lateral inhibition, the function of horizontal cells Figure 51-15 The Optic Disc (also called the optic nerve head) What is it? • point where ganglion cell axons (~1 million) exit the eye to form the optic nerve (2nd cranial nerve). • entry point for retinal blood vessels • creates a blind spot since there are no rods or cones. • located 3-4 mm to nasal side of fovea. • size: 1.76mm (horizontally) x 1.92mm vertically • Has a central depression called the optic cup edematous optic disc Aka, papilledema Function of Amacrine Cells • About 30 different types. • Their primary targets are ganglion cells • Some are involved in the direct pathway from rods to bipolar cells to amacrine cells to ganglion cells. • A few have action potentials • Some amacrine cells respond strongly to the onset of the visual signal, some to the extinguishment of the signal. • Some respond to movement of a light signal across the retina. • Amacrine cells are a type of interneuron that aid in the beginning of visual signal analysis. Most (but not all) amacrine cells release inhibitory transmitters, GABA or glycine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC36 52807/ Figure 51-12 Ganglion Cells • More than 20 different types • Different types respond to the following: • Specific directions of motion or orientation • Fine detail • Increases or decreases in light Two classes of ganglion cells: P and M • Particular colors cells P cells (parvocellular cells): • Project to parvocellular layers of lateral geniculate nucleus (LGN) of thalamus • Small receptive fields, slow impulse conduction, sensitive to color and fine details, relatively insensitive to lowM cells (magnocellular cells): contrast signals • Project to magnocellular layers of lateral geniculate nucleus of thalamus • Larger receptive fields • Fast impulse conduction • More sensitive to low contrast B&W stimuli Figure 50-12 UNIT 10 Chapter 52: The Eye: III. Central Neurophysiology of Vision Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Visual Pathways to the Cortex • • • • • Optic nerve - axons of ganglion cells of retina. Optic chiasm. – all fibers from nasal halves of retina cross to opposite side and join fibers from opposite temporal retina to form optic tracks. Synapse in dorsal lateral geniculate nucleus (LGN) of thalamus. From LGN to primary visual cortex by way of optic radiation. Two principal functions of LGN. – Relay information to primary visual cortex via optic radiation. – “Gate control” of information to primary visual cortex. (of thalamus) Figure 52-1 Lateral Geniculate Nucleus: Relay Function Half of the fibers in each optic tract are derived from one eye, and half from the other eye. Signals from the two eyes are kept apart in the LGN. Layers 2, 3, and 5 receive input from psilateral eye Layers 1, 4, and 6 receive input from contralateral eye Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 26-4 Lateral Geniculate Nucleus: Gate Function LGN controls (gates) how much signal passes to cortex. • LGN receives gating control signals from – corticofugal fibers originating in primary visual cortex (not shown) – reticular areas of midbrain (not shown) • Both inputs are inhibitory and can turn off signal transmission in select areas of LGN. • So, both inhibitory inputs control the visual input that is allowed to pass to cortex. • Also, signals are provided to: A. Control the vergence of the eyes so they converge at the object of interest. B. Control the focus of the eyes based on calculated distance to object of interest. • Information is also provided describing the velocity of major elements in central field of vision, and which way the organism (person) is moving relative to object • Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 26-4 Primary Visual Cortex • Primary visual cortex lies in calcarine fissure. • Distribution from eye is shown. • Note large area of representation of macula (which includes fovea). • Fovea has several 100x more representation in cortex compared to peripheral portions of retina. • Secondary visual areas are visual association areas, where the visual image is dissected and analyzed. Figure 52-2 Analysis of the Visual Image • the visual signal in the primary visual cortex is concerned mainly with contrasts in the visual scene. • the greater the sharpness of the contrast, the greater the degree of stimulation. • also detects the direction of orientation of each line and border. – for each orientation of a line, a specific neuronal cell is stimulated. Visual Perception is a Creative Process • how the brain perceives a visual image is not understood well. • visual perception is thought to be mediated by three parallel pathways that process information on motion, depth and form, and color. Autonomic innervation of eye • Parasympathetic preganglionic fibers arise from Edinger-Westphal nucleus and synapse with postganglionic fibers in ciliary ganglion as shown. • The postganglionic fibers send action potentials through ciliary nerves to eyeball to control: 1. ciliary muscle (lens focusing) 2. Sphincter of iris (constricts pupil) • Sympathetic preganglionic fibers originate in intermediolateral horn of 1st thoracic segment of cord and synapse with postganglionic fibers in superior cervical ganglion as shown. • The postganglionic fibers innervate radial fibers of iris (which open Ciliary nerve Figure 51-11 Control of Accommodation • • Recall that accommodation is the mechanism that focuses the lens system. The lens system focused on a distant object can refocus on a close object in less than 1 s. • Parasympathetic control mechanism is poorly understood • Chromatic aberration: red light rays focus posteriorly compared to blue light rays. Eye can tell which is in better focus and relay information to accommodation mechanism. (seems unlikely since color blind people can still focus) • Convergence: neural signal for convergence cause simultaneous signal to strengthen lens. • Fovea lies in depression of retina. Differences between foveal image and image of surrounding retina may also give clues about which way lens should respond. • Oscillation of the degree of accommodation occurs all the time (2x per second). An image becomes better focused Figure 52-11 Control of Pupillary Diameter • Pupils constrict when the amount of light entering the eyes increases. Functions to help eyes adapt to extremely rapid changes in light conditions. Pupillary light reflex pupil • Parasympathetic nerves excite pupillary sphincter muscle, decreasing pupillary aperture (miosis). • Sympathetic nerves excite radial fibers of iris causing pupillary dilation (mydriasis). • Pupillary light reflex: • Light on retina causes a few impulses to pass from optic nerves to pretectal nuclei. Figure 52-11 Atropine dilates the pupil (mydriasis) and inhibits accommodation …by blocking parasympathetic effects; it is a competitive antagonist for muscarinic acetylcholine receptors, (increased heart rate, dry mouth, decreased sweating/lacrimation, blurry vision, vasodilation, confusion, hallucinations). Mnemonic: "hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter". • Atropine is extracted from the plant, nightshade (Atropa belladonna). • Belladonna (in Italian: bella=beautiful; donna=woman) • Used by Egyptians (Cleopatra), and throughout Europe (late 19th, early 20th century) to enhance beauty. Binocular and stereoscopic vision • • • • • • Binocular – to see (an object) with both eyes simultaneously. Stereoscopic – to see things as 3-D. We have a fixed visual angle of 104⁰, and our eyes are close together. Hence, visual fields overlap as shown, which allows accurate judgment of distance. Slightly different images from each eye are sent to brain, where impulses are fused to make single image. This allows 3-D imaging. Predatory animals (hawks, lions) have eyes set in front, and good binocular and stereoscopic vision. Preyed upon animals (rabbits) have eyes on sides of head and a wide visual field. This arrangement is good for detecting movement, but provides poor stereoscopic vision. Retinitis Pigmentosa • Refers to large group of disorders with clinical and genetic heterogeneity. • Main risk factor is family history • Incidence (1 in 4,000) • Characterized by pigment deposition • Symptoms • Night blindness (rods often go first) • Decreased peripheral vision • Loss of central vision in advanced cases • Treatment • No effective treatment • Sunglasses to reduce UV END UNIT 10 Chapter 53: The Sense of Hearing Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. The Tympanic Membrane and the Ossicular System • Tympanic membrane functions to transmit vibrations in the air to the cochlea (inner ear) • Amplifies the signal because the area of the tympanic membrane is 17 times larger than the oval window. • Tympanic membrane connected to the ossicles: malleus, incus, stapes Figure 53-1 Attenuation of Sound by Muscle Contraction • Two muscles attach to the ossicles – Stapedius (stapes) – Tensor tympani (malleus) • Stapedius is smallest skeletal muscle in body (1 mm long) Attenuation reflex (aka, stapedius reflex, acoustic reflex, auditory reflex): a loud noise initiates reflex contraction, causing ossicular system to develop rigidity. Both muscles involved. attenuates vibration going to cochlea. Can reduce sound transmission by 30-40 decibels. Serves to protect cochlea and dampens low frequency sounds i.e., your own voice (~1000 Hz) or the voice of others. (Humming when you don't want to hear someone else works through the stapedius reflex; this can be a 20-decibel reduction in sound transmission to cochlea) Takes 40-80 msec to activate… • • • • • Cochlea • Encased in bone • Hearing loss: conduction and/or neurological • system of three coiled tubes separated by membranes into the scala tympani, scala media, scala vestibuli • Sound waves cause back and forth movement of the tympanic membrane which moves the stapes back and forth. • This causes displacement of fluid in the cochlea and induces vibration in the basilar membrane. • Organ of Corti lies on surface of basilar membrane; contains hair cells which are electromechanically sensitive. Figure 53-3 Figure 53-1 Organ of Corti • • • • • Receptor organ that generates nerve impulses. Contains rows of hair cells that have stereocilia. Hair cells are the receptor organs that generate APs in response to sound vibrations. The tectorial membrane lies above the stereocilia of the hair cells. Movement of the basilar membrane causes the stereocilia of the hair cells to shear back and Figure 53-7 Nerve Impulse Origination • • Inner hair cells Stereocilia, when bent in one direction cause hair cells to depolarize; when bent in opposite direction hyperpolarize. – this is what begins neural transduction of auditory signal. ~90% auditory signals are transmitted by inner hair cells. – 3-4 X as many outer hair cells than inner hair cells. – outer hair cells may control the sensitivity of inner hair cells for different sound pitches. Figure 53-7 Inner and outer hair cells outer hair cells may control the sensitivity of the inner hair cells for different sound pitches. auditory signals are transmitted by the inner hair cells. Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 30-5 Outer hair cells adjust sensitivity there are nerve fibers running from the brain stem to the vicinity of the outer hair cells, may function to adjust sensitivity by acting on these cells. Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 30-10 Structural components of Cochlea • • • • Basilar membrane contains ~30,000 fibers which project from the bony center of the cochlea, the modiolus. Fibers are stiff reed-like structures fixed to the modiolus and embedded in the loose basilar membrane. Because they are stiff and free at one end they can vibrate like a musical reed. the length of the fibers increases and the diameter of the fibers decrease from the base at the oval window to the helicotrema, overall stiffness decreases 100 X, Short, stiff, high frequency Long, limber, Low frequency Figure 53-4 The round window serves to decompress acoustic energy that enters the cochlea via stapes movement against the oval window. Determination of Sound Frequency and Amplitude • • Place principle determines the frequency of sound perceived. – different frequencies of sound will cause the basilar membrane to oscillate at different positions. – position along the basilar membrane where hair cells are being stimulated determines the pitch of the sound being perceived. Amplitude is determined by how much the basilar membrane is displaced. Figure 53-5 Decibel Unit of Sound • Unit of sound • Sound intensity is expressed in terms of the logarithm of their actual intensity because of the wide range in sound intensity. • A 10-fold increase in sound energy is 1 bel • 0.1 bel is a decibel • 1-decibel is an increase in sound energy of 1.26 times • Ears can barely distinguish a 1-decibel change in sound intensity. Decibel values for various sounds Does the attenuation reflex protect against a shotgun blast? END UNIT 10 Chapter 54: The Chemical Senses—Taste and Smell Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Taste and Smell • Allows one to separate undesirable or lethal foods from those that are nutritious. • Recognize the proximity of other individuals or animals. • Tied to primitive emotional and behavioral functions of the nervous system. Because the tongue can only indicate texture and differentiate between sweet, sour, bitter, salty, and umami, most of what is perceived as the sense of taste is actually derived from smell. Taste Perception • • • • • Sour – caused by H+ from acids (citric acid, acetic acid) – Threshold for citric acid: 2 mM Salty – caused by ionized salts, mainly sodium – Threshold for NaCl: 10 mM Sweet – many chemicals mostly organic compounds – Threshold for sucrose: 20 mM Umami (Japanese, meaning delicious) – Glutamate – Threshold for MSG: <10 mM Bitter – long chain organic substances containing nitrogen – Alkaloids (quinine, strychnine, nicotine, etc.) – Threshold for quinine: 0.008 mM – Threshold for strychnine: 0.0001 mM – (survival mechanism since many poisons are bitter) Babies and young children are exceptionally sensitive to the bitter However, every part of the tongue includes receptors for every basic taste. Location of Taste Buds • Found on three types of papillae of the tongue. – Circumvallate papillae form a V on posterior surface of tongue. (50% of taste buds) – Foliate papillae are located along lateral surfaces of tongue. (25% of taste buds) – Fungiform papillae located over flat surface of tongue. (25% of taste buds) Filiform papillae are the most numerous of the lingual papillae. They are fine, small, cone-shaped papillae covering most of the dorsum of the tongue. They are responsible for giving the tongue its texture and are responsible for the sensation of TOUCH. • Extraglossal taste buds – on the tonsillar pillars, palate, epiglottis, and proximal esophagus. Taste Buds Taste bud • Each taste bud contains ~100 taste receptor cells • Taste receptor cells create a taste pore, where tastants can more efficiently interact with the microvilli (where the taste receptors are located) • Taste receptor cells are depolarized by tastants, creating action potentials in afferent neurons • Afferent neurons that project into the CNS (CNs VII, IX, X) make synaptic contacts with many taste receptor cells • Basal cells are undifferentiated cells that give rise to taste receptor cells every ~12 days Gustatory (taste)Transduction Mechanisms • Ionotropic: tastant ion channels: (salt, sour) • Metabotropic: Gprotein coupled receptors: (sweet, umami, and bitter) • Voltage regulated Na+, K+, and Ca++ channels mediate transmitter release (serotonin, GABA, ATP), which activates afferent neurons. Both ionotropic and metabotropic Stevia herb - steviol glycosides interact with TRPM5 channel, producing a taste sensation 30-100x sweeter compared to sugar. Steviol glycosides can also amplify umami and bitter tastes at higher concentrations. Transmission of Taste Sensations • • • • • Anterior 2/3 of tongue through facial nerve (VII). Posterior 1/3 of tongue through glossopharyngeal nerve (IX). Posterior aspects of the mouth through vagus nerve (X). From solitary nucleus to thalamus. From thalamus to cortex. Figure 54-2 Adaptation of Taste • Taste sensations adapt rapidly. • Adaptation of taste buds themselves accounts for only about 50% of the adaptation. • Central adaptation must occur but the mechanism for this is not known; this is unusual because adaptation for most sensory systems occurs at the receptor. Ageusia – the loss of taste sensation Often confused with anosmia True ageusia, the complete which is a loss of the sense loss of taste, is relatively rare of smell compared to hypogeusia – a partial loss of taste – and dysgeusia – a distortion or alteration Causes of taste. • Neurological damage: Neurological disorders such as Bell’s palsy, Familial dysautonomia, and Multiple sclerosis • Problems with the endocrine system: Cushing's syndrome, hypothyroidism and diabetes mellitus • Medicinal side-effects: antirheumatic drugs, ACE inhibitors, and others • Other causes: Local damage and inflammation, radiation therapy, tobacco use, and denture use. Other known causes include loss of taste sensitivity from aging, anxiety disorder, cancer, renal failure and liver failure. Smell • Least understood of all senses. • Poorly developed in humans. • Olfactory membrane located on the superior part of each nostril. • Contains olfactory cells which contain cilia. • On the cilia are odorant-binding protein receptors. • Binding of chemical odorant to receptor induces the G-protein transduced formation of cAMP which opens sodium channels. Olfaction (aka, Smell) Because the tongue can only sense texture and differentiate between sweet, sour, bitter, salty, and umami, most of what is perceived as the sense of actually derived •taste Leastisunderstood of all from senses. •smell. Olfactory membrane located on the superior part of each nostril. • Olfaction involves CN I which are olfactory receptor neurons (ORNs). They are true neurons, which differentiates them from many other sensory system receptor types. Olfactory receptor neurons (ORNs) • ORNs are located in the olfactory epithelium. • The olfactory membrane has a surface area of about 5 cm2. Figure 54-3 Composite from figure 53-03 and Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 32-1 • ORNs project axons to the olfactory bulb via the cribriform plate A closer look… Olfactory receptor neurons (ORNs) • Bowman’s glands produce mucus (and odorant binding proteins) that help trap odorants • Basal cells are undifferentiated cells that give rise to ORNs every ~45 days • Cilia on ORNs contain receptors, and are the site of transduction Aka, Sustentacular cell Transduction Mechanism • Odorant-binding receptors are located on cilia. • ~1000 different genes code for ORNs, only about 400 genes encode working ORNs. • ORNs can bind to a variety of odorants, with varying affinities. The differences in affinities causes differences in activation patterns resulting in unique odorant Binding of odorant to receptors induces Gprofiles. protein activation of adenyl cyclase, which causes formation of cAMP. The cAMP opens sodium channels causing depolarization. Figure 54-4 Anosmia is the lack of smell • Can be due to traumatic injury, or from disruption to nasal epithelium or central pathways – Traumatic injury can sheer ORN axons in the cribriform plate – Infection (e.g., rhinitis) can block odorants and cause edema – Tumors (e.g., olfactory groove meningiomas) – Smoking decreases sensitivity to odorants – Associated with normal aging and neurodevelopmental disorders (e.g., Alzheimer’s and Parkinson diseases) • Most disruptions to “taste” are from olfactory issues, due to “flavor” being a perception that involves both senses • Constant regeneration of ORNs allows for many forms of anosmia to be temporary How does COVID-19 decrease taste and small? Why does COVID-19 affect smell and taste? While the precise cause of smell dysfunction is not entirely understood, the mostly likely cause is damage to the cells that support and assist the olfactory neurons, called sustentacular cells. These cells can regenerate from stem cells, which may explain why smell recovers quickly in most cases. How long does the loss of taste and smell last? Approximately 90% of those affected can expect improvement within four weeks. Unfortunately, some will END UNIT 11 Chapter 55: Motor Functions of the Spinal Cord; the Cord Reflexes Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. The Spinal Cord Is More Than Just a Conduit for Nerve Fibers • Neuronal circuits for walking and numerous reflexes are contained within spinal cord. • Higher brain centers activate and command these circuits. – walking – maintaining equilibrium Motor Organization of Spinal Cord • sensory fibers enter cord and are transmitted to higher centers, or they synapse locally to elicit motor reflexes. • motor neurons are located in the anterior portion of the cord. – motor neurons are 50 - 100% bigger than other neurons. Anterior Motor Neurons • • alpha motor neurons – large type Aα fibers (~14 microns). – stimulation can excite 3 to >100 extrafusal muscle fibers collectively called a motor unit. gamma motor neurons – smaller type Aγ fibers (~5 microns). – stimulation excites intrafusal fibers, in muscle spindle, a special type of sensory receptor. nterneurons and Propriospinal Fibers • • Interneurons – 30x more abundant than anterior motor neurons. – small and highly excitable – Most signals from brain terminate on interneurons – Comprise neural circuitry for motor reflexes. Propriospinal fibers – travel up and down cord for 1 - 2 segments. – provide pathways for multisegmental reflexes. – important for proprioception Proprioception: from Latin (proprius, “one’s own”) and perception. - sensing of the relative position of body parts and strength of effort used nterneurons - Renshaw cells Renshaw cells are Inhibitory interneurons Descending influences in the anterior horn; they release Glycine, an inhibitory transmitter. • They are associated in two main ways with an alpha motor neuron 1. They receive an excitatory collateral from the alpha neuron’s axon and are thus "kept informed" of how vigorously the Alpha motor neuron is firing. Renshaw cell neuron 2. They send an inhibitory axon to synapse with cell body of the initial alpha neuron and/or an alpha motor neuron of the same motor pool. Inhibitory synapse • In this way, Renshaw cells mediate a Excitatory synapse negative feedback mechanism. • A Renshaw cell may be supplied by more Muscle than one alpha motor neuron collateral, and it may synapse on multiple motor neurons. • Clinical Significance of Renshaw cells Tetanus (aka, Lockjaw) • Renshaw cells are targeted by Descending influences Clostridium tetani causing tetanus. • Spores of the bacteria can be found Tetanospasmin in dust, dirt, and animal droppings. Toxin A person can become infected when these spores enter the bloodstream through a deep cut or wound. The spores then spread to the central nervous system and produce a toxin Alpha motor Renshaw cell called tetanospasmin. neuron • This toxin inhibits the release of Glycine from Renshaw cells, causing alpha motor neurons to become hyperactive, and muscles Strychnine Poison Inhibitory synapse to constantly contract. • It’s a pesticide particularly for killing small Excitatory synapse vertebrates like birds and rodents. Has no known medicinal effects. It is sometimes Muscle mixed with street drugs. • Binds to and inactivates glycine receptors on alpha motor neuron and thus muscles continually contract and may prove fatal if the diaphragm is involved. Types of muscle fibers • Extrafusal fibers – make up bulk of muscle – stimulated by alpha motoneurons – provide force for muscle contraction • Intrafusal fibers – smaller than extrafusal fibers – encapsulated in sheaths to form muscle spindles – run in parallel with extrafusal fibers, but much shorter (~10 mm) Sensory Receptors of Muscle • Muscle Spindle – located in muscle belly – senses muscle length and rate of change in length. • Golgi Tendon Organ – located in tendon – senses tendon tension and rate of change in tension. Signals from muscle sensory receptors are (mainly) for intrinsic muscle control. They (mainly) occur subconsciously. They transmit information to cerebrum and cerebellum (as well as to spinal cord). Muscle spindles – detect both static and dynamic changes in muscle length – distributed throughout muscles – consist of intrafusal muscle fibers in parallel with extrafusal muscle fibers – density varies according to function • larger muscles with coarse movements have few (e.g., quadriceps) • smaller muscles with fine movements have many (e.g., extraocular muscles, muscles in hand and neck) The Muscle Spindle Intrafusal fibers (3 to 12 per spindle) – no actin/myosin in center of fiber; hence, no contraction in center (center functions as sensory receptor) – innervated by gamma motor neurons (type Aγ). – Two types of intrafusal fibers 1. Nuclear bag intrafusal fibers • detect rate of change in length (fast, dynamic changes) • Innervated by Type Ia sensory afferents 2. Nuclear chain intrafusal fibers • detect static changes in length • Innervated by Type II sensory How muscle spindle works Muscle spindle reflexes oppose (correct for) increases in muscle length (stretch) 1. Stretching muscle (increasing length) also stretches spindle. This stimulates sensory Type Ia and Type II afferents. 2. Type Ia fibers stimulate αmotoneurons in spinal cord, causing contraction and shortening of entire muscle. 3. Thus, the stretch is Function of original γ-motoneurons opposed and muscle length is • innervate intrafusal fibers maintained. • adjust sensitivity of muscle spindle (so it will respond appropriately during muscle contraction) • α-motoneurons and γ-motoneurons are co-activated (so that muscle spindles can be sensitive to changes in length during contraction). How muscle spindle works A. Stretching spindle activates receptors (and normally causes Ia fibers to stimulate α-motoneurons) B. Contraction of muscle without contracting ends of spindle makes stretch response unavailable C. Simultaneous contraction of both muscle and spindle keeps stretch response intact muscle spindle sustained stretch of muscle Ia discharge tension pull weight stimulate αmotoneuro n contracti on Ia response filled in stimulate γmotoneuron contracti on Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill How muscle spindle works Static Response. • when spindle is stretched slowly number of impulses in Type Ia and Type II afferents increases in proportion to degree of stretch. • this is the ‘static response’. Dynamic Response. • when center of spindle is stretched rapidly - number of impulses in Type Ia afferents increases in proportion to rate of change of the length. • this is the ‘dynamic response’. Physiologic Function of the Muscle Spindle • comparator of length between the intrafusal and extrafusal muscle fiber. • opposes a change in muscle length. • when the muscle is stretched the spindle returns it to its original length. • leads to the stretch reflex. The Stretch Reflex 1. sudden stretch of muscle excites muscle spindle. 2. afferent impulses to cord excite αmotor neuron, which results in contraction of muscle. 3. At same time, synergistic muscles are activated; antagonistic muscles are inhibited 4. this reflex opposes further stretch of muscle • Number of synapses: monosynaptic reflex arc • Stimulus: muscle stretch • Afferent fibers: Type Ia • Response: contraction of muscle Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig36-2b1 Smoothing function of Stretch Reflex Stretch reflex is important for preventing jerkiness of body movements A. Stimulation at 8 Hz causes smooth contraction, illustrating smoothing effect of muscle spindle system B. Sensory afferents from muscle spindle was sectioned 3 months ago. Note jerkiness of muscle contraction. Patellar Reflex (knee jerk) 1a 1. Strike patellar tendon with tendon hammer 2. Muscle spindle stretches (in quadriceps femoris) 3. Type Ia afferent stimulates αmotoneuron in L4 (without interneurons – monosynaptic reflex arc) 4. Antagonistic flexor (hamstring) relaxes via inhibitory interneuron 5. α-motoneuron stimulates quadreceps to contract Westphal’s sign – absence or decrease in 6. Multiple Leg kicks oscillations of leg is sign of a cerebellar disease. patellar reflex. Could be caused by many things… receptor damage, peripheral nerve disease, lesion in motor cortex or pyramidal tracts, interruption of sensory and/or motor impulse transmission in femoral nerve… How Can We Change Muscle Length ?? Co-activation of alpha and gamma motor neurons • causes contraction of both muscle and ends of spindle. • results in a shortened spindle with an intact stretch response (otherwise spindle would hang loose within muscle) • feedback from spindle (via Type Ia) reinforces activation of alpha motoneurons Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill Co-activation of alpha and gamma motor neurons Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 36-9 co-activation prevents spindle from being unloaded during contraction; hence, proper damping function of spindle is maintained. Golgi Tendon Organ • • • • • • • low-threshold mechanoreceptors located in tendons increased muscle tension compresses nerve endings, opening stretch sensitive ion channels formed by branches of Type Ib afferents Autogenic inhibition reflex: a sudden relaxation of muscle at very high muscle tensions (protects against muscle tear) However, Golgi tendon organs signal muscle force through the entire physiological range, not only at high levels of tension. function is to equalize force among muscle fibers. only affects an individual muscle (adjacent muscles are not affected) Golgi Tendon Organ •Number of synapses: Disynaptic reflex arc •Stimulus: muscle contraction (tension) •Afferent fibers: Type Ib •Response: relaxation of muscle Transmission of muscle length and tension information to higher centers • signal from Muscle Spindle and Golgi tendon are also transmitted to higher centers (not just the cord). • this informs brain of instantaneous changes in muscle tension and length. • information is transmitted at 120 m/sec. • important for feedback control of motor activity (discussed later). Flexor Withdrawal Reflexes • painful stimulus causes limb to withdraw from stimulus. • neural pathways – nociceptor activation transmitted to cord. – synapses with interneurons that diverge to muscles for withdrawal, inhibit antagonist muscles, and activate reverberating circuits to prolong muscle contraction. – duration of after discharge depends on strength of stimulus. • Crossed Extensor Reflex: – painful stimulus elicits an extensor reflex in opposite limb. – extensor reflex begins 0.2 - 0.5 seconds after painful stimulus (i.e., after flexor reflex). – serves to push body away from stimulus, also to shift weight to opposite limb. Flexor Withdrawal Reflexes •Number of synapses: Polysynaptic reflex arc •Stimulus: pain •Afferent fibers: II, III, IV •Response: ipsilateral flexion; contralateral extension Other Reflexes for Posture and Locomotion • pressure on bottom of feet causes extensor reflex. – more complex than flexor-crossed extensor reflex. • basic walking reflexes reside in spinal cord. Reflexes that Cause Muscle Spasm • pain signals can cause reflex activation and spasm of local muscles. • inflammation of peritoneum can cause abdominal muscle spasm. • muscle cramps caused by painful stimulus in muscle – can be due to cold, ischemia, or over-activity. – reflex contraction increases painful stimulus and causes more muscle contraction.

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