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129 Cards in this Set
- Front
- Back
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3 nociceptors |
- mechanical -thermal -chemical |
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where are nociceptor free nerve endings found? |
skin & deep tissue, joints, muscle & bone |
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how can nociceptors be modulated? |
presence of chemical like prostaglandine which greatly enhance receptor response to noxious stimulus - tissue injury can release prostaglandins -lower activation threshold of receptors - aspirin like drugs inhibit synthesis of prostaglandins , (pain killing effect) |
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A-delta fibres |
-transmit pain impulses from nociceptors -largest and fastest fibre (myelinated) -signals from cold,warmth, & mechanical stimuli -sharp brief initial pain |
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C fibres |
-transmit pain impulses from nociceptors -slow and small (unmyelinated) - heat, cold, mechanical also, just slower than A-delta -dull aching pain |
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bradykinin |
activates slow pain pathway -activating by enzymes released into ECF by damaged tissue -stimulate polymodal nociceptors and inflamation response |
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substance P & higher levels of pain processing |
-pain neurotransmitter - activates ascending pathways that transmit nociceptive signals to higher levels for further processing - higher levels include (cortex/thalamus/reticular formation) -somatosensory localize pain - pain can be percieved in absence of cortex (thalamus) - ReticF increases alertness associated with noxious encounter - thalamus/RF interconnect to hypothalaus to elicit emotional response, limbic syste important in perceiving unpleasnt aspects of pain |
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glutamates affect on AMPA receptors & pain |
permeability changes resulting in action potential in dorsal horn neuron which transmit pain to higher centres |
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glutamates affect of NMDA receptors & pain |
Ca2+ entry into dorsal horn neurons initiating second messanger system that make neuron more excitable than usual, makes very sensitive ex. touching sunburn - dont want more damage |
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chronic/neuropathic pain |
sometimes occurs in absence of tissue injury - pain is percieved becasue of abnormal signalling within pain pathways ex. strokes that damage pathways can lead to abnormal persistent sensation of pain |
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analgesic system |
-suppreses pain by blocking release of substance P - depends on prescence of opiate receptors (morphine) - opiates bind to receptors on afferent pain-fibre terminal, suppresing release of SubP, stopping pain signal -reticular formation plays role |
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endogenous opiates (3) |
endorphins, enkephalins, dynorphins |
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'runners high' |
endorphins released by prolonged exercise |
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some types of stress induce analgesia |
sick |
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protexting eye from injury |
- bony socket positioned in - eyelids (shutters) - blinking and tears keep lubed and clean -eyelashes |
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where are tears produced and what happens when we cry |
lacrimal gland continuously and when crying cant handle profuse production and overflows |
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3 layers of eye (outermost to innermost) |
1. sclere/cornea 2. choroid/ciliary body/iris 3. retina |
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glaucoma |
if aqueous humour isnt drained as quickly as formed, excess causes pressure to rise within eye - can lead to blindness (causes retinal/optic nerve damage) |
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eye clolour? |
pigment in iris |
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pupil gets smaller when? and para or sympa |
circular muscles contract. para -bright light to decrease amount entering |
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pupil gets bigger when? para or sympa |
radial muscles contract. sympa - dim light to allow more entrance |
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astigmatism |
curvature of cornea is uneven, rays arent equally refracted |
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accomodation |
ability to adjust strength of lens |
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ciliary muscle |
2 major components - ciliary muscle and capillary nertwork producting aqueous humour
-circular ring of smooth muscle attached to lens by suspensatory ligaments - controlled by ANS & sympa - relaxation and para- contraction |
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presbyopia |
- lens made up of cells no nucleus or organelles, cant make new or repair,, cells in middle farthest away from vitrueous humour, nutrient source, cells die and become stiff with age, lose shape, so people 40 & up usually start needing glasses |
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cataract |
-elastic fibres in lens normally transparnent but if become opaque so light rays can't pass thru, u have cataract - surgically remove lens and artificail or glasses |
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myopia (nearsightedness) |
-where close object usually needs accomodation, abnormal strength of lens or too long eyeball, dont need accomodation for near but now need for far which u dont normally need
-far source is focused in front of retina and blurrry - need concave lens |
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heperopia (farsightedness) |
- eyeball too short or lens too weak - far objects focused on retina only w/accomodation where near are focused behind even with accomodation -needs convex lens |
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laser eye surgery, why? |
to premanantley change shape of cornea to compensate for refractive errors |
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when lens is flattened weak. ciliary muscle and suspensatory ligament? what stimulation? |
relaxed ciliary. suspensatories tight. sympathetic. far vision |
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when lens is rounded, strong. ciliary muscle and suspensatory ligament?what stimulation? |
contracted ciliary. slackend suspensatory. parasynpathetic. near vision, need more curve and refractive ability |
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3neural layers of retina |
back to front: 1. cones and rods 2. bipolar cells 3.ganglion cells |
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optic nerve formed out of? |
axons of ganglion cells |
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optic disc aka ____ |
blind spot -optic nerve and blood vessels leave here -no rods and cones, no image detected |
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fovea and macula lutea |
no ganglion or bipolar cells or rods, only lots of cones for exremely high acuity, centre of retina, why we turn to look at things
-macula lutea is the surrounding of fovea and has slight ganglion and bipolars |
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macular degeneration |
- loss of photreceptors in macula lutea due to old age - doughnut vision, only have peripheral |
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photoreceptor basic and 3 parts |
specialized neuron in retina, rods and cones 1. outer segment - detects light stimulus (rod shaped in rods) (cone shaped in cones) 2. inner segment - middle - meabolic machinery 3. synaptic terminal- facing bipolar cells - transmits signal generated on light stimulation to next cells in visual pathway |
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outer segment of photoreceptor |
- detects light stimulus (rod shaped in rods) (cone shaped in cones) - stacked discs containing light sensitive photopigment molecules |
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photopigments |
when acitvated by light, action potential- transmit info to brain for processing - 1.opsin - intergral protein of dics membrane 2. retienne - derivative of vitamin A, bound within interior of opsin molecule - light absorbing part |
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how many photopigments in each? rod/cone |
rod - 1 - shades - rhodopsin is their photpigmnt cone- red, blue, green |
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phototransduction. what do photoreceptors do differently |
light stimuli to electric. photoreceptors hyperpolarize |
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photreceptor actiivty in dark |
Na channels in photorecptors activated by cGMP 2nd messenger, in absence of llight cGMP is high
- so Na channels opne, donstant depolarization, this spreads to synaptic terminal and keep VG Ca open which triggers release of neurotransmitter which is also in terminal |
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photorecpetor activity in light |
retiene changes shape in light, activates photopigment, ctivates G protein transducin in rods/cones, activates phosphodiesterase which degrades cGMP
- lets Na channels close, hyperpolarization - spreads to synatic terminal - close Ca reduce NT
- photorecpetors inhibited by adequeate stmulus and excited by absencse of stmulus
- brighter the light , greater reduction in NT release |
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photoreceptor NT effect |
inhibits bipolars who cant send message to ganglion to send to brain, so lack of NT excites |
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bipolar cells |
-transfer signal to ganglion cells from photoreceotrs - graded potentials but ganglion do AP
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rods |
- 30 x more than cones -intensity of shades of grey - high sensitivity -low acuity - night vision - much convergence in retinal pathway - more numerous in periphery |
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cones |
- 30 times less than rods - colour - low sensitivity - high acuity - day vision - little convergence in retinal pathway - concentrated in centre (fovea/maula lutea) |
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dark adaptation |
- light breaksdown photopigments, reducing sensitivity -longer in dark, regenerated and sensitivity increases |
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light adaptatio |
- photopigments begin to break down rapidly and adjust, this burns out rods and cones are used for the day vision |
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night blindness |
-dietary dficiencies of vitamin A which is used to make retienne - although photopigments are reduced, still enoughcone pigment to see in bright light - cant see at night cause rods arent functional - thus carrots(vitamin A) 'good for eyes' |
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how we see diffrent colours, not just red green blue |
visual cortex, percieves colour based on percenage of each colour cone used |
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colour blindness |
lacking a particular cone, genetic or nerve/eye/brain damage.
- rely on 2 cones to create colours recieved,
-some cant distinguish green/red so at traffic light rely on intensity to see when to go |
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visual field |
what can be seen w/o moving head |
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info that reaches visual cortex is not replica of visual field because (4) |
1. retina sees upside down and backward because bending of light rays- brain flips
2. rods and cones supress and enhance selected info for sharper imaging - on/off centre ganglion cells - on centre enhances middle when light most intense there and off centre enhances outside when more intense there
3. various aspects like form, colour, depth, movement, sepereated and projected in parallel pathways to different regions of cortex, when sepearete parts processed/integrated by higher visual regions, whole thing reassembled
4. left half of cortex recieves from right visual field as detected by both eyes and vic versa - |
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lesion in specifc- visual processing regions of brain |
may be unable to combine components of visual expression ex. (can be very specific) can recognize inadament objects but not farmiliar faces |
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optic chiasm |
-optic nerves cross here -underneath hypothalamus - fibres from medial half of each eye cross over but lateral stays same side - this brings together halfs of each visual field from each eye |
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lateral geniculate nucleus (in thalamus) |
-seperates info recieevd from eyes and relays it via fibre bundles known as optic radiations to diff zones in cortex (each proccesed diff aspect, ex. form, depth, movement)
-also has topographical map, and fovea is largest representation
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depth perception |
- overlap of two eyes in visual field allows for depth perception (binocular field of vision) - brain uses slight difference in each eye to tell distance
-some depth perception is possible with 1 eye, past experiences, and if u see car and building, and car looks bigger u know its closer
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double vision |
disparate views fro both eyes are seen simultaneously either because
- eyes aren't focused on same object simultaneously cause of defects of extrenal eye muscle
or
- binocular information is improperly integrated |
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cortical cells (3) |
-fires when particular illumination pattern for which its programmed - simple and complex stacked on top of eachother within cortical columns on primary visual cortex -hyper complex found in higher visual processing areas |
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simple cortical cells |
ex. bar viewd vertical, horizontal, other oblique orientation |
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complex cortical cells |
respond to movement of critical axis of orientation |
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hyper complex cortical cells |
respond to edges, corners, curves |
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aqueous humour |
-btwn cornea and lens
- fluid that carries nutrients to cornea and lens |
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choroid |
-middle layer of eye
- pigmented to prevent scattering of light rays in eye -contains blood vessels to nourish retina - anteriorly specialized to form ciliary body and iris |
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cornea |
- outermost layer of eye
- refrative ability |
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iris |
- visible pigmented ring of muscle within aqueous humour
- varies size of puil/ responsible for eye colour |
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lens |
-between aqueous/vitreous humour
- variable refractive ability during accomodation |
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sclera |
- tough outer layer of eye, anterior portion is formed cornea
- protective, forms white of eye |
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vitreous humour |
- semifluid, jelly substance helps maintain shape of eye |
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ear 3 portions basic |
external, middle, inner ear
middle/external - transmit airborne sound waves and amplify
inner ear -1. cochlea - contains receptors for sonversion of sound waves into nerve impulses -2.-vesitbular apparatus - sense of equilibrium |
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timbre |
- enables listener to distinguish source of sound waves ex. know if its mother or GF |
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how to determine location of sound |
- sound reaches one ear first - coming from one way, head blocks going to second ear |
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chew gum when flying |
tympanic membrane feels pressure as middle ear pressure is higher so opening of eustachian tube allows 'pop' and pressure to equalibrate |
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fluid accumulation in middle ear? from where? effect? |
throat infections thru eustachian tube. fluid is painful and interferes with sound conduction |
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middle ear bones (ossicles) |
transfers vibratory movements of tympanic membrane to fluid of inner ear
1.malleus - attached to tympanic 2.incus - middle bone 3. stapes -attached to oval window |
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how middle ear amplifies waves to inner ear to set cochlear fluid in motion |
- tympanic membrane more surface are so pressure=force/unit area, increased pressure - lever action of ossciles provides mechanical advantage |
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how middle ear protects delicate sensory apparaus from damage |
several tiny muscles in middle ear contract for sound over 70db tightening typanic membrane and reducting transmission to inner ear, slow though so works for prolonged but not short like explosions, in war had guns with loud pre fire so used to sound when actual shot |
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how sound transmitted in inner ear |
pressure waves take shortcut and pass thru vesitbular membrane into cochlear duct and thru basilar membrane into lower compartment where cause round window to bulge in and out, becuase organ of corti ride on basilar hair cells move up and down and bas membrane ossiclates |
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inner hair cells |
transform mechanical into electrical - stereocilia contact stiff tectorial membrane they get bent back and forth whle basilar membrane shifts their position in relation to tectorial
- back and forth mechanical deformation of hairs opens and closes mechanically gated ion channels in hair cell and causes hyper and depolarizations
-inner hair cells communicate via chemical syapse with terminals of afferent nerve fibres making uo auditory (cochlear) nerve
- depolarizarion increases NT release which increases rate of firing in afferents |
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outer hair cells |
electromotility - actively/rapidly change length in response to changes in membrane potential
- depol - shorten hyper - lengthen
- amplify motion of basilar membrane
- enhance response of inner hairs |
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pitch discrimination |
different regions of basilar membrane naturally vibrate maximally at different frequencies
- narrow end near oval window - high pitch - wide-end near helicotrema - low pitch, everything inbetween progresses increasingly |
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loudness discrimination |
- greater tympanic deflection converted to greater amplitude of basilar membrane movement which is interpreted by CNS as louder
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primary auditory cortex |
-tonotopically organized - corresponding basilar membrane regions
- organ of corti to auditory cortex has many synapses, most important is medial geniculate nucleus of thalamus and brain stem
- brain stem uses for arousal
-MGN sorts and relays upward
-signals go to both temporal lobes because fibres partially cross over in brain stem so disruption post brain stem in auditory pathway doesnt affect other ear |
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conductive deafness |
- sound waves arent adequately conducted thru extermal and middle portions of ear to set inner ear fluid in motion
- earwax, rupture of eardrum, middlel ear infections, fluid accumulation, restriction of osssicular movement |
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sensorineural deafness |
- transmitted to inner ear but not into nerve signals that are interpreted as sound
- organ of corti, auditory nerves, ascending autitory pathways or auditory cortex
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neuralpresbycusis |
- partial hearing loss - old age, hair cells wear out
MP3 is causing in young now doe! |
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hearing aids |
- conductive deafness
- increase intensity of airborne sounds and may modify sound spectrum to tailor to either higher/lower frequencies depending on persons hearing loss
- receptor cell-neural pathway must still be intact |
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cochlear implants |
transduce sound into electrical signals that directly stimulate auditory nerve
- bypasses defective cochlear system
- not completely normal hearing but can recognize sounds |
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what is key to speaking reading, writing lanuage |
hearing, not hearing from birth makes it extremeely hard but if lost later in life, much easier |
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ampulla and cupula |
ampulla- swelling at bottom of semicircular canals
cupula - protrudes into amullas and sways in direction of movement |
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vestibular hair cells |
one kinocilium and 20-50 stereocilia, arranged in rows of increasing height
-stereocilia linked at tip-links
- when stereocilia deflected, tenstion on tip links pulls mechanically gated ion channels in hair cell
- depolarize - toward kinocillium -hyper polarize - away from kinocillium
- hair cells synapse on terminal endings of neuron who join to form vesitbular nerve, which joins with auditory nerve to form vestibulocochlear nerve
- depolarization realeases NT increasdd firing |
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vestibular apparatus - semicircular canals |
because of inertia, during acceleration/deceleration, fluid goes opposite way of motion bending cupula and hairs opposite way of motion |
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vesibular apparatus - otolith organs (2) |
utricle and satricle
- info of head relative to gravity & rate of linear motion
- kinocilium and stereocilia straight up at rest, tilted down go witi direction and gelationous gel is heavy, accelerating running going opposite like semicirculars |
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motion sickness |
- sensitve to motions of vestibular apparatus, cause dizziness and nausea |
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menieres disease |
fluid imbalances within ear - both vestibular and cochlea (auditory) contain same inner ear fluid, both have symptoms from this
- vertigo,, ringing in ears, loss of hearing, dizzyness, cant stand straight and spinning objects |
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vestibular nuclei what does it help co-ordinate and with what else's help? |
signals from vestibular go thru vestibulocochlear nerve to vestibular nuclei in brain stem (and sigs go to cerebellum too) where vistibular info is integrated with input with muscles, skin, joints to maintain -balance -posture -control of eye muscles, to be fixed on one point despite head moving - perceiving motion and orientation - |
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external auditory meatus (ear canal) |
- directs sound to tympanic membrane
-secretes proective earwax |
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pinna (ear) |
collects sound waves and channels down ear canal |
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scala vestibuli/tympani |
vestibuli - upper compartment of cochlea
tympany - lower compartment
-both contain perilymph |
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cochlear duct (scala media) |
-tube in middle runnign thru cochlea
- contains endolymph and houses basilar membrane |
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basilar membrane |
- floor of cochlear duct - vibrates in unison with perilymph movements, bears organ of Corti, the sense organ for hearing |
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Organ of Corti |
- on basilar membrane
- contains hair cells, inner hair cells undergo receptor potentials when hairs are bent as result of fluid movement in cochlea |
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tectorial membrane |
stationary and hairs of organ of COrti bend against it |
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round window |
- vibrates in unison with perilymph
- only for pressure dissapation in cochlea |
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utricle |
- sac-like structure in bony chamber btwn cochlea and semicircular canals
detects - 1. changes in head position away from vertical 2. horizontally directed linear acceleration |
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saccule |
- sac-like structure in bony chamber btwn cochlea and semicircular canals
detects - 1. chnages in head position away from horizontal 3. vertically directed linear accelration |
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gustation and olfaction |
mechanism of taste and smell respectively |
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taste buds and taste receptor cells |
-chemoreceptors for taste lie here - most on upper surface of tongue - 1 taste bud consists of ~50 spindle shaped taste receptor cells - each taste bud has small opening, taste pore thru which fluids hit up receptors
-taste receptor cells are modified epithelials tons of microvilli increasing SA, regenerate evry 10 days
- binding of tastant alters cell ionic channels inducing depolarization |
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tastant |
taste-provoking chemical |
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only chemicals in solution csn bind to receptors for taste (saliva) |
OH YES |
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cortical gustatory area |
area in parietal lobe adjacent to tongue area, where signals from taste end up
-also stops in brain stem and thalamus on way up, b-stem also projects to hypothalamus and limbic for emotional response |
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taste discrimination |
each receptor cell responds in varying degree to each of 5 tastes but usually favours one
-also influenced by smell, loss of sense of smell, taste is remarkedly reduced |
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salty taste |
-stimulated by salts
- direct entry of Na thru channels in receptor cell and depolarize |
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sour taste |
-acids containing a free H+ ion - H+ blocks K+ channels, decrease in passive movement of K+ out of cell, reduces interal negativity and depolarize |
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sweet taste |
- glucose (or other similar structure)
- activate G protein --> cAMP, results in phosphorylation and blockage of K+ ions and depolarize |
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bitter taste |
- alkaloids(caffeine, nicotiine...toxic plant derivatives) & poisonous substances
- protective mechanism to discourage ingestion
- 50-100 bitter receptors, each responds to diff bitter flavour
- G protein, gustducin- very similar to transducin starts second messonger |
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umami taste |
-AA especially glutamate
-glutamate binds to G-protein-->2nd mess-->details pathway unknown
-distinctive taste of flavour additive MSG (monosodium glutamate) very popular in CHan dishes |
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supporting cells (nose) |
-secrete mucus, coating nasal passage |
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basal cells (nose) |
-precursors for new olfactory receptor cells, replace every 1-2 months |
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olfactory receptor cells |
afferent neuron, receptor lies in olfactory mucosa, axon transverses in brain, axons of these form olfactory nerve
- receptor has cilia where odourants bind to
to be able to smell something
1. dissolve in mucus coating olfactory mucosa 2. easily vaporized so molecules can enter nose |
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detecting and sorting odour components |
1000 different types of olfacotry receptors - each receptor responds to one discrete smell - binding activates g-protein triggering cAMP -->Na+ open-->depolarization receptor potential-->action pot in afferent
- frequency of AP depends on conc of stimulus
- afferent fibres pass thru bone and synapse in olfactory bulb
-synapse on glomeruli-->mitral cells then they go to either primary olfactory corex part of limbic system or they go thru thalamus to cortex , for conscous perception and fine discrimination of smell
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glomeruli |
small ball like neural juctions that receptor cells synapse on |
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mitral cells |
cells on which olfactory receptors terminate in the glomeruli that refine smell signals and relay them to brain for further processing |
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odour discrimination |
-based on diff patterns of glomeruli activation - more than 10000 scents
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adaptability of olfactory system |
-sensitivity to new odour diminishes quickly - olfactory receptors adapt slowly specific to particular ordour
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-why we stop smelling something when odour physicslly is gone? |
odour eating enzymes in olfactory mucosa, also clears away harmful chemicals, possibly linked to lizer enzymes who also janitors |
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vomeronasal organ |
-another sense organ of nose
- detects pheremones, bind to receptors and AP to limbic system which elicits emotional/sexual response |
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pheremones |
-nonvolatile chemical signal passed subconsciouslly from person to person - triggers action potential to limbic system elicting emotion and sociosexual response, never reach higher awareness |
