Neruo final
Terms
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- DCN
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- projects to inferior colliculus
- sound identification - VCN
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- 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
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- afferant cerebellar
- from inferior olivary nucleus (which was from red nucleus)
- multiple synapses on a single Purkinje neuron - mossy fibers
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- afferant cerebellar
- from pontine nucleus
- form parallel fibers that from few synapses on MANY Purkinje neuron - Major basal ganglia inputs
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- Cortex -> caudate\putamen
- Substantia nigra -> caudate\putamen
- Subthalamus -> globus pallidus - Major basal ganglia outputs
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- globus pallidus -> thalamus and subthalamus
- caudate\putamen -> globus pallidus and substantia nigra - caudate\putamen input and output
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- 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
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- 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
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- from Spinocerebellum (vermis)
- posture, balance - Interposed Deep Nucleus
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- from Spinocerebellum
- limb movement
- sends axons through superior cerebellar peduncle - Dentate Deep Nucleus
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- from Cerebrocerebellum
- motor planning
- sends axons through superior cerebellar peduncle - Vestibular Deep Nucleus
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- from Vestibulocerebellum and axons go throuhg inferior cerebellar peduncle (weird)
- Balance, Eye Movements - Superior peduncle
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- mostly outputs (projections from the cerebellum)
- damage causes intention tremor (loss of output to cerebral motor cortex) - Middle peduncle
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- 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
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- 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
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- 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)
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- 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
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- 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
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- Short Term Memory Loss
- Amygdala, hippocampus, entorhinal cortex (olfactory bulbs, too) - middle alzheimers
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- Memory, Confusion, Lethargy,
Errors in Judgment
- Widespread areas of cortex, sparing motor and sensory - late alzheimers
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- Vegetative State, Loss of Control of Body Functions
- all brain areas - amalyoid plaques
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- 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
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- 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
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- chrom 21 (2%) -> insoluble amyloid plaques containing the A-beta
- chrom 1 (50%) -> Mutations in presenilins 1 or 2 - sporatic AD
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- 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
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- none
- Anticholinesterases may spare some neurons
- One NMDA antagonist approved
- Statins may reduce cance - nuronal turnover in humans
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- 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
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- 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
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- myelinating cell of the CNS
- up to 50 myelin segments each
- attacked in MS - astrocytes
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- 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
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- 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
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- 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
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- 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
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- 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
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- dop, NE and Epi
- synthesized from Tyrosine - Indoleamine
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- seretonin
- synthesized from tryptophan
- originates in the raphe nuclei and projects broadly to cortex, thalamus, hypo, hippo cerebellum, and SC
- target of prozac - Imadazoleamine
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- 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
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- from the substantia nigra to the striatum (caudate-putamen)
- Neurons in this pathway are lost in Parkinson's disease. - Mesolimbic dopaminic projection
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— 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
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- 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
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- 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
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- selectively block serotonin reuptake (fluoxetine/Prozac)
- Current first line treatment; effective in half to 2/3 of patients - Schizophrenia
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- 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
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- Dopamine receptor antagonist
- extrapyramidal SEs
- (haloperidol/Haldol) - 2nd generation antipsychotics
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- Dopamine receptor antagonist w/ activity against other R’s such as serotonin
- fewer extrapyramidal SEs
- (Clozapine) - Reticular Formation
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- 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
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- 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
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- 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
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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
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- 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
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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
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Motoneurons to muscles of pharynx and larynx
(IX, X, XI) - Gag Reflex
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- 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:
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- MLF to EOM nuc
- VST
- VP of Thalamus
- Vestibulocerebellum - Voluntary Control of lateral gaze
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Frontal Eye Field.
PPRF
Nucleus of VI and III - Vestibulat control of lateral gaze
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Vestibular nuclei
PPRF
Nucleus of VI and III - Lateral Pontine deficit
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- 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
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- 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
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- 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
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- anterior spinal art infarct
- light touch, bi (medial lemniscus)
- upper motor neuron syndrome, bi (pyramids)
- Difficulty moving tongue, slurred speech (hypoglossal nucleus and nerve)