Ch 15- The Special Senses Flashcards
cards for the 94 slides
five special senses
vision, olfaction, gustation, hearing, equilibrium
most dominant sense
vision, has most sensory receptors
conjuctiva
transpart mucous membrane
conjunctiva function
produces lubricating mucous, preventing dry eye
palpebrae
eyelids, allow open or close.
orbicularis oculi muscle- what is it what does it do
skeletal muscle tissue under eye- allows eye to close
levator palpebrae superioris muscle- what is it what does it do
upper eyelid muscle, allows you to stop eye opening or keep it- pulls eyelid up
lacrimal apparatus
produces and drains tears, also protects.
lysozyme
lubricate for eye surface, washes away foreign bodies in eye and kills bacteria and other pathogens
lacrimal apparatus makeup
lacrimal glands (produce and release tears), lacrimal canaliculi (drains tears at medial portion), nasolacrimal duct(drains tears from cannaliculi into nasal cavity)
extrinsic eye muscle function
allows movement of the eye in orbit, each attach to the sclera of the eye (white)
6 extrinsic eye muscles
superior rectus, inferior rectus, lateral rectus, medial rectus, superior oblique, inferior oblique
lateral rectus
moves eye laterally
medial rectus
moves eye medially
superior rectus
elevates eye, turns medially (up or down)
inferior rectus
depresses eye, turns medially (up or down)
inferior oblique
elevates eye, lateral movement (counteracts direction eye is pulled)
superior oblique
(depresses eye and turns it medially(counteracts direction of eye pull)
what do oblique muscles do
balance out rectus muscles
fibrous layer
outermost coat pf eye, 2 regions
the 2 regions of fibrous layer
sclera and cornea
sclera
white of eye, gives shape and anchor for the muscles
cornea
transparent layer at anterior region, allows light to enter, bends the light. Has pain receptors, regenerates fast, no blood vessels with no immune system
vascular layer
middle coat with 3 regions
3 vascular layer regions
choroid, cilliary body, iris
choroid
well vascularized layer, absorbed light with dark color, allows easy brain interpretation bc no scattering
cilliary body
cilliary muscle (controls lens shape) cilliary processes (secretes aqueous humor), suspensory ligaments (holds lens in place and emits tension from ciliary muscle to lens)
iris
controls the melanin, colored portion of eye, has sphincter pupillae and dilator pupillae
pupil
central opening, allows light to enter eyeball
sphincter pupillae
bright light, pupil decreases in size bc layer thickens
dilator pupillae
dim light, pupil increases in size bc layer narrows
retina
innermost eye layer, has the photoreceptors, responds to light and color. has pigmented layer and neural layer.
pigmented layer of retina
superficial layer, absorbs light, stores vitamin A, makes it so you can produce and regenerate the photoreceptors.
neural layer
deepest layer, generates AP to brain, has photoreceptor cells, rods and cones plus bipolar and ganglion cells
rods
dim light and peripheral visio, outer retina layers
cones
bright light, allows color vision. in fovea central’s ands macula lutea,it is less sensitive to light
bipolar and ganglion cells
generate AP to light stimuli
optic disc
blind spot, no photoreceptors, Brain fills in missing gaps and its in back of eye
macula lutea and fovea centralis
macula: only cones, photoreceptors receive direct light and pushes to side when light strikes cones, ACUTE vision here
fovea: center of macula, 1/1000th of visual field
lens
transparent and flexible structure, has lens fibers for thickness, disadvantage over time bc lens fibers build up and makes it harder to change shape so vision loss occurs
anterior segment
aqueous humor, supplies nutrioents and O2 to structures and removes waste washes it away, it is constantly drained and produced (rate of this must be equal)
glaucoma
too much aqueous humor produced
posterior segment
vitreous humor, behind lens, lasts a lifetime, contributes to pressure on eye and holds retina in place as well as transmits light
visible light spectrum
400-700 nm, light strikes object bounces off it and then strikes the eye. the color of object is what waves are absorbed and what is reflected. WHITE is reflected BLACK is absorbed
light refraction
bending of light as it passes from one substance to another with different density
speed through light mediums
faster transmission in air, slower in solid. light travels ay constant speed thru single medium, refraction is important for vision bc air travel to cornea then must be able to reflect light for stimulation of the photoreceptors
lens and cornea and focusing light
cornea will bend the light, but won’t change shape. lens changes shape to fine tune the refraction- less power is less bulge, more power is more bulging.
relaxation of cilliary muscles
increased tension in suspensory ligaments, pulled tight, so the lens flattens and bends less light, less refractory power
contraction of cilliary muscles
decreased tension in suspensory ligaments, go slack, lens bulges, high refectory power and bends light very well.
looking at an objet far away…
lens flattens, less refractory power
far point of vision
point where lens doesn’t need to change shape to focus, 20+cfeet, distant object means light entering rays are parallel so it can bend easily to focus in on retinal
lens accommodation
ciliary muscles contract, lens will bulge when object is up close, must be rounded
pupil constriction
don’t want scattering here would confuse visual signal, smaller diameter to tell how much light goes in, prevents the diverging rays from entering eye
convergence of eyes
closer object means more conversion, keeps object focused on foveae (highest resolution) and medial rotation
near point of vision
4inches, but increases with age we lose ability to focus close to face, these light rays are more divergent as they enterr the eye, more divergent light rays striking retina means brain is confused so we want less divergence when near
phoptorecepots, rods and cones
very modified and dif from other neurons, outer segment has folded photopigments into discs which respond to light stimuli.(actual response to light AP generated) inner has embedded in neural layer of retina, metabolic processes of them with connection to outer cell body segment.
rods
have more photopigments than cones, sensitive to light, used in the dark, no color vision, all rods synapse on one ganglion cell. (AP PRODUCED, BRAIN RECEIVES, WHERE IS TI FROM?, JUST KNOWS ROD STIMULATED BUT LESS ACUITY)
cones
low sensitivity, light conditions, color vision red green blue, each cone synapses with ITS OWN GANGLION (CONE MUST BE BOMBARDED TO BE ACTIVE, BRAIN KNOWS WHERE IT IS WHEN AP IS SENT DUE TO GANGLION, MORE. ACUITY AND CLEAR VISION)
phototransduction
light stimuli becomes electrical signal at retina
3 cells involved with light processing
rods/cones (photoreceptor cells that make graded potentials in response to stimuli), bipolar cells, ganglion cells
bipolar cells
create IPSP of EPSP with graded potentials
ganglion cells
generate AP that is propagated along optic nerve, sent to visual cortex
retina in the dark
photoreceptor ion channels r open, receptor is depolarized to -40 MV. response doesn’t happen here bc w/out stimuli its depolar
retina. in the light
photorecprot ion channels r closed, hyper polarized to -70MV, used transducer (G protein) signal system with 11 cis retinol absorbing light converted to all trans retinol
how info is processed in the dark
ion channels OPEN, Na+ ENTERS, photoreceptor DEPOLARIZES to -40 mv. Ca 2+ channels OPEN and neurotransmitter is released between photorecpeot and bipolar cells. NO NEUROTRAN is released at bipolar and ganglion. NO AP IS GENERATED BY GAGLION- so nothing sen tin dark bc no ap can happen
G-protein signalung system for phototransduction
11 cis retinal goes to all trans retinal, produces transducin, binds to phosphordiestras, ions close, GMP cannot bind, ion channels close, so hyperpolarization happens so light can be generated!
how info is processed in the light
light stimuli causes ion channels to CLOSE, Na+does not enter, hyper polarizes to -70mv, Ca 2+ ion Channel CLOSES, NEUROTRAN NOT RELEASED, bipolar cell DEPOLARIZES bc EPSP with neurotransmitter, ca2+ then OPENS and neurotransmitter can be released between bipolar and ganglion, so AP CAN GENERARE and it sent to OPTIC NERVE TO CORTEX FOR INTERPERATION
light adaption
dark to light conditions, rods get bombarded with stimuli and white light occurs, rods turn off cones turn on, cones aren’t as sensitive so retinal sensitivity decreases, adaptation takes 60 seconds, and acuity is reached in 5 min as well as good color vision
dark adaptation
light to dark, and has temporary vision loss, cones turn off rods turn on, retinal serenity increases bc rods are here. 30 minutes toadapt
visual cortex pathway
optic nerve exits back of eye and ganglion cells go to primary visual cortex, optic chasm is when medial fibers from each optic nerve crosses over (not lateral fibers tho), and optic tracts go to visual cortex and boom
optic tracts:
carry fibers from lateral to same side of eye, and medial to opposite side
fibers in visual cortex
most fibers in tracts travel to primary visual cortex of occipital lobe, but some go to superior colliculi (reflex center controlling extrinsic eye muscles), pretectal nuclei (mediates pupil light response), and suprachiasmatic nucleus (which sets biorhythms sleep n wake)
depth perception
170 degree visual field, left and right overlap and bth eyes can see that overlap so we get 2 images, the visual cortex combines the 2 to get the depth perception, which allows us to locate objects in space, but if one eye is gone then boom there goes depth perception.
olfaction
chemoreceptors respond to stimuli dissolved in a solution- smell!
where are olfactory receptors found
olfactory epithelium, in root of nasal cavity
3 cell types in the olfactory epithelium
olfactory sensory neurons (bind to chemical), supporting cells, and olfactory stem cells
olfactory cilia
hair like projections found in olfactory epithelium, they increase the receptive area of neuron, mucous surrounding cilia dissolves airborne . without mucous, we could not smell.
axon synapse in brain
axons synapse with olfactory mitral cells in olfactory bulb, which are neurons, and forms the glomeruli. (mitral cells produce the AP to be sent)
how smell occurs
must activate sensory neurons and transduction of smell has to happen
activation of sensory neurons
odorant dissolves in mucous, an odorant is anything we can smell. the odorant will then bind the receptors of the cillum membrane.ion channels open for graded potentials
transduction of smell
graded potential is created by sensory neuron, this is not AP, if strong enough mitral cells generate AP, but diff ions make dif effects on it.
Na2+ and Ca2+ will create graded potential by depolarizes sensory neurons.
if Ca2+ is continuous neuron will adapt and the potential will stop the production.
longevity of olfactory neurons
they are superficial so they get destroyed fast, only last 30-60 days, strong smells or fast air intake or sneezing makes them destroyed. the regeneration ensures we don’t lose our sense of smell over time
pathway to olfactory cortex
bundles of mitral cells make the olfactory tract, which is how impulses flow from olfactory bulb to cortex. can to go olfactory cortex or even go to limbic system
olfactory cortex vs limbic system
in olfactory cortex, smell is consciously interpreted or identified.in limbic system, smell has emotional response bc activates sympathetic or parasympathetic system.
gustation
chemoreceptors are found on tastebuds, located on papillae of tongue.
3 types of papillae
fungiform papillae, have 1-5 taste buds each. vallate papillae- each one has many tastebuds. foliate papillae- taste bud number varies with age, younger have more and aging causes loss.
each taste bud has 2 epithelial cells
gustatory and basal epithelial cells
gustatory epithelial cells
receptor cells for taste, gustatory hairs which are microvilli projecting from tips of the cells, binds to tasting to produce a graded potential not AP. they are wrapped in sensory dendrites, which generate AP to be sent to cortex.
basal epithelial cells
stem cells, replace lost or damaged gustatory cells, respond to chemicals leading to taste sensations. these r necessary bc we lose taste buds so often, they get replaced every 7-10 days.
6 taste sensations
sweet sour salty bitter umami and long chain fatty acids. one taste cell Responds to 1 modality. but, one taste bud can have multiple epithelial cells so we can taste everything over entire tongue.
taste physiology
chemical tastant must be dissolved in saliva. tastant binding gustatory cell makes graded potential occur, neurotransmitter release to sensory dendrite elicits and AP, so brain can now interpret.
salty, sour, bitter/sweet/umami
salty: Na+ influx depolarizes gustatory cell
sour: H+ acts intracellularly rot open ion channels
bitte ror sweet or umami: gustducin opens ion channels to depolarize membrane
pathway to gustatory cortex
facial nerve carriers info from anterior 2/3 tongue, most sensory work done here w taste. glossopharyngeal nerve carriers info from the leftover 1/3 posteriorly. most fibers travel to primary gustatory cortex- but some go to limbic/hypothalamus (emotional response OR fight/flight w bad food)
do olfaction and gustation contribute to the other
YES, brain combines into from both to refine taste
hearing 3 major ear regions
external ear, middle ear,inner ear
external acoustic meatus
tube extends auricle to tympanum, allows sound to pass deeper regions inner, funnel sounds until tympanic membrane.
tympanic membrane, tympanum
divides outer ear from middle ear (eardrum) and vibrates in response to sound waves (frequencies or amplitudes)
middle ear
has incus malleus and stapes, stapes is smallest and attaches to oval window. they vibrate at the same frequency when tympanum vibrates.
tensor tympani and stapdeius
contract in respons eto extreme sounds, protects the gentle small bones.
oval and round window
membranes which divide middle from inner ear. helps sound transmission. this is not an open space.
pharyngotympanic tube
runs from middle ear to throat, opens tube to equalize pressure in middle ear. need this bc it connects ,middle ear to throat which helps balance the pressure, only vibrates if pressure is equal, and tube ensures it is equal. ex: we chew gum on airplane to open and equalize pressure in middle ear
inner ear
cavity carved into bone, which as 3 divisions for the cochlea and vestibule/semicircular canals. cochlea is fluid filled that converts sound to AP for hearing, the latter are fluid filled with recptors for equilibrium and balance. but fluid must flow in both to activate.
bony labyrinth
system of channels that go in temporal bone, cavity in bone, filled with perilymph (like CSF), surrounds and supports membranous labriythn. PROTECTS SENSORY RECEPTORS AND HELPS SUSPEND SENSORUY RECEPTORS IN CAVITY.
membraneous labyrinth
sacs and ducts within bony labrytnh and filled with endolymph, (LIKE ICF). these sensory receptors for hearing and equilibrium are found here, and get stimulated bc as they flow through membrane ion touches receptors to stimulate it.
cochlea
spiral shaped with membraneous labyrinth, Scala vestibule, scala tympani, and scala media. it stops at helicotrema (dead end)
scala vestibuli / scala timpani
begins at oval window, part of bony labyrinth/ ends at round window. they are continuous and meet at helicotrema. filled w the perilymph which freely flows through vestibule
scala media
cochlear duct, part of membranous labyrinth, has endolymph. has stria vascularis which produces and secretes endolymph. also has basilar membrane which forms floor of scala media (flexible and moves in reponse to sound waves)
spiral organ of scala media
receptor region that has cochlea hair cells, and supporiutng cells
sound properties 2 thinfssssss
sound is a mechanical wave. it causes vibration of particles in the medium it travels through. compression (pushed particles together) and rarefaction (particles are spread apart). sound waves r alternate rarefactions and contractions- and sound travels fastest in a solid.
frequency n tone
pitch, number of sound waves that pass a point in a period of time. this is determined by wavelength. shorter wave mean shigher frequency. tone is a sound consisting of a single frequency.
human hear range
20-20k Hz
amplitude
indicates loudness, the height off the wave. 0-120 DB, over 120 is painful bc too much rattling.
Soudn transmission
vibrate tympanic membrane, malleus vibrates in respondent tympanum, as well as incus and stapes, bc they are all attached to the tympanum. stapes transmits vibes to oval window dividing middle and inner ear.
wave production
stapes push on oval window, so round window pushes perilymphby increasing pressure. the pressuremus be released for movement of perilymph
basilar membrane path of perilymph
from scala media sound waves, hair cells get stimulated spiral organ and generates AP for sound perception by brain.
helicotrema path
under 20 Hz low frequency, sop basilar membrane won’t vibrate and no sound perception happens.
basilar membrane Is tuned to vibrate specific frequencies along length, how?
oval window to helicotrema has different fibers of different length, near oval window very stiff and short fibers for less bending- so for high frequency to be there must be bombarded. learn helicotrema, fibers are ling and loose, where low frequency is.
sound transduction
movement of basilar membrane for inner hair cells, which have sterocillia. tallest stereocillia are embedded in tectorial membrane at top of spiral organ and joined together by TIP LINKS, which OPEN mechanically gated ion channels.a
basilar mmebrane at rest
some tip links open for small ion flow, so inner hair cell is slightly depolarized. no sound there
if stereocuillia pivots to tallest hair
ALL tip links open, all ion channels open so K and Ca enter with large rush, and strong depolarization happens. This generates graded receptor potential. once neurotran from inner hair cell is released to cochlear nerve, AP is generated and we still get AO even when no stimulus bends the basilar membrane or inner hair cells
stereocillia bends to shortest hair
ALL tip links close, K and Ca don’t enter, inner hair cells hyperpolarizes, no receptor potential, neurotransmitter no longe released so NO AP!w
what do outer hair cells do?
efferent fibers, change flexibility of basilar membrane. can make it more stiff or flexible. it receives info- does not send it. so it can increase hasir cell responses and protect outer hair cells by stiffening with loud sounds. membrane bends for more or less easy responsiveness of inner hair cells. NO AP HERE
primary auditory cortex time
mostly ipsilateral some contralateral, each cortex gets info from both ears.
pitch
multiple parts of basilar membrane stimulated at the sam time. hair cell impulses
loudness
louder sound is more perilymph movement bc more rocking of basilar membrane.
sound localization
intensity and timing- if identical its above below in front or behind. if different comes from L or R side
equilibrium - 2 structures responsible for iy
sensation or awareness that comes fro changes in head posiiton. vestibule and semicircular canals which are endolymph filled
vestibule
most central portion of bony labyrinth of inner ear. responds to linear movememt and acceleration.s
semkicurklcualr canals
rotational mivmevet,antewrior posterior and lateral.
saccule in vestibule
continuous with cochlea, small
utricle in vestibule
contunos w semicular canals
maculae
linear movement sensory receptor
maculae anatomy
flat patch with sterocullia and kinocillia, innervate day vestibular nerve. oloith membrane is a jelly base with otolith stones on top (dense n heavy). they drag back with forward movement
hair bending with otolith membrane- maculae will only respond to changes in head ppoiosiiton
TILT FORWARD bend to kinocilium, hair cells depolarize w AP increase
TILT BACKWARDS away from kinociliu,. hair cells hyper polarize.AP decreases. uprigjht heasd is just steady AP in nerve.m
utricle vs saccule hair cell orientation and perceptions
utricle: horizontally oriented in head with vertical hair cells
saccule: vertically oriented can only bend ip or down . (elevator example)
rotational acceleration
semicircular canals, ampullae with membrane swelling ayt end opf receptor ducts. receptor has crista ampullares (with ampullary cupula, the gel that surrounds the hair cells, it’ll respond to endolymph movement)
canal flow when head spins
endolymph flows in opposite direction of rotational ,movement. hair cells depolarize when it pushes on ampullary cupula. if its constant speed, isn’t stimulated. when rotation stops, opposite direction so hyper polarizes with less neurotransmitter
vestibular nuclei pathway
Ap only generated when maculae and crista ampullares is stimulated. will travel ti cerebellum or vestibular cortex.
vestibular cortex pathway
vestibular nuclei sends impulse to reflex centers of brain, and body position gets fixed/ receives visual and somatic info
cerebellum pathways
corrects body movement, coordinates skeletal muscle activity and muslce tone to maintain body posture and head position as well as balance.
what happens if cerebellum conflicts with vestibular pathway?
brain confused, nauseous, barfing, motion sickness. once movement stops conflicitonstops.
