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142 Cards in this Set
- Front
- Back
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Ionic makeup of endolymph
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high K+ and Ca++
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What do hair cells stick into: endo or perilymphh
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endolymph
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What structure marks the tall end of a hair bundle
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kinocilium
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What else besides the kinocilium compromises the hair bundle
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about 30 "stereocilia", which aren't really cilia but are actin-filled projections.
30 stereocilia are arranged like a staircase |
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what is the kinocilium made of? the stereocilia?
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kinocilium: MT
stereocilia: Actin |
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What connects the tips of stereocilia?
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tip links
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what are hair cells dervied from?
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neuroectoderm
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Movement of hair bundles in which direction will cause increased firing of 8th nerve fiber?
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Movement toward KINOCILIIUM (this stretches tip link...)
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"How did we know that auditory transduction is mechanicotransduction and not chemotransduction?
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It is so fast. cf phototransduction, which is much slower.
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How are hair channels opened mechanically?
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bending toward kinocilium stretches tip links. this physically opens ion channels on the stereocilia...
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What is going on whe hair cells are straight up?
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Still some level of strech inducced transduction...about 15% of the strech-linked channels are open. tonic release of NT.
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What happens ionically when strech channnels open?
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Hi K+ and Ca++ from the endolymph flows into the hairs.
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What does this ion flow do?
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+ flow into cell. this depolarizes it.
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Which ions pass thru stretch channel? Why?
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K+ mainly
Ca++ also and also Na+ Any cation, basically, will flow in via its electrochemical gradient. not a selective channel. |
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What is Meniere's syndrome?
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Symptoms:
vertigo attacks tinnitus fulneess in ear eventual hearing loss Causes: dilation/rupture of membranous labyrinth |
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How do strech channels adapt to continued stimulus?
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Channel attached to myosin motor that asociates with actin core of the sterocilia.
With continued open stimulation, Ca influx causes Myosin motor to move downward. This relaxes tension in tip fiber, and stretch activated pores close. The opposite happens with continued bending of hairs away from kinocilium. Myosin goes up shaft, taking up the slack in the tip fibers |
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What are the divisions of heriditary deafness?
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1) syndromic: associated with other problems
2) nonsyndromic: only hearing problems |
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Name a genetic cause of hereditary deafness:
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mutations in several unconventional myosins.
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What are the major causes of hair cell loss?
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1) hereditary defects
2) infections 3) ototoxic drugs (streptomycin,etc) 4) accoustic trauma 5) presbyacusis |
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How can some ototoxic drugs cause hearing loss?
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They can plug the stretch-activated channels in the stereocilia
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What general category of drugs is ototoxic?
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aminoglycoside antibiotics
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What is TTS?
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Temporary threshhold shift
Temporary hearing loss after continued exposure to loud sounds may be due to breakage of tip links, which can regenerate somewhat over a period of hours |
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where are the hair cells that mediate balance?
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In the otolith organs and the semicircular canals
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What do hair cells in otolith organs detect?
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Static head position
Linear acceleration |
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What do hair cells in semicurcular canals detect?
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They mediate dynamic head movement by detecting angular acceleration
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how is utricle oriented
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Hair cells pointing straight up
horizontal-oriented macular plane |
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How is saccule oriented?
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vertical oriented macular plane
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Where are hair cells/receptors in the semicircular canals?
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on the ampullary crest
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what is the cupula?
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The elatinous mass that hair undles from duct hair cells project into, in the ampullae of the semicircular ducts
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what is the relationship between dB level and sound intensity?
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every 20 sb = 10 fold increase in sound pressure
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what db level does hair cell damage occur?
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120
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what is the normal human frequency hearing range?
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20 to 20,000 Hz
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Vowels and consonents: frequencies?
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consonants: hi frequencies
Vowels: lo frequencies |
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Where does stapes press on inner ear?
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oval window
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what are the middle ear muscles? Fxn?
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Stapedius
tensor tympani (malleus) dampen vibration during loud soounds |
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what is otosclerosis?
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bone proliferation of stapes at oval window...causes hearing loss
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How do you know if you have conductive hearing loss instead of sensorineural hearing loss?
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1) hearing loss at all frequencies
2) bone conduction intact |
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What is in the scala vestibuli?
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perilymph
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What is in the scala media?
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endolymph
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What is the organ of corti?
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Neuroepithelium on the basal membrane in the cochlea
Consists of 1) inner and outer hair cells 2) gelatinous tectorial membrane 3) supporting cells |
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describe tonotopic nature of basilar mmembrane
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each segment of the basilar membrane vibrates maximally at a diiscrete frequence, from low at the beginning (wider) to high frequency at the top.
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how many rows inner and outer hair cells?
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1 inner
3 outer |
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Describe ratio of inner and outer hair cells and their connection to cn VIII afferents
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10 outer hair cells will converge on one nerve fiber
1 inner hair cell will converge on 10 nerve fibers so most afferent within the nerve 90+% are carrying input from inner hair cells |
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which scala does wave go up? which one down?
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Up the scala tympani, down the scala vestibuli
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What specialized feature do outer hair cells have? what might it be involved in?
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they have a membrane structure that actually allows them to contract. This may be the basis of otoaccoustic emissions.
It also exerts forces on the tectorial membrane that may increase sensitivity and tuning sharpness. |
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what is place coding?
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It is how nerve cells at each segment on the basilar membrane are "tuned" to have their lowest firing threshhold when activated by a particular frequency. So while other frequencies can activate it, it must be much louder..
this tonotopic organization is maintained all the way thru the cortex. |
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what is phase locking?
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At low frequencies (only), 8th nerve fibers will tend to fire at the same phase of each wave, precisely preserving frequency information (1 beat, 1 fire).
this is another way to code information, in addition to place coding (infering info based on WHERE the nerve is coming from) |
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How is amplitude of sound wave coded for?
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Increase of tone and you recruit more fibers to fire (ones slightly off tune, since you are now above their threshhold?)
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what are the 2 methods of sound localization? Which nucleus is involved with each?
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1) compare difference of intensity in each ear. Lateral superior olivary comples.
2) compare difference in timing in each ear--which ear does sound reach first? Medial superior olivary complex. |
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What is inferior collocilus involved in?
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sound localization
probably the beginning of sound identificatioon |
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which frequencies get tonotopicaly expanded territory in the cortex?
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those in the speech range
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Which has more surface area: cerebrum or cerebellum?
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cerebellum
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Which has more neurons: cerebrum or cerebellum?
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tie (20 billion)
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what kind of learning might the cerebellum be involved in?
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non-declarative
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describe the cerebellar plasticity/eye patch experiment
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cut lateral rectus of one eye to weaken it. It is slower to track target. If you patch it and have person look to weakened side, ok eye is normal and patched damage eye undershoots. If you patch normal eye and have it look to target, damaged eye hits target but patched normal eye overshoots.
BUT: with time and recovery, there is recovery of the lost function when patching occurs. SUGGESTION: cerebellum might be involved in learning needed to compensate for injury |
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Describe Friedrichs ataxia
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Hereditary ataxia
Autosomal recessive affects large neurons in spine Progressive ataxia, especially of trunk Nystagmus, weakness, spasticity, REDUCED DTR Usually associated with an unstable GAA (glut) repeat in the FRATAXIN gene Worse when passed from father--more repeat expansion |
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Describe SCA
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Spinocerebellar atrophy
Autosomal DOMINANT Loss of Purkinje cells (mainly) Associated with CAG repeats in ataxin gene (a nuclear kinase) |
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Repeats and diseases:
GAA CAG CGG CTG |
GAA: Friedrichs ataxia
CAG: Spinocerebellar atrophy, Huntingtons CGG: Fragile X CTG: myotonic dystrophy |
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What is the function of the basal ganglia?
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think of them as a traffic cop: gating multiple stimuli that might evoke a motor act. they decide which one goes when
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What makes up the basal ganglia
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Caudate/putamen
Globus pallidus Subtantia nigra Subthalamus |
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What parts of the cerebbral cortex project to the basal ganglia
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just about all of it! BG must recieve info re senation, motivation, emotion in deciding how to gate impulses
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Describe the 3 prominent neurotransmitters involved in basal ganglia connections
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GABA: inhbitory
Glutamate: excitatory Dopamine: excitatory |
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What do you call motor disorders related to problems in basal ganglia? What does this group inlcude?
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"Dyskenisias":
Chorea (rapid flicking) Bradykinesia (poverty of movement) Rigidity, stiffness Tremor at REST) |
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Where is the neuron loss in parkinsons disease:
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pars compacta of the substantia nigra (dopamineric neurons)
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What does dopamine agonsist help/not help in parkinsons:
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Helps bradykinesia, rigidity, slow gate
Does not help tremor at rest |
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What does help PD tremor?
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cholinergic ANTAgonists.
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Describe 2 surgical interventions for PD
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Pallidectomy (selective lesion of globus palllidus)
Lesion of thalamus Transplant fetal dopaminergic neurons |
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Describe pathophysiology of huntingtons:
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Degeneration of caudate and putamen
(enlargement of lateral ventriclles) |
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What does CAG code for
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glutamiine. polyglutamine forms nuclear inclusions/is insoluble
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what disease are lewy bodies associated with?
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PD
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What is Werner's syndrome
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accelerated aging due to DNA helicase defect
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Which matter do you lose more of wiht age?
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White > gray
atrophy more common than actual cell loss |
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What are 3 possible mechanisms of CNS atrophy?
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1) compromised blood flow
2) Trophic factor deprivation 3) Free radicals |
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Estrogen and aging
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seems to act as a neuro growth factor--increase dendritic spine number. But it turns out it may actually promote dementia wiht time
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What might be the aging pacemaker
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hypothalamus...
causes decreas in GHRH (GH release) and GnRH (estrogen release) |
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Define dementia
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Multiple cognitive defects that SIGNIFICANTLY disrupt function
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What are the major types of Alzheimers disease? Describe
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1) sporadic. 80-90% of cases. Late onset. Weak genetic association.
2) familial. 10% cases. Onset before 60. Strong genetic association (1, 14, 21--downs!) |
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Where do you find amyloid plaques and tangles in AD?
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Limbic system
Cerebral cortex |
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Are plaques and tangles sufficient to cause AD?
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no. both are found in nondemented brains.
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How do plaques form?
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Abberant cleavage of APP leads to formation of bad A-beta fragment, which aggregate and form extracellular plaques
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What are tangles?
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Intra and extracellular neurofilament groups that include Tau protein in abnormal helical arrangments
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what gene is involved in familial AD
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presenilin, may have role in APP processing
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what protein is implicated in sporadic AD?
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Apo E.
Lipid transporter that is found in amyloid plaques. Normal apoE may be required for Tau stabilization; abberrant apoE leads to tangle formation |
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Which apoE allele is the bad one for sporadic AD?
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apoE4
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what 3 events are required for regeneration
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1) replacement of lost neurons
2) regrowth of lost axons 3) reformation of specific connections |
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Why is frog retinal neuron regrowth not really regeneratino?
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It was not evolved to make frog more viable, and doesn't surve that purpose in the wild. this is just an artifact of a DEVELOPMENTAL adaptation
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Where is theere constitutivve neuron proliferation in mammals?
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granule cells
in olfactory bulb and dentate gyrus of hippocampal formation. Confirmed with labelling experiments on people just before they died. |
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what did the labelling of granule cells in mice in enriched/not enriched environment show?
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In enriched environment, there is not necessarily more granule cell proliferation (not more labeled neurons). But there seems to be less turnover...that is, the rate of dying of those cells is decreased. Thus, the bassal regeneration rate is > death rate, and with time it appears that more granule cells are labeled.
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Rat experiment of stem cells injected for parkinsons disease
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50% had symptom alleviation
20% had metastatic tumors (there WAS differentiation of stem cells into neurons and glial cells) |
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What is nogo?
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protein expressed in white matter of CNS. Seems to have something to do with why in CNS, the oligodendrocyte environment seems to inhibit axonal regrowth. If you add nogo antibodies, you can induce some axonal growh from nicked axon. These block the inhibitory epitopes on CNS myelin
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Describe regrowth of axons in the periphery
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Unike in CNS, they do regrow. But even in PNS, Regeneration is not specific to the correct targets.
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recovery in children
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seems to be better. may actually be some "reorganization" type plasticity. You can reroute an intercostal nerve to arm after brachial plexus is ripped...
Over time, arm movement is not associated with respiration! Not clear if reorganization is at cord or cortex level. |
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do glia retain the ability to divide/
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yes. and they do, especially in response to injury
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Types of glia in the 2 NSs.
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PNS:
Schwann cells CNS: oligodendrocytes astrocytes ependymal cells microglia |
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what happens to schwann cell if axon dies/
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it becomes phagocytic. also secretes growth factors (NGF)
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do schwann cells always myelinate
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no, sometimes they can just "ensheath" the axon
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describe the 2 classes of astrocytes
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1) fibrous. long processes, mainly in white matter tracts
2) protoplasmic. veil-like processes, more in gray matter. they ENVELOPE SYNAPSES. |
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name 2 things astrocytic processes do
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1) line the outer surface of brain and blood vessels to form glia limitans
2) ensheath neuronal cell bodies, unmyelinated axons, dendrites, nodes, and synapses |
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how are astrocytes coupled
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gap jxns. capable of spreading ca, K, ATP
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What happens to astrocytes after injury in CNS
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become phagocytic, may proliferate and form a glial scar
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describe ependymal cells
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1) line surfaces of ventricles
2) have cilia and microvili 3) LACK tight jxns, so CSF can equilibrate with ISF around brain tissue 4) specializes ependymal cells in choroid plexus secrete CSF |
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what are microglia
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resident macrophages of CNS
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how are microglia arranged in cns
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spaced apart somewhat regularly, unlike the neurons that are all tangled together
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what is the major site of HIV replication in the brain
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microglia
can cause dementia |
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what kind of channels are at nodes?
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Na
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how do glial cells buffer?
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they act as a sink for extracellular K. They are permeable to K (almost exclusively), and they are connected by gap jxns to form a functional syncytium. so they are an infinite sink for excess K
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How do glia function in neurotransmission
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1) they themselves cannot propogate an AP
2) they can insulate synaptic inputs 3) they can uptake NT 4) they can also release some modulating NT into the synapse |
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Glia and NMDA receptors
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can release D-serine, needed before NMDA receptors can respond to glutamate.
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can Glial cells even modulate the NMJ
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YES! injection of stimulatory subunit of G protein in a perisynaptic schwann cell caused decline in effected postsynaptic current after excitation!
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What happens when you add glutamate around astrocytes?
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you see propogation of intracellular Ca waves through the astrocyte syncytium
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where are most CNS tumors derived from?
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glia
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name the monaminergic neurotransmitteres
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1) dopamine
2) epineprine 3) norepinephrine 4) serotonin 5) histamine |
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Name the catecholamines
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dopamine
norepinephrine epinephrine |
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Describe Catecholamine synthesis
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1) starts with TYROSINE
2) Tyr hyroxlyase makes L-DOPA 3) DOPA decarboxylase --> dopamine 4) Dopamine hydroxylase --> NE 5) NE demethylation: Epinephrine |
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Serotonin sytnethesis
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1) starts with TYPTOPHAN
2) Tryp hydroxlase --> 5-HTP 3) 5-HTP decarboxylase --> serotonin |
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Histamine synthesis
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HISTIDINE --> Hist decarboxlyase --> HISTAMINE
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What causes release of monoamine containing vesicles from terminal?
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Ca+ influx
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What are most monoamine receptors?
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most are g protein-coupled
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How are monoamines dealy with after release
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1) degredation on postsynaptic terminal (COMT)
2) active semi-selective reuptake (NET, SERT, DAT) 3) ...followed by degradiation in presynaptic terminal by MAO 4) or reloading into vesicle by vesicle surface VMAT |
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Where does the dopaminergic system project from and to?
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FROM: substantia nigra/ventral tegmental area of midbrain
TO: 1) Nigrostriatal 2) Mesolimbic (amygdala, hippocampus, cingulate). 3) mesocortical |
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describe more the 3 components of the dopaminergic system
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1) nigrostriatal. Project to C/P (striatum). PArkinsons path
2) mesolimbic. Ventral tegmental midprain to limbic system. Reward pathway 3) mesocortical. Ventral tegmental midbrain to prefrontal cortex. Schizophrenia? |
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Describe location of noradrenergic system
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1)STARTES: locus coeruleus in brainstem
2) PROJECTS: widely. Has to do with depression.... |
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Describle location of histaminergic system
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1) originates in TUBEROMAMILLARY NUCLEUS of hypothalamus.
2) PROJECTS: sparsely but widely. Involved in arousal and attention. Affected by benadryl, which crosses blood brain barrier. |
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How do amphetamines and cocaine work?
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alter catecholamine levels by blocking reuptake of monoaminergic NT
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What might cause depression?
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downregulation of monoamines, esp catecholamines and serotonin
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Describe treatments for depression
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1) MAO inhibitors. Bad side effects. stop breakdown of monoamines
2) tricyclic antidepressents: block reuptake of monoamines 3) SSRI: selectively block reuptake of serotonin 4) ECT: effective 85% of the time! NOTE: remember that psychological effects occur several weeks after the action of the drug starts! |
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What treats bipolar disorder/
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Lithium
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Is schizophrenia usually associated with violent behavior?
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no
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Name some anatomical changes associated with schizophrenia
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enlarged ventricles
widening of sulci/brain atrophy decreased activityy in prefrontal cortex |
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What is a theory of what causes schizophrenia?
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excess dopamine. So many antischizophrenia drugs are dopamine receptor antagonists (HAldol, etc)
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Which dopaminergic system is associated wiht schizophrenia?
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mesocortical.
Mesolimbic: drug addiction Nigrastriatal: parkinsons... |
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side effect of clozapine:
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weight gain
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What are some side effects of antipsychotic drugs (dopamine antagonists)
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1) parkinsonism
2) acute dystonia (spasms) 3) tardive dyskenesia (stereotyped involuntary movements of the mouth that show up later) |
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Is consciousness a function of sensory input?
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no. If you cut off all sensory input,, you still have sleep wake cycles
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what structure maintains consciousness?
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Reticular formation, a loose aggregation of cells extending from medulla to midbrain
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what are the main functions of the reticular formation?
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1) regulate respiration and heart fxn
2) maintain wakefulness 3) regulate sleep |
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How does REM sleep amount change with age?
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declines wiht age. Fetuses have mostly REM sleep. With age amt of rem sleep declines
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What structures do slow wave and REM sleep depend on?
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REM: raphe nucleus (serotonergic)
Slow wave: locus corrueleus (noradrenergic) |
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What happens with "real" rat slleep deprivation?
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body weight goes down
Food intake goes up |
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What regulates motor inhibition in REM sleep?
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locus corueleus in the pons
(catecholaminergic/noradrenergic) |
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inheritance pattern of narcolepsy.
Gene? |
autosomal recessive
gene codes for "orexin" |
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What all is orexin associated with?
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diminished orexin in CSF associated with narcolepsy with cataplexy
increased orexin levels associated with food deprivation (hunger signal) inject orexin in animals-->increased eating, obesity, reduced sleep |
