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93 Cards in this Set

  • Front
  • Back
DCN
- projects to inferior colliculus
- sound identification
VCN
- projects to SOC
- sound localization
lateral SOC
detects loudness differences - cells sensitive to smaller differences at one end and cells sensitive to bigger at the other
medial SOC
detects timing differences - each neuron is tuned to a specific f and a specific interaural time difference
nucleus of lateral lemniscus
processes temporal aspects of sound
inferior colliculus
begins analysis of complex sounds like speech
medial geniculate
thalmic relay of sound to cortex
1o auditory cortex
has tonotopic organization - the higher auditory areas like somatosensory and visual cortex do not
climbing fibers
- afferant cerebellar
- from inferior olivary nucleus (which was from red nucleus)
- multiple synapses on a single Purkinje neuron
mossy fibers
- afferant cerebellar
- from pontine nucleus
- form parallel fibers that from few synapses on MANY Purkinje neuron
Major basal ganglia inputs
- Cortex -> caudate\putamen
- Substantia nigra -> caudate\putamen
- Subthalamus -> globus pallidus
Major basal ganglia outputs
- globus pallidus -> thalamus and subthalamus
- caudate\putamen -> globus pallidus and substantia nigra
caudate\putamen input and output
- output (to gobus pallidus) is inhibitory
- input is excitatory
Parkinsons disease etiology
damage to dopaminergic neurons of the substantia nigra pars compacta
Dopamine agonists
relieve bradykinesia, slow gait, rigidity in Parkinsons disease
Cholinergic antagonists
alleviate tremor in parkinsons
intentional lesion to treat parkinsons
globus pallidus or thalamus
Huntingtons etiology
- first refered for mental symptoms
- profound degeneration of caudate and putamen due to loss of GABAergic projection neurons
- CAG repeats make too much glutamine - autosomal dominant
Fastigal Deep Nucleus
- from Spinocerebellum (vermis)
- posture, balance
Interposed Deep Nucleus
- from Spinocerebellum
- limb movement
- sends axons through superior cerebellar peduncle
Dentate Deep Nucleus
- from Cerebrocerebellum
- motor planning
- sends axons through superior cerebellar peduncle
Vestibular Deep Nucleus
- from Vestibulocerebellum and axons go throuhg inferior cerebellar peduncle (weird)
- Balance, Eye Movements
Superior peduncle
- mostly outputs (projections from the cerebellum)
- damage causes intention tremor (loss of output to cerebral motor cortex)
Middle peduncle
- exclusively inputs (projections from contralateral pons)
- damage leads to ataxia (cerebro-ponto-cerebellum)
- lesion to pontine nuclei on one side leads to contralateral gait ataxia
Inferior peduncle
- inputs from spinal cord, vestibular system, and inferior olive
- outputs to vestibular nuc and brainstem
- damage least so ataxia (DSCT, inferior olive), nystagmus (vestibular nuclei), and vertigo
otolith organs
Hair cells here detect static head position and linear acceleration
semicircular canals
Hair cells here mediate dynamic head movement (angular acceleration)
utricle
horizontal of otolith organs
saccule
up down of otolith organs
Friedreich's Ataxia
- autosomal recessive, from unstable GAA (glutamate) repeat in the FRDA gene, for frataxin, in mitochondria only
- gets large neurons of myelinated axons in the dorsal root and posterior columns AND spinocerebellar and corticospinal tracts
- progressive ataxia, esp trunk, Spasticity, Weakness,
Reduced tendon reflexes, Nystagmus
Spinocerebellar Atrophies (SCA)
- autosomal dominants
- from loss of Purkinje cells, but can get SC, brainstem, BG, and retina
- 20 forms, associated w/ unstable CAG (glutamine) repeats in ataxin (nuclear kinase) genes
02 radicals and aging
- Lipofuscin “aging pigment” has oxidized lipids and proteins and accumulates in neurons w/ age
- Antioxidants abundant in brain
- O2 free radicals -> atrophy and neuron loss
- Postmitotic cells (neurons, muscle) show the most damage
- Iron (catalyzes free radical production) accumulates w/ age
GH, IGF-I
brain trophins
Early alzheimers
- Short Term Memory Loss
- Amygdala, hippocampus, entorhinal cortex (olfactory bulbs, too)
middle alzheimers
- Memory, Confusion, Lethargy,
Errors in Judgment
- Widespread areas of cortex, sparing motor and sensory
late alzheimers
- Vegetative State, Loss of Control of Body Functions
- all brain areas
amalyoid plaques
- Amyloid precursor protein (APP) is normal constituent
- usually cleavad to soluble peptide, but in AD, it an insoluble (A-beta) that aggregates w/ otuer molecules -> EC plaques
- may inhibit NMDA receptors, so no glutamate excitation
- inflam around them killes Ns
neruofibrillary tangle
- come last, can kill neurons
- They are IC and EC groups of neurofilaments w/ protein Tau in abnormal paired helical arrangements
familial mutations leading to AD
- chrom 21 (2%) -> insoluble amyloid plaques containing the A-beta
- chrom 1 (50%) -> Mutations in presenilins 1 or 2
sporatic AD
- ApoE is lipid transporter found in plaques - influences axonal transport and required for tau to stabilize microt's
- ApoE2 and 3 - do this well, ApoE4 - may cause tangles
AD treatment
- none
- Anticholinesterases may spare some neurons
- One NMDA antagonist approved
- Statins may reduce cance
nuronal turnover in humans
- only been shown in granule cells of the hippocampus
- depression may be linked to less ability to regenerate
regrowth of axons
- grow more in periphery b/c central cells have oligodendroctyes instead of schwann cells - they have NOGO-A which inhibits groth - give NOGO-A Ab, and it will grow more
schwann cell
- Myelinating cells of the PNS
- 1 cell makes 1 m segment
- ensheath cell bodies, dendrites, unmyelinated axons, and synapses
- If the axon dies, they lose myelin, phatocytize, and secrete GFs like NGF
oligodendrocytes
- myelinating cell of the CNS
- up to 50 myelin segments each
- attacked in MS
astrocytes
- processes line brain and BVs to form the glia limitans
- Ensheath neuronal cell bodies, unmyelinated axons, dendrites, nodes of Ranvier, and synapses
- coupled by gap jxns -> a syncytium capable of spreading
small things (K+, Ca+, ATP)
- after CNS injury, phagocytic and increase in size and # to seal off wound -> glial scar
ependymal cells
- line ventricular surfaces
- have microvilli and cilia on apical - lack tight junctions to provide a permeable barrier so CSF can equilibrate w/ brain tissue
- Specialized ones in choroid plexus secrete CSF
microglia
- in CNS, can sense and respond to changes in nearby neurons
- major site of HIV infection and replication in brain
glial cells and K
- very permeable to K, buffer against high []'s
Glutamate-Glutamine Shuttle
Glutamate->Glutamine in glial cells, the other way around in neruons
d-serine and glial cells
- NMDA receptors need glycine site occupied
- D-serine is as effective as glycine
- synthesized by serine racemase, an enzyme only in astrocytes (so they can block excitation)
GTPgS and glial cells
inject this into glial cells and 50% decline in post syn current
Ca and glial cells
- Ca++ waves in astrocytes triggered by glutamate
- IC propagation is from Ca++ evoked release of Ca++ from IC stores
- Ca++ waves represent a possible non-neuronal signaling mechanism
- propagate differently from APs (more slowly)
Catecholamines
- dop, NE and Epi
- synthesized from Tyrosine
Indoleamine
- seretonin
- synthesized from tryptophan
- originates in the raphe nuclei and projects broadly to cortex, thalamus, hypo, hippo cerebellum, and SC
- target of prozac
Imadazoleamine
- histamine
- synthesized from histadine
- originates in hypo's tuberomammillary nuc, projects broadly
- implicated in arousal and wakefulness
- Benadryl are H1R blockers that cross the BBB and act as sedatives
Enzymatic NT Degradation
COMT (post) and MAO (pre)
Active NT uptake
(DAT, NET, SERT)
Nigrostriatal dopaminic projection
- from the substantia nigra to the striatum (caudate-putamen)
- Neurons in this pathway are lost in Parkinson's disease.
Mesolimbic dopaminic projection
— originates in the ventral tegmental portion of the midbrain
- projects to the limbic system, including the amygdala, nucleus accumbens, hippocampus, and cingulate
Mesocortical dopaminic projection
- neurons from the ventral tegmental portion of the midbrain that project rostrally to regions such as cortex, especially the prefontal cortex
- aka mesofrontal or mesolimbocortical
Noradrenergic system
- broad projections from locus coeruleus to cortex, thalamus, hypo, hippo, SC and cerebellum
- implicated in arousal, attention, and feeding
drugs that cause Dopaminergic
Activation
- nicotine
- opiods
- caffiene
- sex
- cocaine
Amphetamines and cocaine
alter catecholamine levels by blocking reuptake of monaminergic transmitters such as DA and NE
MAO inhibitors
block breakdown of monoamines (phenelzine) - Rarely used now due to side effects
Tricyclic antidepressants
inhibit uptake of DA, NE, and serotonin by DAT, NET, and SERT. (desipramine)
SSRIs
- selectively block serotonin reuptake (fluoxetine/Prozac)
- Current first line treatment; effective in half to 2/3 of patients
Schizophrenia
- excess dopaminergic transmission - Antipsychotic drugs block DA receptors
- 1st generation antipsychotic (neuroleptics), potency correlate w/ affinity for DA receptors
- Many antipsychotics cause extrapyramidal motor side effects like PD
- Drugs that increase DA activity can cause psychoses. (L-DOPA, cocaine, amphet)
1st generation antipsychotics
- Dopamine receptor antagonist
- extrapyramidal SEs
- (haloperidol/Haldol)
2nd generation antipsychotics
- Dopamine receptor antagonist w/ activity against other R’s such as serotonin
- fewer extrapyramidal SEs
- (Clozapine)
Reticular Formation
- Primitive functions, such as regulation of resp and CV
- Maintaining wakefulness
- Regulating sleep, including
NREM sleep (Slow-Wave) 3-4 stages and REM sleep (Fast-Wave, Paradoxical)
Slow-wave sleep
depends on the integrity of the raphe nuclei in the medulla, which are rich in serotonin
REM sleep
depends on the integrity of neurons in the locus coeruleus of the pons, which are rich in noradrenalin - particularly motor inhibition
Motor inhibition
- regulated by catecholinime neurons in locus coeruleus in the pons - if destroyed, animals act out their dreams
- may be protective - prevents injury
- Inappropriate activation of REM sleep -> narcolepsy / cataplexy syndrome
narcolepsy gene
- orexin is diminished
- increases when an animal is food deprived
- obesity pill could block it, but could produce narcolepsy - may also serve to maintain penile erection
Spinal Nucleus V - Overview
V, VII, IX, X - sensory
Solitary Nuc Overview
VII, IX, X - sensory
Nuc. Ambiguus Overview
IX, X, XI - Motor
Spinal Nucleus V - in depth
pain from face (V)
- from cornea (V)
- from anterior 2/3 of tongue (V)
- From posterior 1/3 of tongue (IX)
- from the ear (VII, IX, X)
from the meninges
- Above the tentorium (V)
- Below the tentorium (X)
Corneal Reflex
- Sensory input from cornea is via the trigeminal nerve to the spinal trigeminal nucleus (pain and temperature of the face).
- Motor output is via the facial nucleus and nerve to close the eyelid.
- Reflex is bilateral because spinal nucleus of V projects to both facial nuclei
Solitary nucleus - in depth
rostral is taste
- from anterior tongue (VII)
- from posterior tongue (IX)
- from epiglottis (X)

Caudal is visceral sensation
- from pharynx (IX, X)
- from carotid body and carotid sinus (IX)
- from larynx (X)
- from viscera of thorax & abdomen (X)
Dorsal Vagal Motor Nucleus
(X) - Parasympathetic preganglionics to gut, respiratory structures and heart
Nucleus ambiguus - in depth
Motoneurons to muscles of pharynx and larynx
(IX, X, XI)
Gag Reflex
- Sensory input from (IX) to solitary nucleus.
- Motor output is via nucleus ambiguus (and sometimes phrenic nucleus).
Edinger-Westphal nucleus
parasympathetic preganglionic output for pupillary constriction (III)
Some axons in VII, IX, X
parasympathetic preganglionic output controlling tears, saliva, and mucus
Nuc. VIII Outputs:
- MLF to EOM nuc
- VST
- VP of Thalamus
- Vestibulocerebellum
Voluntary Control of lateral gaze
Frontal Eye Field.
PPRF
Nucleus of VI and III
Vestibulat control of lateral gaze
Vestibular nuclei
PPRF
Nucleus of VI and III
Lateral Pontine deficit
- AICA Infarct
- Fine touch (princ. nuc. V) and P & T (spinal tr. V) to ips face
- P & T to contralateral body (spinothalamic Tr.)
- Voluntary movement -entire ipsi face (nuc, nerve VII)
- lateral gaze to side of lesion (VI and PPRF)
- Horner syndrome - ipsi face
- ipsi vertigo, nystagmus, deafness (VIII)
- ipsi ataxia (middle cereb. peduncle)
Medial Pontine deficits
- contra arm and leg, (CST)
- light touch (medial lemnis)
- Inward deviation of ipsi eye (VI - nuc/N)
- Possible impairment of conjugate gaze to side of lesion (VI nuc. and PPRF)
- Ipsi paralysis of the face (VII- nuc/N)
Lateral Medullary deficits
- PICA Infarct
- P & T - contra body
- P & T - ipsi face
- Horner’s - ipsi face
- dysphagia and hoarseness (nucleus ambiguus)
- vertigo, nausea and nystagmus (vestibular nuclei)
- ataxia (inferior cerebellar peduncle, cerebellum)
medial Medullary deficits
- anterior spinal art infarct
- light touch, bi (medial lemniscus)
- upper motor neuron syndrome, bi (pyramids)
- Difficulty moving tongue, slurred speech (hypoglossal nucleus and nerve)