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515 Cards in this Set

  • Front
  • Back
the anterior 1/6 of the sclera is referred to as?
the transparent cornea
what are the 3 concentric tissue layers of the eye?
sclera
uvea or choroid
retina
anteriorly the choroid forms what?
the bulk of the ciliary body containing the ciliary muscle and the stroma of the iris
where is aqueous humor produced?
in the posterior chamber by teh ciliary body, but then drains through Canal of Schlem
the shape of the eye is maintained by ?
intraocular pressure
what produces aqueous humor?
the ciliary body which is secreted into the pos chamber
where is the pos chamber?
teh space b/n iris and lens
how does glaucoma occur?
if the canal of shelm is interrupted/osbsructed causing increase in intraocular pressure
this canal is what aqueous humor drains through
what causes pappilledema?
the meninges surround the eye so any increase in intracranial pressure will exert pressure in the subarachnoid space around the optic sheath which will interfere with axonal transport in the optic nerve. the built up CSF will push on optic disk
what is located in the vitreous humor?
phagocytic cells that clean up debris
what is the most powerful focusing element of the eye?
cornea (40D)
2x as powerful as the lens
how many D is the resting lens?
20D
explain the flow of light through the eye?
enters cornea then through lens then hits the layers of the retina and is convertd to electrical activity as it passes to the photoR and back as graded potential until the ganglion cells converts it to AP to travel via optic nerve
which type of lens has a greater FL?
concave causes increased FL
convex causes decreased FL
what is a diopter?
the inverse of the focal length
D=1/FL
used to describe the power of the lens
what does it mean that D are additive?
you can use 2 lens with power of 2 to get a power of 4D
what is myopia? caused by?
near sighted
too much curvature of the corneal surface or too long of an eyeball
light ends up focusing before retina
what type of lens will corect myopia?
concave lens to increase FL
what type of lens will correct hyperopia?
convex to decrease FL
waht is hyperopia? caused by?
far-sighted
eyeball too short or cornea too thin
light focuses after retina
what is the process that controls the refractive (bending) capacity of the lens?
accomodation
what is the shape of our lens when we are viewing distant objects?
flat
least refractive power
waht is the shape of our lens when we are viewing near objects?
thick and round
high refractiv power to focus the image
what is the lens suspended in place by?
CT bands called zonule fibers that are attached to ciliary mm
what component of the neural-musclar connextion of accomodation keeps the lens flat (viewing far objects)?
muscular force of zonule fibers keep the lens flat b/c their force dominates
what happens in accomodation to focus on near objects?
the zonule fibers relax, so the intrinsic elasticity of the lens can dominate and the lens rounds back up
the zonules RELAX b/c the ciliar mm CONTRACT
as the ciliary mm contract, less tension is exerted on the zonule fibers so they can relax and the lens rounds up
what is presbyopia?
the decrease in accomodation with age due to increaesed rigidity/loss of elasticity of the lens
can only accomodate to about 21D (normal 34D)
besides accomodation, what is another method for improving the resolution of an image?
reduce the size of the pupil to increase the depth of the feild
what is the aperature of the iris called?
pupil
shape of iris mm?
sphincter mm: circumferentially organized sphincter muscle
dilator: radially arranged
what type of fibers innervate the mm of the iris?
spincter mm controlled by PNS
dilator m controlled by SNS
what are the 3 physiological events that occur when our eyes accomodate? together, what are they called?
1. pupil consticts
2. eyes converge
3. eyes accomodate
Near Reflex
the 3 actions of the near reflex are all coupled through what?
the pregang PNS innervation coming from the Edinger-Westphal nuclues in the brain
where in the eye is light energy converted to electrical activity?
in the retina
compare the sensitivities of cones and rods?
cones: require many photons
rods: so sensitive they they can detect 1 photon of light
what are the output cells of the retina?
ganglion cells
send their axons to the brain (optic nerve)
job of bipolar cells?
relay info from the photoR to the ganglion cells
what are the interneurons of the retina?
horizontal and amacrine cells
mediate lateral interactions b/n cells in the outer and inner plexiform layers
why is the retina paradoxically aranged?
the 1st cells to encouter light are the ganglion cells then bipolar then photoR
reqd that photoR be last b/c they need pigment epithelium to survive
what is the fxn of Pigment Epi?
place where outersegments of photoRs are embedded
secretes GF that are critical and absorbs light so it doesnt interfere
problem in retina detachment?
the photoR require being embedded in pigment epi for GF and vasculature of choroid
explain the type of NT release in neurons of retina
photoR: graded release/local
bipolar: graded release/local
ganglion: AP (needed b/c travels from retina to thalamus)
explain what happens in phototransduction?
light is absorbed by GPCR, rhodopsin (in rod). this causes a conformation change in 11-cis retinal to become trans-retinal. this conf change activates G protein Transducin. The alpha subunit of transducin activates PDE which then decreases cGMP in cell. all the cGMP cation channels close and Na can't enter the cell. the cell is now hyperpolarized causing a decrese in NT release
what terminates the signal activated in phototransdxn?
arrestin; prevents rhodopsin from activating transducin now retinal dissociates from rhodopsin
rod-mediated vision is called?
scotopic and occurs at low light levels
night blindness is associatd with what?
losing rods
rods are extremely sensitive to light
cone-mediated vision is called?
photopic and occurs in bright light conditions
how are cones defined?
by their absorption spectra: long(red), middle(green) and short(blue) wavelenths
the differentce in absorption is determined by the type of opsin each cone makes
cones absorb photons according to what?
their opsins and the intensity of the response is entirely dependent on the number of photons each absorbs
how is our perception of color derived?
from the releative levels of activity in all three sets of cones: red,gree, blue
which opsins are on the X chromosome
red and green thus a higher prevalence of this form of color blindess in men than women
what is the specialized and distinct region on the retina where are highest acuity vision occurs?
the fovea thus we move our eyes ot the optimal position to have the image fall on our fovea
where is the fovea located?
in a depression w/n the macula lutea (w/n retina)
where is the macula lutea?
w/n retina near optic disk
what is the optic disk?
wherere the axons of the ganglion cells leave the retina as the optic nerve
contains NO neurons thus is "blind spot"
where is the blind spot and why is it called that?
located in optic disk which is where the axons of ganglion cells leave the retina
called blind spot b/c there are no neurons located there so no image is picked up (no photoRs)
where in the retina are the most cones? rods?
cones: fovea especially foveola (no rods at all)
rods: periphery
what is unique about the foveola?
no rods at all
all other retinal neurons are pushed aside so that nothing obscures the capture of light by the cones
no blood vssls run through
*cones are very dependt on PE for nuorishment
why is foveal vision such high acuity?
cones synpase on 1 bipolar cell which synpases on 1 ganglion cell (midget ganglion)
1:1 ratio
maximizes acuity but is SLOW
what is neuron connectivity like in areas of retina that are not the fovea?
several rods and cones converge on the same ganglion cell (15:1)
why would you want convergence of rods? what happens to spatial resolution?
spatial resoln decreases but increase in sensitivity b/c so many rods will be sending input to single ganglion cell
*don't care what stimulus loos like (fine resoln) just need to know that there is a stimulus somewhere
when would you not want convergence of rods? where do you find this?
dont want convergence when need to know exactly what the stimulus lookds like/high color, detailed
want this in fovea
what is retinitis pigmentosa
mutations in rhodopsin causing apoptic death of rods directly
indierct death of cones
what is age-related macular degeneration (AMD)? 2 forms?
progressive loss of central vision
photoR die
wet AMD and dry AMD
compare the types of AMD
wet: least common, excessive growth of vasculature leaks blood into retina damaging photoR
dry: most common (90%), retinal PE dies indirectly killing photoR
what are "on-center" bipolar cells and "off-center"
on center: respond to light in the center of receptive field
off center: respond to light that lies aruond the center in a concentric circle
why do we have both on and off center ganglion cells?
to distinguish b/n objects that are brighter or dimmer than their background
which type of bipolar cells do cones release glutamate onto?
both! on center and off center but they have different glutamate Rs
compare the glutamate Rs on the bipolar cells
on-center: metabotropic, mGluR6 b/c hyperpol by glutamate
off center: ionotropic , AMPA and Kainate b/c depol by glutamate
are all ganglion cells exciatory?
yes!
what happens when a cone absorbs light in the center of a receptive feild?
light on cone causes hyperpolarization b/c PDE activated
less glutamate is then released on on-center and off-center cells
the OFF center are less excited b/c not much glutamate was released, but the ON center were less inhibited/activated therefore stimulating ON center ganglion cells
what form of bipolar cels are depol by glutamate? hyperpol?
depol: OFF center
hyperpol: ON center
the axons that emanated from the temporal side of the retina will travel to what side of optic tract?
ipsilateral
the axons that emanated from the nasal half of the retina will travel to what side of optic tract?
cross at chiasm and travel to contralateral optic tract
where do the ganglion cell axons going to go?
exit the retina and form the optic nerve then encounter the optic chiasm in the diencephalon
after the chiasm, the ganglion fibers run in the optic tract
where do the majority of ganglion cell axons ending up synapsing?
lateral geniculate nucleus (LGN) in the thalamus which then project to the thalamus
besides the LGN, where else do ganglion cell axons projecting to?
superior colliculus in midbrain, pretectum, suprachiasmatic nucleus of the hypothalamus
superior colliculus is impt in what?
coordinating eye and head mvmts
pretectum is impt in what?
coordinating pupillary light reflex
suprachiasmatic nucleus of hypothalamus is impt in waht?
circadium ryhthms
what type of ganglion cells project to suprachiasmatic nucleus of hypothalamus??
ganglion cells that make melanopsin which can absorb light thus they do not depend on rods or cones for light info..thus we have circadium rhythms in the absense of rods and cones
what is the parvocellular pathway?
cones 1:1 relationships
more precise/resolution
aka: midget ganglion
if you cut the optic tract, what type of deficit will you have?
deficit in both eyes
axons from the nasal retina of the left eye travel with what axons?
axons from temporal part of the right eye to the right brain
what is the magnocellular pathway?
involves rods (15:1)
highly sensitive
low resolution
what are the 3 classes of ganglion cells that project to the LGN
high acuity
color
motion
info from the left half of the visual world is represented where on visual cortex?
on the right half of visual cortex
what is the diff b/n optic tract and optic nerve?
axons in optic tract contain axons from both eyes, while axons in the optic nerve contain axons from only one eye
what is the diff b/n binocular and monocular visual fields?
binocular: seen by both eyes
monocular: seen by only 1 eye
where do inversions of images occur?
only in retina
after retina, image remains inverted and is mapped as inverted in visual cortex
where is the visual cortex?
along calcarine sulcus in the occipital lobe
what comprises the majority of the caudal region of the occipital lobe? why?
large area of cortex for macula b/c of 1:1 inputs
explain the organization of visual field mapping in occipital lobe
upper visual field is underneath the calcarine sulcus
lower visual field is above the calcarine sulcus
b/c of path taken by optic radiation
the fibers of optic radiation representing sup retinal quadrants have what type of info? inf retinal quadrants?
sup retinal quadrant fibers: info from inf visual field
inf retinal quadran fibers: info from sup visual field
what is Meyer's loop? where is it located? what type of info?
br from optic radiation that runs through the temporal lobe en route to visual cortex
carries info from sup part of contralateral visual field
what will you damage if you damage left MCA?
meyers lop
lose sup portion of visual field from both eyes
large visual field defects are called?
anopsias
small visual field defects are called?
scotomas
if you lesion R optic nerve..
lose vision in R eye
if you lesion center of optic chiasm..
bitemporal (heteronomous) hemianopsia "tunnel vision"
left superior quadrantanopsia is due to what type of damage?
damage to Meyers loop
cells in our cortex detect what?
edges (from bars of light) and they are oritenation selective
LGN axons project to and synapse where?
layer 4 of the primary visual (striate) cortex
AKA Area 17
LGN neurons are what type of neurons? Layer 4 neurons?
LGN: 2ndary neurons that synapse in Area 17
Layer4/Area 17: 3ry neurons
how is the visual cortex divided up?
into columns, called ocular dominance columns based on orientation from each eye
what are the 3 major features of a visual stimulus that our nervous system extracts?
form
color
movment
what are the 2 major pathways carrying visual info?
magnocellular pathway
parvocellualr pathway
magnocellular process __
parvocellular processes ____
magno: motion
parvo: form and color
cells of magnocellular pathway? parvo?
magno: large, M ganglion
parvo: small, P ganglion (midget)
receptive fields of magnocellular vs parvocellular?
magno: large receptive field
parvo: small
how do magnocellular cells and parvo cells respond to stimuli?
magno: transiently
parvo: sustained
where is majority of info coming from in magno pathways? parvo?
magno: non-fovea retina
parvo: cones in fovea that are sensitive to diff in wavelenthg of light therefore very good color info
damage to magno pathway results in what? parvo?
magno: loss of motion sensitivity; inability to detect rapidly changing stimuli
parvo: impaired color and form recog.
waht type of resolution is magno pathway provide? parvo?
magno: high temporal resolution that determines location, speed and direction of moving object
parvo: high spatial resolution that determines the shape, size and color of objects
magno pathway is located where?
dorsally in parietal lobe: info about motion
parvo pathway is located where?
ventrally in temporal lobe where object recognition (inf temporal gyrus) and color will be processed
explain the circuitry of Pupillary Light Reflex
The reflex pathway consists of retinal ganglion cells, which convey information from the photoreceptors to the optic nerve which synpase in the pretectum ipsilaterally. It bypasses the LGN and the primary visual cortex. From the pretectum neurons send axons to neurons of both the Edinger-Westphal nuclei whose axons run along both the left and right oculomotor nerves. Neurons in the EW nuclei then project ipsi to synapse on PNS neurons in cilary ganglion.(Oculomotor nerve axons synapse on ciliary ganglion neurons)
Neurons in the ciliary ganglion travel through a short nerve to synapse on the pupillary sphincter and cause it to constrict
what is located w/n occulomotor nucleus besides the LMN that supply the mm controlled by this nerve?
column of pregang PNS neurons called E-W nucleus which projects to ipsilateral ciliary ganglion
the PNS neurons in the ciliary ganglion innervate what?
pupillary sphincter and ciliary muscle
the pregang PNS neurons in pupillary light reflex synapse where? the postgang synapse where?
pregang PNS synapse on ipsilateral ciliary gang on postgang PNS
post gang PNS synpapse on pupillary sphincter and ciliary mm to cause it to constrict
what is an afferent defect in eye?
damaged right optic nerve
problem w/ sensory
(CNII=sensory CNIII=motor)
another name for blind pupil?
amaurotic pupil or afferent pupillary defect
efferent pupillary defect involves a defect in what?
CN III parasympathetic pathway
if we shine a light in the L eye and get a consensual response, what does this tell us?
CN II and III are ok in L eye
CN III ok in R eye (b/c constricted)
if we shine a light in the R eye and get a consensual response but no direct response what does this tell us?
CN III intact in L
CN II not intact in R b/c no direct response; pupil didn't constrict b/c stimulus was removed from good eye
R eye is dilated
what is anisocoria?
pupil sizes different
seen in damaged occulomotor nerve
how do you know if you have an efferent pupillary defect?
shine line in R eye and R eye constricts but L eye stays dilated therefore II and III ok in R, but problem with III in L
when shine light in L eye, it stays dilated but R eye constricts therefore II ok
what are the fxns of CN II and III in pupillary light reflex?
The optic nerve is responsible for the afferent limb of the pupillary reflex, or in other words, senses the incoming light. The oculomotor nerve is responsible for the efferent limb of the pupillary reflex; in other words, it drives the muscles that constrict the pupil.
what 4 things do you see in optic nerve damage on one side?
The ipsilateral (on the side with the damage) direct reflex is lost
The contralateral (on the other side) direct reflex is intact
The ipsilateral consensual reflex is intact (because light shone into the opposite eye can signal to the brain, causing constriction of both pupils via the normal oculomotor nerves
The contralateral consensual reflex is lost (because light shone into the eye on the damaged side cannot signal to the brain)
what 4 things do you see in occulomotor damage on one side
The ipsilateral direct reflex is lost
The contralateral direct reflex is intact
The ipsilateral consensual reflex is lost (because light shone into the opposite eye can signal the brain, causing attempted constriction of both pupils, but constriction fails on the damaged side)
The contralateral consensual reflex is intact (because light shone into the damaged eye can still signal to the brain via the normal optic nerve, causing attempted constriction of both pupils, which works on the other side via the normal oculomotor nerve on that side)
how is the ipilateral consensual reflex differt in optic nerve damage v/s occulomotor nerve damage?
optic nerve damage: ipsilateral consensual reflex intact
occulomotor damage: ipsilateral consensual reflex lost
how is the contralateral consensual reflex different in optic nerve damage vs occulomotor nerve damage?
optic nerve: contralateral consensual reflex lost b/c damaged eye deosnt sense light and can't signal brain
occulomtor damage: contralateral consensual reflex is intact b/c normal optic nerve therefore able to signal to brain
age related hearing loss is called:
presbycusis
sound is transmitted to the brain via electrical signals from what ?
cochlea
what are the 2 impt tasks that must be accomplished by auditory system?
1. sound localization (where it is coming from)-requires both ears
2. spectral content of sound (the freq and intensity)
what is amplitude? what is it measured in?
loudness/intensity
measured in dB
waht is frequency? what is it measured in?
pitch
Hz
how many dB is normal speech? what is the dB threshold of pain?
normal speech: 60dB
pain: 140dB
what happens in ostosclerosis?
stapedial foot becomes fenestrated which results in hearing loss of about 30dB
what is hyperacusis?
painful sensitivity to sound that can occur during Bell's palsy due to loss of control over the stapedius muscle
what is the fxn of stapedius mm?
dampen the sound by stiffening the ossicles which reduces their ability to transmit sound to cochlea
in Bells palsy have loss of control over this mm leading to hyperacusis
what are the 2 mech that mediate teh large gain in pressure by the middle ear?
1. size ratio b/n large tympanic membrane compared to small oval window (20:1)
2. lever ratio of the ossicular chain
therfore the middle ear is considered a transformer b/c it incrases the mechanical energy focused onto the fluid filled inner ear
what type of cells are hair cells?
neuroepithelial cells that release NT when activated
what are teh 3 chambers of the cochlea?
scala vestibuli
scala media
scale tympani
where is the spiral ganglion located?
embedded in bone of cochlea
sensory afferent
what is the central process of spiral ganglion?
CN VIII
what lies above organ of corti? below?
above: scala media
below: scale tympani
whre does the transdxn of mechanical energy to electrochemical neural potentials take place?
cochlea (auditory portion of inner ear)
wht is tonotopy?
the map or organization of sound according to its freq that is maintained all the way to auditory cortex
what is the cochlea embedded in
spongy bone called mediolus that has cell bodies of the spiral ganglion cells
another name for scala media?
cochlear duct whch contains the actual auditory receptrs: hair cells in the Organ of Corti
where is the organ of corti (what does it lie on)?
basilar membrane and contains the transdxn apparatus that consists of 1 inner hair cell and 3 outer hair cells
the stereocilia of the tall inner and outer hair cells are embedded in what?
tectorial membrane
under sound induced vibration, what happens to the hair cells?
the shear force of the vibration moves the tectorial membrane which indirecly causes bending of the hair cells towards longest sterocilia causing transdxn cation channels to open (K and Ca) causing depol
what happens to tectorial membrane and basilar membrane during sound induced vibratin?
tectorial membrane moves toward longest sterocilia
basilar membrane moves upward
what happens when shear force moves tectorial membrane in direction of shortest sterocilia?
cation trasdxn channels close causing hyperpol turning off stimulus
what links the sterocilia of the hair cells ?
tiplinks
when do the hair cells depolarize?
when the cell is deflected towards the tallest sterocilium b/c cation selective channels(K) open near the tips of the sterocilia due to tension from the tiplinks. Now Ca channels open and NT vesicles are released onto the sensory afferent fibers in 8th nerve
what is resting potential in scala media? what is the importance of this?
+80mV
insures that there is both a concentration gradient and an electrical gradient that favors K flow into the hair cell
*want to have very high + environment so when given the opportunity, the K will want to leave media and enter hair cell
where is endolymph found? perilymph?
endolymph: scala media
perilymph: scala tympani, vestibuli
difference in K concentratsion in the different scale?
scala media: high K 80mv
scale tympani: low K 0 mv like CSF
what surrounds the base of hair cells? what are the stereocilia embedded in?
perilymph surrounds the base of hair cell
but stereocilia are embedded in endolymph to insure a K flow into hair cell to cause depol (respond very rapidly to slight deflection)
what is the stria vascularis?
makes endolymph and K which enters hair cells and causes depolarization
waht happens if you damage the stria vascularis?
damage to endolymph therefore cant depol hair cells or CN VIII therefore no transdxn to brain
describe the symmetry of the basilar membrane. what is teh importance of this?
apex: floppy
base: stiff
necessary for the cochlea to perform a spectral to spatial transformation
hair cells at apex of basilar membrane are stimulated by what type of freq? at base?
low at apex
high at base
high freq have their maximal deflection where?
near the oval window
what innervates the inner hair cells? outer?
IHC: 95% innervted by sensory afferent fibers
OHC: efferent fibers coming from the brain/superior olivary complex
is it the OHC or IHC that are responsible for the amplification of low INTENSITY sounds?
Outer hair cell are responsible for the amplification of low intensity sounds thus they play a role in sensitivity and tuning of the cochlea
w/o OHC, what would be lost?
the sharp tuning and high sensitivity (response to 20-40dB) would be lost
which hair cells act as cochlear amplifier?
OHC
most hearing loss is due to loss of what?
OHC therefore lose cochlear amplifier
why is it impt that the OHC can contract?
when they contract in response to small electrical currents, it helps the basilar membrane respond to low sound tones by incraseing the vibration of the basilar membrane which then increases the stimulation of IHC increasing their receptor potential which increases the stimulation of the sensory afferents in CN8
what are otoacoustic emissions?
the activity of OHC creates these emission which can be measured. first induce sound stimulus that stimulates vibration, + OHC which vibrates back to outer membrane. with a microphone at tympanic membrane one can record the emissions
waht test is done routinely in newborns to assess their hearing? why?
otoacoustic emissions b/c it requires a fxnl middle ear to get info to tympanic membrane as well as inner ear with OHC
what is tinnitus?
ringing in the ears
b/c the otoacoustic emissions can be seen pathologically
what happens after the central processes of the spiral ganglion enter the brainstem at the pontomedullary jxn?
they bifurcate with 1 branch going to the dorsal cochlear nucleus and the other branch going into the ventral cochlear nucleus
what is the binaural pathway?
compares the imput from both ears therfore localizes sound
fxn of monaural pathway?
impt in analyzing the freq and intensity of a sound
compares input from only 1 ear
which nucleus is heavily involved in the binaural pathway?
ventral cochlear nuclues
what happens after sensory affernts synapse in VENTRAL cochlear nucleus?
involved in binaural pathway
sensory affernts synapse there and post-synaptic cells then send their axons to the ipsilateral and contralateral medial superior olivary complex (MSO). this is where binaural info first converges. from the MSO, axons project into ipsilateral lateral lemniscus to terminate in inferior colliculus
when you hear lateral lemniscus, think?
auditory
lateral geniculate nucleus think?
visual info
medial geniculate nucelus think?
auditory info
sup collicular think? inf colliculs?
sup: visual
inf: auditory
waht is the path of the monaural pathway?
axons from dorsal cochlear nucleus go right past the superior olive and terminate in nuclei of the lateral lemniscus on contralateral side of brainstem. from their axons project to ipsilateral inf colliculus
from both monaural and binaural pathways, projections from inf colliculus travel to thalamus where they synapse where?
medial geniculate complex then off to primary auditory cortex which is in sup temporal gyrus in the temporal lobe
where is the primary auditory complex located?
sup temporal gyrus in temporal lobe
superior olive think?
binaural pathway
sound localization
if lesion in 1 cochlear nucleus?
deaf 1 ear (from cochlear nucleus up)
if leasion in 1 lateral lemniscus?
Not deaf in that ear
what is a conductive hearing loss?
mechanical problem *damage outer ear or middle ear
damage to actual mechanical transfer of sound to the inner ear
ex: ossification/damage of ossicles, chronic ear infxns, cerumen (wax plug)
what is sensorineural hearing loss?
results from damage to the inner ear, to hair cells, ganglion cells, auditory nerve and or in the brain
in sensorineural hearing loss, what are the freq sounds that are first lost?
high freq and all sounds critical to understanding speech
how do you hear by bone condxn?
involves direct transmission of vibrations form the skull to the fluids of the inner ear, bypassing the outer and middle ears
hearing loss by testing bone condxn indicates a _____ problem?
sensorineural
where do you place the tuning fork in Weber test? in Rinne?
Weber: on vertex of skull
Rinne: on mastoid process until subject no longer hears it, then held in air next to ear
normal Weber test?
hears equally well on both sides
normal Rinne test?
hears vibration in air after bone condxn is over
condxn deafness in one ear with Weber test?
sound is louder in diseased ear b/c masking effect of environmental noise is absent on the diseased side
condxn deafness in one ear with Rinne test?
vibrations in air not heard after bone condxn is over
what is the results of Weber test if there is nerve deafness in one ear?
sound louder in normal ear
what is the result of Rinne test if there is a nerve deafness in one ear?
vibration heard in air after bone condxn is over (b/x hearing by bone condxn involves direct transmission of vibrations from the skull to fluids in inner ear)
what are the axices for audiogram?
x: test freq (Hz)
y: hearing threshold (dB)
in the case of conductive hearing loss due to chronic otitis media, hearing by bone condxn is ____, and hearing by air condxn is ____
bone: normal
air: impaired
what are some ex of how sensorineural loss can occur?
response to ototoxic drugs (drugs used for malaria)
mefloquine to block AchR
acoustic neuroma
LOUD noises
what is the best solution for sensorineural loss?
cochler implant
how is hearing threshld related to sensitivity?
threshold is inversely related to sensitivity
very sensitive = low threshold
what is the normal range of freq (Hz)?
20Hz-20,000 Hz
low freq are located at what point of basilar membrane? high freq?
low: apex
high: base
frequency think...
basilar membrane
what does it mean for your threshold and sensitivity if you can't hear high freq?
increased threshohld
decreased sensitivity
* if pus or cerumen in ear
w/ conductive deafness, can you still hear in inner ear?
yes
only a mechanical damage that affects outer and middle ear
an acoustic nearoma is what?
in periphery blocking CN VIII
also called schwann cell tumor or schannoma
cause of sensorineural loss
where is the spiral ganglion located?
w/n temporal bone
thus when tuning fork is placed on temporal bone, it gets the fluids osscilating and hair cells transduce that freq that is carred to spiral ganglion then from there to coclear nuclei
where are the cochlear nuclei located?
pontine medullay jxn
ventral tegmental area (VTA) think..
dopamine
release dopamine on nuclues acumbins
substantia nigr think..
dopamine
segments of anatomical midbrain
tectum (roof)-most dorsal of midbrain
tegmentum (middle-contains CN nuclei)
base
if you are addicted to cocaine, dopamine is released from where onto what?
from ventral tegmental area (VTA) on nucleus accumbuns
at what level can chemoselective neurons in the nose discriminate thousads of different odors?
nanoM concentrations
how many odorant R are per neuron
1 odorant R/ neuron
olfactory goes directly to where?
cortex NOT thalamus
turn over every 1-2 months
where is the olfactory R neuron located?
olfactory epithelium of nose
what type of neuron is the olfactory neuron?
bipolar, unmyelinated located in olfacory epi of nose
which chemosensory neuron acts like a distance R?
olfactory neurons: travel all way to cortex
describe the firing capabilities of olfactory neurons?
generate continuous, tonic level of AP from 1/20 sec - 3AP/sec
waht are the only CNS neurons capable of continually reproducing throughout life?
olfactory neurons
in the subventricular zone: develop new neurons every 1-2 months
how often do olfactory neurons regenerate? do they recognize the same smell?
every 30-60 days from basal cells in olfactory mucosa
new neuron expresses the same odor sensitivity w/ same mitral cell in the olfactory bulb
how do odorants reach the chemosensitive cilia?
they bind to and are TRANSPORTED to the Olfactory Binding Protein (OBP) in the mucus to the chemosensitive cilia of the olfactory R neuron
the odorants then react with the Olfactory R proteins on the neuron ciliary membrane
is the olfactory receptr a direct or indirect r?
indirect
is a Gprotein linked R with 7 membrane spanning domains
similar to the INDIRECT ligand gated R's for neurotransmitters
binding of odorant to OR activates what?
Golf taht stimulates adenylate cyclase which Increases cAMP which opens up cation channesl to cause depolarization (local potential**)
what is the job of olfactory binding protein?
transports odorants in the mucus to the chemosensitive cilia of OR neuron
when the Golf increases cAMP waht happens next?
cAMP opens up cyclic nucleotide gated (CNG) cation channel that lets Na and Ca in resulting in a slow deol Receptor potential**
what type of potentials are found on sensory neurons?
receptor potential/generator potential
what type of 2nd mssgs amplify the odorant signal?
if odorants are unable to stimulate AC directly, they activate PLC which breaks down PIP2 releaseing IP3 which increases conductance of Ca ions at the cilia membrane
passive electronic conductance ___ with distance as it heads towards axon hillock to encode
decreases with distance
how are odorant signals terminated?
by protein kinases and enzymes that catalyze covalent modification of odor producing molecules
is encoding passive or active?
encoding is an active process b/c it involves converting a local potential into an AP
before you can encode an odor what must happen?
transduce the incoming energy (pain, temp) into R potential
then you can encode # and pattern of APs which is active
descrive the sensitivity of olfactory system for odor detection?
very high sensitivity (low threshold)
recognize 20,000 odors with only 1,000 OR proteins
where does the odotype may exist?
olfactory bulb
how do olfactory neurons synapse in olfactory bulb?
there is a convergence of axonal projections from nurons in the olfactory epi that express the same OR gene to one pair of glomeurli
(different ORs are sending info about the smell or turkey to the same glomeruli)
*high convergence gives high sensitivity to olfactory system
waht is the concept of labeled line?
the few glomeruli that are activated at lowest conc of odorant represents input from the subset OR neurons whose R's have the highest affinity for that odor
what do secondary sensory olfactory neurons innervate?
primary olfactory cortex
*no thalamic relay
besides projecting to primary olfactory cortex, where else do fibers of olfactory tract project to?
directly to amygdala (corticomedial nucleus) and olfactory tubercle (ant. perforated substance)
where is teh amygdala located and what is it impt for?
deep on medial temporal cortex
deep to uncus
part of limbic system-emotional signifivance to stimuli
what is the odotopic map located ?
olfactory bulb
what is anosmia? due to?
inability to smell
mxnl block of airway, tumor, infecn, fractur of cribiform plate
infxn: 20% with URT infxn will have complete death of OR
Kallmann's Syndrome
early smptm. in Parkinsons
what is Kallmanns syndrome?
genetic defect OR nruons fail to reach olfactory bulb
wont have GnRH: testes and ovaries affected
hypogonadism
what is specific anosmia?
lowered sensitivity to single odorant or few related cmpds
what is hyposmia?
diminshed sense of smell
due to commmon head cold, CF, Parkinsons (loss of dopamine in olfactory bulb)
waht is Cacosmia?
olfactory hallucinations of repugnant smells
ex.smell burning tires
appear as part of unicinate epileptic seizures
what is dysosmia?
distorted sense of smell
damage OE
ex: when eat turkey smells like perfume; drink coffee, smells like urine
waht is gustation?
sensation of tasting
what are the 3 CN's that pick up taste?
7, 9 (palate, pharynx, epiglottis)
10 (upper esophagus)
what is the site of stimulus transdxn (R cell) in taste bud?
sensory neuroepithelial cells
this is the R cell
how are neuroepithlia cells of tast bud structurally organized?
fxnly polarized
apical border exclusive from BL b/c Tight Jxns
apical border has microvilli
do you only have 1 primary afferent fiber synapsing at the base of each neuroepithelial cell in taste buds?
no..branches from several
activity on a primary affernt nerve represents the input from many R cells from different tast buds
what is the life span of neuroepithelia of tast bud?
short
turn over every week
what is the only part of neuroepi R cell (taste bud) that is exposed to cmpds in oral cavity?
microvili
site where sensory trasdxn takes place
what are the 5 basic taste submodaliteies? what CN is associated with each?
sweet-7
bitter-9
amino acid (umami)
sour-7 & 9
salty-7
(sour, sweet, salty = 7)
what CN is responsible for all sensation for head?
CN 5
pain in oral cavity, corneal abrasion, sensation "slimy"-fine touch, irritant gases
what CN are respnonsible for taste?
7, 9
waht CN are responsible for motoring tongue?
12
taste R cell transduce waht type of moleucles and whre? how do they commmunicate with affernt gustatory nerves?
sapid molecules (tastant) on apical border
communicate w/ afferent gustatory nerves by synaptic transmission (exicitatory transmitter released from vesicles in BL border of taste R cells)
what type of channels are present on taste receptor cells to transduce sapid molecules?
Na, K and Ca vg ion channels(salty, acids)
indirect ligand gated channels (sweet, bitter, umami)
compare conductance vs resistance
conductance : green light GO!
resistance: red light (stop!)
channel close = no conductance
R=1/g(conductance)
g what a shame the channel closed - lipids and gases can come through but ions cant
in order to have a ion conductance(g) you need what?
ion current(I)
current (I) depends on what?
concentration gradient and electrical gradient (nernst)
do we have post synaptic neurons in our taste R cells?
no! b/c it is neuroepithelial cell
a typical interaction b/n tastant and transdxn site results in waht?
change in membrane conductance
depolarization causing R potential
when Rpotential reaches threshold, AP cuaess increase Ca with release of Glu and serotonin at BL border
what NT are releaed on afferntt sensory nerve in tast receptor cells?
excitatory: glutamate and serotonin
what are the 3 types of info extracted from sapid chemical stimuli?
quality: sweet, satly, ect
intensity: magnitude
hedonic value: pleasant
is water sapid?
no!
which taste submodalities bind to R proteins and are 2nd mssgr mediated?
bitter
sweet
umami
they are indirect, with metabotropic Rs
how do bitter tastes get relayed to taste receptor cell?
quinine, coffee, K, Mg
bind to R which activate G protein, Gustducin, which stimulates IP2 to release Ca
how do sweet tastes get relayed to taste R cell?
sucrose, artificial sweetners
bind to R which activate G protein what stimulates increase cAMP and closes K leak chanells
what can you do to taste only sweet?
close ionotropic channels with amiloride
how do sour/salty tastes activate taste R cell?
act DIRECTLY via ionotropic ion channels (fast!) let Na in
get immediate depol generating an AP
*sour depolarize cell by INWARD flux of CATION, H
*salty have Na invlux therough vol independent amiloride inhibitable Na channels in apical border
how do salty tastes activate taste R cell
ionotropic channel
Na influx through V independent amiloride inhibitable Na channels in apical membrane
desribe the 5-HT R
uses 2nd mssge system
indirect
metabotropic
do taste afferent nerve fibers cross the midline on their way to CNS
no
what are teh 1st, 2nd, 3rd, 4th synapses for taste to reach CNS?
1. neuroepithelial cell with afferent primary sensory nerves (7, 9, 10)
2. brain stem: Rostral solitary nuclear complex in medulla
3. thalamus VPM
4. cortex: gustatory region post central gyrus
what is the rostral solitary nuclear complex assoiciated with? where is it?
medulla
2nd synapse for afferent primary taste sensory nerves (7,9,10)
whre does tast project to in thalamus?
VPM
cross section through rostral solitary nucleus looks like a donut therefore think
taste! in medulla-2nd synapse
middle of donut-tract with axons
donut: nucleus
gustatory cortex other name
insula
information from the insula in the gustatory cortex can be sent where?
amygdala to ascribe emotional memorty to taste and smell
what is labeled line vs across neuron coding?
“across neuron” hypothesis proposes that the pattern of responses to a particular stimulus across ALL fibers is the central feature of coding
(ex: will determine if taste is salty by looking at AP of all taste submodality R inputs)
labeled line only looks at salty R inputs and if APs are in large amts then teh taste is coded as salty
what are the 3 types of classic NT?
1. amino acids
2. biogenic amines (catecholamines, serotonin, histamine)
3. Ach
what are the 2 inhibitory Nt? excitatory NT?
inhib: glycine, GABA
excit: glutamate
what does the Goldman eqn tell us?
permeability and concentration
Vm is always closest to Eion that is most permean
what are the 3 different types of protein R's?
1. ligand (indirect and direct)
2. vgated: change in membrane charge
3. mxnl ex tiplinks
what does GAT stand for?
GABA
Amino Acid
Transporter
what is the result of drugs that block the inhibitory action of GABA?
produce excitation and convulsions
high anxiety, out of control
what are teh 2 classes of drugs that modulate GABA(A) r's? what do they attach to?
anti-anxiety-bensodiazepines
anti-convulsant-barbituates
Ben and BARBI attach to Cl channels
how is GABA produced in pre-synaptic cell?
glucose converted to glutamate which is then converted to GABA
glutamate to GABA requires glutamic acid decarboxylase + B6 (pyradoxal phosphate)
why is B6 reqd in infant formula?
rqd for prodxn of GABA (glucose is precursor)
w/o GABA won't have proper brain development
what happens to GABA after its released onto post-synaptic cell?
binds to GABA R's on Cl channels then comes right off (only stays on channel if Ben and Barbi are present)
will then be recycled through GAT into pre-synaptic or brought throug GAT into glial cell
action of benzoadiasepines?
action of barbituates?
ben: anti-anxiety
barbi: anti-convulsant
compare GABA(A) and GABA(B) R's in terms of ligand gated channel type.
GABA(A): direct gated
GABA(B): indirect gated
compare GABA(A) and GABA(B) R's in terms of action
GABA(A): increases Cl conduction (g)
GABA(B): blocks Ca channels and activates K channels (think B for block)
compare GABA(A) and GABA(B) R's in terms of R modulators
GABA(A): ben and barbi
(B): none
compare GABA(A) and GABA(B) R's in terms of agonist
(A): muscimol
(B): baclofen
compare GABA(A) and GABA(B) R's in terms of antagonists?
(A): picrotoxin
(B): bicuculline
what is the structure of GABA(A) R's?
3 subunits
very diverse: hundreds of different GABA R's are possible
compare GABA(A) and GABA(B) R's in terms of speed of postsynaptic ptoentials
(A): fast-metabotropic
(B): indirect, G protein coupled. signif slower and longer postsynaptic potentials than those genereated through iotrogenic R's
wht has a R similar to the GABA(A) R that opens a Cl channel on the post synaptic membrane?
Glycine
-not as common as GABA
where is Glycine mostly found?
spinal cord and lower brainstem inhibitory interneurons
what inhibits Gly channels? what is the response?
- + - = +
Strychnine produces convulsions by blocking Gly channels in AL
action of Strychnine?
overfire AL causeing sk mm convulsions b/c strychnine blocks Gly channels
action of excitatory amino acid transmitters in the CNS?
open up Na and K channel
what is the major excitatory transmitter in CNS? what are the types of R's?
glutamate
NMDA and non-NMDA based on sensitivity to Glu agonsit NMDA
what blocks the NMDA R? what enters?
Mg blocks channel
Ca enters
too much neuronal excitotoxicity b/c of Ca involves what?
overactivity of NMDA R as Ca enters continuosly
Ca is reqd for memory and learning
what makes the NMDA R unique?
both v and ligand gated
how do you drive out the Mg in the NMDA cation channel?
membrane depol in addition to Glu to open cation channel
on the motor end plate, how do generator pot get converted to AP? where?
in the troughs of the end plate whre Ach is released on nAchR--very fast!! this creates and endplate Na current and you get an EPP-graded, local
Na then travels passively towards neg electrodes "elecronic condxn"
must convert local P to AP in order to reach t-tubules
what are the names of the Non-NMDA R's (3)?
Kainate
quisqualate A
quisqualate B
what is the only Non NMDA R that is indirect
quisqualanate B
what is the antagonist for NMDA R
PCP (phencyclidine)-angel dust
what is EATT?
exciatatory amino acid transporter located on presynaptic cells and glial cells
lets in recycled glutamate
what is glutamate derived from? what enzyme?
glutamine by glutaminase
(glutamate degraded to glutamine by glutamine synthetase)
what happens to glutamate that has bound NMDA R's and has now come off?
recycled back to presynaptic cell or to glial cell to be remade into glutamine
enters either cell via EATT
biogenic amines act mainly as ___
neuromodulators -indirect G protein coupled R's SLOW!!
what are biogenic amines derived from?
L-amino acids and produced by certain neuron groups only that express enzymes for syn of NE or Epi
what are the catecholarmines considered? what are the cats? what are teh cats derived from?
considered biogenic amines
derived from tyrosine
dopamine
NE
Epi
tyrosine to Dopa by what enzyme? dopa to dopamine? dopamine to NE?
t-dopa: tyrosine hydroxylase
dopa-dopamine: dopa carboxylase (aromatic a.a. decarboxylase)
dopamine-NE: dopamine beta hydroxylase
what are the 2 prominent dopamine containing nuclei in brainstem?
substantia nigra (SN)
Ventral Tegmental Area (VTA)
substantia nigra projects to where? impt for what? what is the name of these fibers?
to basal ganglia
impt in motor control
nigrostriatal dopaminergic fibers=motor regulation
VTA projects to where? impt for wht? name of these fibers?
nuclus accumbens (part of basal ganglia but not motor)
impt for reward-addiction circuits in the limbic system
mesolimbic dopaminergic fibers = reward prediction, behavior, pleasure
nucleus Accumbens think?
Addictions
mesolimbic dopaminergic fibers= reward prediction
part of BG but NOT motor
both VTA and Substantia Nigra project to where? imprt for? names of these fibers?
prefrontal cortex
impt in MOTIVATION and COGNITION (D1 R's)
mesocortical dopaminergic fibers = working memory processes
what nuclus in hypothal has cell bodies releasing dopamine that inhibit Prl?
arcuate nucleus
where is the mesolimbic dopamingic fiber relaying ?
from VTA to nuclus accumbens
relay info about reward prediction, behavior, pleaseure
what and where is the nigrostriatal dopaminergic fibers relaying?
substantia nigra to basal ganglia
motor regulation
what and whre is the mesocortical dopaminergic fibers relaying?
working memory processes
where is the basal ganglia located that gives it a wrong name?
telencephalon thus should be called basal nuclei
dopamine stimulants inhibit?
dopamine reuptake
lithium inhibits?
dopamine relesae
what inhibits dopamine relesae?
lithium
whre are D1 R's located?
pre frontal cortex
involved in gene transcription in consolidation of emotionally rich "flashbulb" memories
ex: high stress, post traumatic stress syndrome
permantly change a part of brain
NE is released from?
ANS POSTgang sym neurons in SNS (in the periphery)
what is the locus ceruleus?
cluster of NE producing neurons in brainstem reticular formation whose axons innervate wide areas of the cerebral and cerebellar cortices (throughout CNS and cerebellum bathes them in NE)
ganglion indicates periphery except?
basal ganglia
does the post-gang neuron of ANS that releses NE have myelin? what does it release NE on?
no
"effector" smooth or cardia m not skeletal
locus ceruleus (blue spot) think?
cluster of NE producing neurons
ampthetamine stimulates __ release?
NE
what drug stimulates NE release
ampthetamine
is NE inhibitory or excitatory?
both ..depends on if alpha or beta receptor activated (true for all biogenic amines)
hippocampal pyramidal cells think?
temporal lobe
memory
how is NE inhibitory in hippocampal pyramidal cells?
blocks the slow Ca activated Kca conductance associated with afterhyperpol follwing a train of Ap's
by blocking the show undershoot phase, NE increases the number of AP's elicited by prolonged depols
has does NE increase the freq of AP's in hippocampal pyrimadel cells?
blocks Kca conductance channels
if no K present, don't hyperpol, get more APs bc closer to depol potential
how is NE excitatory in heart?
by stimulating B1 adrenergic R and opening ion channel indirectly
tachycardia
what is an ex of indolamine biogenic amine? derived from?
serotonin derived from tryptophan
SRI antidepressants and Tricyclic antidepressants inhibit reuptake of what?
serotonin
what type of R's do novel anxiolytics activate?
1A Serotonin Rs that are indirect
these are high anxiety
what drugs bind direct serotonin r's?
antiemetrics
what is localized in raphe neuclei?
serotonin with widespread distribution to CNS
firing rate of dopamine and NE is dependnent on what?
state of consciousness
major neuromodulator
what is teh imidazole biogenic amine?
histamine derived from histidine
where is histamine localized?
small region of hypothal --tuberomamillary nucleus-VLPO area
histaminergic neurons regulate what?
brain energy metabolism and wakefullness
what is the transmitter that is NOT an amino acid nor derived from one?
Ach
difference b/n nAchR and mAchR in terms of channel type?
nAchR: direct
mAchR: indirect
difference b/n nAchR and mAchR in terms of action?
nAchR: increases condxn of BOTH Na and K
mAChR: open or close K, Ca or Cl channels
difference b/n nAchR and mAchR in terms of agonists
nAchR: nicotine
mAchR: muscarine
difference b/n nAchR and mAchR in terms of inactivator?
acetylcholinesterase for both (enzyme)
difference b/n nAchR and mAchR in terms of blockers
n: curare, rabies virus, bungaro
m: atropine
myasthenia gravis from knocking out n or mAchR?
nicotinic
what is teh NT at all NMG? what R? inhibitory or excitatory?
Ach on nAchR
Ach is excitatory in NMJ
in NMJ, what produces the End plate current and EPP?
Ach bound to n1AchR
what is the transmitter at all pregang neurons and PNS post gang neurons?
Ach
PNS both neurons release Ach
where are the nAchRs 1 and 2 found?
n1: at all NMJs
n2: ANS postgang
is Ach excitatory or inhibitory to ANS postganglinic neurons? what is the R?
excitatory
n2AchR
is Ach excitatory or inhibitory to cardiac muscle? wht is the R?
inhibitory
m2AchR
(there are muscarinic and adrenergic Rs in cardiac m)
whre is Ach produced?
by group of neurons in basal nucleus of Meynert in the forebrain
widespread synapses throughout brain
is Ach a biogenic amine?
no
what NT is impt in temporal lobe hippocampus memory?
Ach
degenerate in Alzeihimers disease
where do neuropeptides come from? are they excitatory, inhibitory?
secretory proteins formed in neuron cell body on polyribosomes attached to Er
can be excit, inhib or both
when axon terminal supply is out of neuropeptides, what does it do?
must ship new supply of peptides from cell body before releae into synaptic cleft can occur again
what is an ex of coexistence of neuropeptides and small molecule transmitter in same axon?
Ach and VIP
enkephalin is what?
neuropeptide (5aminoacids) with R's in substantia gelatinosa
what is the presynaptic R for adenosine called?
autocoid: feedback mxn for further transmitter release
b/c ATP is usually packeaged as co-transmitter, when ATP + Ach is released, ATP is degraded to andenosine which has its own R on presynaptic neuron called autocoid
ATP is a __
purine along with adenosine, adenine (new NT)
what blocks adenosine Rs?
Xanthines (caffeine and theophylline)
what are Endocannabinoids?
"new NT"
Anandaminde and 2-AG(endogenous NT) that bind to endogeneous cannabinoid R's
inhibit release of GABA transmission
produced by degradation of lipids
what do Endocannabinoids do?
inhibit release of GABA transmission
what type of ganglion relesae NO?
same one that relesaes Ach: PNS post gang
NO: vasodilation of penis
precursor, rate limiting step, removal mxn, and type of vesicle for Ach?
precursor: choline + acetyl CoA
rate L: CAT
Removal: AchEase
vesicle: small
precursor, rate limiting step, type vesicle for Glutamate?
precursor: glutamine
RL: glutaminase
vesicle: small
precursor, rate limiting step, type vesicle for GABA?
precursor: glutamate
RL: GAD
vesicle: small
precursor, rate limiting step, type vesicle for Glycine
precursor: serine
RL: phosposerine
vesicle: small
precursor, rate limiting step, type vesicle for catecholamines
precursor: tyrosine
RL: tyrosine hydroxylase
vesicle: small
precursor, rate limiting step, type vesicle for serotonin?
precursor: tryptophan
RL: tryp hydroxylase
vesicle: large*
precursor, rate limiting step, type vesicle for histamine
precursor: histidine
RL: histindine decarboxylase
vesicle: large
precursor, rate limiting step, type vesicle for ATP
precursor: ADP
RL: mt. oxidative phosp; glycolysis
vesicle: smalle
precursor, rate limiting step, type vesicle for neuropeptides
precursor: amino acids
RL: synthesis and transport
vesicle: large*, dense core
precursor, rate limiting step, type vesicle for endocannabinoids?
precursor: membrane lipids
RL: enyzamatic modification of lipids
vesicle: none
precursor, rate limiting step, type vesicle for NO?
precursor: arginine
Rl: NO synthase
vesicle: none
which of the NTs are considered small?
"classic" and new
stored in small vesicles
synthesized in nerve terminal
which of the NTs are considered large?
neuropeptides
stored in large vesicles
synthesized in neuron body
what is conjugate eye movement and where is it coordinated from in brain?
frontal eye feild in frontal lobe
look at clock on R, hit L frontal eye field and both eyes look to R (contralateral side)
what area of the brain is responsible for peronality, goal setting, cognition?
pre frontal cortex
what area of the brain lights up with increased blood flow as you rehearse motor activity before you do it?
prefrontal cortex
L motor strip innervates what?
R somatic strip
at the highest CNS level, what does sensory info do?
generates a mental image of the body and its relatinship to the environment
*critical to know where you are in space
difference in terms of energy b/n sensory and motor systems
sensory: takes physical energy and converts it to electrochemcial energy by transducing RP and encoding AP
motor: allows neural info (electrochemical) to be transformed into physical energy (contractile force generated in mm)
list the hierarchy of the voluntary motor control system
lowest: spinal cord and brainstem
intermeidate: cerebellum and motor cortex
highest level: neocortex association areas, basal ganglia
what is the lowest level of motor system and what is the fxn?
brain and spinal cord
execute movments
activate AL to generate goal directed mvmts and postural adjustments and simple stereotyped reflex movmts
what is teh intermediate level of motor system and what is the fxn?
cerebellum and motor cortex
tactics of movmt
ex: remembers tactics to ride a bike
desending upper motor control commands and ascending soensry info used to produce spatiotemporal seq of mm contractions reqd to smoothly and accuralty achieve a strategic goal
wht is the highest level of motor system and what is the fxn?
neocortex association areas and basal gaglia
strategy
determines the goal of the mvmt and mvmt strategies that best achieves the goal
associate sensory input with motor
ex: no dopamine, can't get out of chair b/c no strategy
what part of the brain remembers tactics to ride a bike?
cerebellum
what levels of motor hierarchy do sensory inputs go to?
all levels
what layer is sensory cortex? what layer is premotor cortex?
both layer 4
what tract runs b/n motor cortex (M1) and spinal cord?
corticospinal tract (UMD)
what tract runs b/n motor cortex and brain stem?
corticobulbar/corticonuclear
what NT does corticobulbar/nuclear release?
Glu b/n runs b/n motor cortex and brainstem thus still in CNS
what type of R's would you need to hit a baseball?
nicotinic
what type of Rs would you need to salivate?
muscarinic
what type of R's do you want on sk ms?
nicotinic
what MN runs b/n brainstem and spinal cord?
AL
are there alpha MN (AL) in the brainstem?
yes, ex CN 7, 12
innervate head (MN in spinal cord innervate body)
what AL's leave the brainstem?
those innervating the head (AL in spinal cord innervte body)
CN 7, 12
do the cerebellum and basal ganglia directly innervate alpha MN's?
No! they compare wht you want to do and how you will accomplish that goal (ex: taking steps to walk)
wht is the disease of the cerebellum?
ataxia: uncoordinated mvmts due to cerebelluar hemorrhage
this is b/c cerebullum does not directly innervate alpha MN, instead it compares what you want to do with how you will accomplish the goal
what part of the brain sets the level of activity?
basal ganglia
what type of mvmts wil you have if you damage the basal ganglia? classic disease?
slow motor mvmts=hypokinesia
b/c basal ganglia sets the LEVEL of activity
Parkinson's: decrese mvnts
Huntingtons's: increase mvmts
to reach basal ganglia, sensory input must go through where?
thalamus: ventroanterior (VA) and ventrolateral (VL)
thalamus enters sensory cortex at layer __
4
what are the 3 types of mvmt?
1. voluntary mvmt
2. reflex mvmt
3. rythmic motor patterns
wht type of mvmt is the most complex?
volutantary
what are the characteristics of voluntary mvmt?
purposeful
goal oriented
effectivness of voluntary mvmt improves with experience and practice
do you need external sensory stimuli for volutary mvmt?
no! b/c goal-oriented
mvmts initiated by thoughts or emotions
how does the sensory association cortex play a role in voluntary mvmt?
associates thoughts and emotions (in lymbic and prefrontal cortex) into mvmts
what type of mvmt is this: if your hands are tied you can pick up the keys with your feet
purposeful voluntary mvmt
allows flexibility of mvmt strategy
what is the simplest mvmt LEAST affected by voluntary control?
reflex mvmt
characteristics of Reflex Mvmt
INvolutary
rapid
sterotyped
graded by stimulus strength
wht are rhythmic motor patterns?
walking ,chewing
combo of voluntary and reflex movmts
stereotyped seq of motor activity
repetitive mvmts continue automatically in a reflex manner
*initiation and termination are under voluntary control
waht does the motor system require?
info about the environment and body
1. continous inflow of sensory info from proprioceptors and vision, hearing and body surfce R's
2. degeneration of primary afferents
what is the worst proprioceptor to lose?
vestibular apparatus
informs motor system of position, acceleration of body in space
what defects will a pt have if they have degeneration of primary afferents? what will they be able to sense still?
they won't be able to sense limb or joint position, detect motion of their joints, cannot detect tension generated in mm, manual dexteritiy impaired
*will still be able to sense pain and temperature b/c no myelin
will maintain steady position if they cn see thier limbs and body (b/c stretch R's dont work)
where is LGN located? MGM?
LGN:layer 4 in occipital cortex
MGM: layer 4 in mediotemporal lobe
signs of UMN lesion
weakness (no glu)
no atrophy
no fasiculations
hyperreflexia
hypertonia
+ Babinski
signs of LMN lesion
weakness (no Ach)
atrophy (AL damaged)
fasiculations (involuntary twitch--very subtle)
hypOreflexion (b/c require both sensory and motor for deep tendon reflex)
hypOtonia
what would a persion with UMN lesion walk like?
leg extended and arm flexed
swing leg out
resting tremor
parkinson's disease
intention tremor
problem with cerebellum
ex: only tremor when try to swat at mosquito
ex of LMN damage
polio
spinal cord injury
ALS
S2-S4 innervate what?
smooth muscle in lower abdomen ex genitalia
where are PNS PREgang neurons for S2-S4 located? where do they synapse?
IML of spinal cord
synapse in PNS ganglia in pelvic pathway and relese Ach
the postgang PNS nxons then rlease Ach on mAchR and NO on penis
ANS..think motor to ___
smooth muscle
NO sensory going back b/c voluntary mvmt
compare site of PNS pregang neurons to SNS pregang neurons w/n spinal cord?
PNS: S2-S4 to smooth m in lower abdomen
SNS: T1-L2
both leave spinal cord at IML
what do SNS pregang release? what do SNS postgang release? exception?
pre: Ach on n2AchR
post: NE onto alpha or beta adrenergic on smooth muscle (only AL on skletal)
exceptions: post to sweat glands release Ach on mAchR
post to kidneys release dopamine on D1R's cuaisng vasodilation
what is relased by SNS post on sweat glands?
Ach on mAchR
what is released from SNS post on kidnesy?
dopamine on D1R's causing vasodilation
what are the 4 PNS CN's?
3, 7, 9, 10
have pregang that release nAchR
postgang release Ach on mAchR in cardac or smooth
to block release of pregang PNS neurons use what drug?
curare b/c nAchR
to block release of postgang PNS nuerons onto effector muscles us what drug?
atropine b/c mAchR
purpose of SNS and PNS ?
to regulate and maintain a steady state via their antagonistic actions
are there alpha MN in ANS?
no! only automatic control
not skeletal innervation
are afferent pathways that sense conditions of body and send info to hypothal part of ANS ?
no
this info is sent to autonomic centers in the brain (hypothal), medulla, and spinal cord
they respond by activating visceral afferents by activating efferent reflex impulses by the ANS
Ex: Baroreceptor reflex
in some cases both visceral and somatic afferent can initiate autonomic reflexes
what can modify the activity of the ANS?
strong emotion
ex: high stress-neurogenic or psychogenic diarrhea: excessive stmulation of PNS which increases teh motility and secretion of mucus in the distal colon
how does autonomic outflow differ from the somatic outflow ?
in the location of the motor neuron cell body
somatic: cell bodies IN CNS
autonomic: in ganglia OUSTIDE CNS
how many synaptic jxns are involved in efferent autonomic reflex chains? where are they?
1 synapatic jxn
b/n outflow from CNS and the effector organ
located in ganglia OUTSIdE CNS
whre can inhibition of ANS occur? compare with somatic system
at either the pre or post gang neurons
inhibiton of pre in CNS is similar to somatic system-the only pt for inhibition of skeletal muscle is at AL in spinal cord
does the adrenal medulla have post gang?
no! directly release NE and Epi into blood, which will bind anywhere R's are present
compare where ganglia of PNS vs SNS are situated
SNS ganglia not embedded in effector organs
PNS ganglia are embedded in effector organ and the post gang is usually short
what activates SNS ?
fear, trauma, hypoglycemia, cold, stress, painful stimuli, exercise
do PNS and SNS discharge as a unit?
only SNS discharges as a widespread effect
PNS never**discharges as a whole system, activation is discrete
PNS neurons originate from CN nuclei:
3, 7, 9, 10 and cranial segments S2-S4
fxn of PNS:
balances or opposes the actions of SNS
nerves that release Ach are termed?
cholinergic neurons:
All somatic neurons
all ANS Pregang (both SNS and PNS)
all PNS POSTgang
only SNS POST suppling sweat glands, blood vssls and piloerrector mm
nerves that release NE and Epi are termed? what are some typical ones?
adrenergic neurons
typical: MAJORITY of SNS post (except those to sweat glands or kidneys)
adrenal medulla secretes more?
Epi than NE
are cholineric neurons or adrenergic destroyed faster?
cholinergic by cholinesterases
adrenergic more slowly and can diffuse into blood circulation
what are dopaminergic neurons?
nerves the release dopamine
found in kidney located in renal blood vssls that cause vasodilation in kidney
what are peptidergic neurson?
nerves that release peptides such as GnRH, VIP, Neuropeptide Y, ATP (colocalized with NE in postgang noradrenergic neurons)
all muscarinic R's are stimulated by what? located whre?
stimulated by Ach
located in all effector organs (PNS)
in sweat glands, sk blood vssls, pilorector mm
all nicotinic R's are stimulated by waht? located were?
stimulated by Ach
located on dendrites and soma of POST gang (both PNS and SNS)
found in somatic motor system on sk mm
are adrenergic R's indirect or direct? located where?
indirect ligand gated
located on majority of effector organs (SNS)
what adrenergic R's do NE and Epi have greater affinities for?
NE: alpha
E: beta
are peptidergic R and dopaminergic R indirect or direct?
indirect
most effector organs receive innervation from waht? which predominates?
both SNS and PNS
the final change in organ fxn depends on the balance of activity b/n the 2 competeing regulating systems
*at rest, only one system PREDOMINATES despite dual innervation
who has sole innervation by SNS?
adrenal medulla
blood vssls
kidney
liver
pilorector mm
sweat glands
time frame of different R's?
Nicotinic: milliseconds for EPSP
Dopaminergic: seconds for IPSP
M2: seconds for slow EPSP
Peptides: minutes for late, slow EPSP--maintain longer contxn
waht does SLUD-BBB stand for?
predom tone at rest by PNS
S: salivation (3, 7, 9, 10)
L: lacrimation (7)
U: urination
D: defecation
B: bradycardia
B: blurry vision
B: bronchoconstrxn
who controls the predom tone at rest for blood vssl? what is the tone?
SNS
*constrixn by alpha (dilation by beta)
what is the effect of SNS and PNS on eye-pupil?
SNS: mydriasis (dilation)
PNS: miosis (constriction)* predom tone
what is the effect of SNS and PNS on ciliary muscle?
SNS: relaxation
PNS: contraction *predom tone
what is the effect of SNS and PNS on salivary glands?
SNS: thick mucus
PNS: watery secretion *predom tone=salivation
what is the effect of PNS and SNS on blood vssls?
SNS: constricion (alpha)
PNS:none
what is the effect of SNS and PNS on heart?
SNS: increase rate, contractility
PNS: decrease rate, contractility *predom tone is bradycardia
what is the effect of SNS and PNS on bronchial muscle?
SNS: relaxation
PNS: contraction *predom toni is bronchoconstrxn
what is teh effect of SNS and PNS on GI tract?
SNS: decrease motility
PNS: increase motility *predom tone is defectation
waht is the effect of SNS and PNS on urogenital tract?
SNS: decrease urination
PNS: increase urination *predom tone
a baseline vasoconstrixn is regulated by what nervous system and why is vasocontrxn?
SNS regulates blood pressure by altering blood vssl diamter by keeping a steady tonic SNS firing to arterioles
how does discharge of noradrenergic firing change to cause constrxn and dilation of arterioles?
increased discharge=constrxn
decreased discharge=dilation
when do we have pupil dilation? waht nervous system controls this?
SNS
dilation called Mydriasis
youth, emotion "love detector"
darkness, pain
when do we have Miosis? waht nerves system controls this?
PNS
pin point pupil
age, boredom, tired, NON-REM sleep and Anesthesia
if you have just given your pt anesthesia and lifted up their eyelid what will yo usee?
pin point pupil: miosis
also in age, boredom, tired NON REM sleep
sphinctor mm of eye is innrvated by waht?
PNS-CN 3
have mAchR for Ach
if you block constriction of pupil with atropine, what is this called?
Cycloplegia
where are the cell bodies for pregang CN 3 innervating sphinctor mm of eye?
Edinger Westphal nucleus
what must you do for near vision?
incresae PNS
contract ciliary muscle
lens becomes round
what must you do for far vision?
decrease PNS
relax ciliary muscle
lens bcomes flat
what is the problem with Horner's syndrome?
knockout sup cervical ganglion (where preSNS synapse on post SNS for dilator muscle of eye)
won't get dilated pupil b/c that is where pregang SNS secretes Ach on post gang
eye constricts
if flash light on pupil and pupil constricts further this tells you that spinchter mm is intact therefore PNS-CN3 is ok
what does ptosis tell you?
lesion in sym pathway
what NT is released on IML pregang SNS neurons from T1-L2?
glutamate
from hypothal
waht does PNS and SNS do to K and Ca conductace?
PNS: increases resting K conductance, decrease Ca conductanceconductance to slow heart rate
SNS: increase HR by increases K conductace for fast repol anc also increases Ca conductance
what adrenergic Rs are responsible for increasing heart rate and contractility?
sNS innvervation of Beta2 adrenergic R's
how does the baroR reflex work?
primary prob: rise in BP
increase sensory afferent firing (baroR's)
decresae SNS activity firing of vasoconstrictors
incrase PNS firing of vagus=vasodilation by increaseing mAchR activatin to decrease HR
force of contraction decreaed b/c less activation of B1R's thus get decrease in CO
BP back to normal
increase in BP causes a ____ in BaroR firing
increse BP = increase firing
what CN's relay info about change in blood pressure to solitary nucleus?
CN 9, 10