Neruo Final

Front 1

DCN

Back 1

- projects to inferior colliculus
- sound identification

Front 2

VCN

Back 2

- projects to SOC
- sound localization

Front 3

lateral SOC

Back 3

detects loudness differences - cells sensitive to smaller differences at one end and cells sensitive to bigger at the other

Front 4

medial SOC

Back 4

detects timing differences - each neuron is tuned to a specific f and a specific interaural time difference

Front 5

nucleus of lateral lemniscus

Back 5

processes temporal aspects of sound

Front 6

inferior colliculus

Back 6

begins analysis of complex sounds like speech

Front 7

medial geniculate

Back 7

thalmic relay of sound to cortex

Front 8

1o auditory cortex

Back 8

has tonotopic organization - the higher auditory areas like somatosensory and visual cortex do not

Front 9

climbing fibers

Back 9

- afferant cerebellar
- from inferior olivary nucleus (which was from red nucleus)
- multiple synapses on a single Purkinje neuron

Front 10

mossy fibers

Back 10

- afferant cerebellar
- from pontine nucleus
- form parallel fibers that from few synapses on MANY Purkinje neuron

Front 11

Major basal ganglia inputs

Back 11

- Cortex -> caudate\putamen
- Substantia nigra -> caudate\putamen
- Subthalamus -> globus pallidus

Front 12

Major basal ganglia outputs

Back 12

- globus pallidus -> thalamus and subthalamus
- caudate\putamen -> globus pallidus and substantia nigra

Front 13

caudate\putamen input and output

Back 13

- output (to gobus pallidus) is inhibitory
- input is excitatory

Front 14

Parkinsons disease etiology

Back 14

damage to dopaminergic neurons of the substantia nigra pars compacta

Front 15

Dopamine agonists

Back 15

relieve bradykinesia, slow gait, rigidity in Parkinsons disease

Front 16

Cholinergic antagonists

Back 16

alleviate tremor in parkinsons

Front 17

intentional lesion to treat parkinsons

Back 17

globus pallidus or thalamus

Front 18

Huntingtons etiology

Back 18

- 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

Front 19

Fastigal Deep Nucleus

Back 19

- from Spinocerebellum (vermis)
- posture, balance

Front 20

Interposed Deep Nucleus

Back 20

- from Spinocerebellum
- limb movement
- sends axons through superior cerebellar peduncle

Front 21

Dentate Deep Nucleus

Back 21

- from Cerebrocerebellum
- motor planning
- sends axons through superior cerebellar peduncle

Front 22

Vestibular Deep Nucleus

Back 22

- from Vestibulocerebellum and axons go throuhg inferior cerebellar peduncle (weird)
- Balance, Eye Movements

Front 23

Superior peduncle

Back 23

- mostly outputs (projections from the cerebellum)
- damage causes intention tremor (loss of output to cerebral motor cortex)

Front 24

Middle peduncle

Back 24

- 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

Front 25

Inferior peduncle

Back 25

- 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

Front 26

otolith organs

Back 26

Hair cells here detect static head position and linear acceleration

Front 27

semicircular canals

Back 27

Hair cells here mediate dynamic head movement (angular acceleration)

Front 28

utricle

Back 28

horizontal of otolith organs

Front 29

saccule

Back 29

up down of otolith organs

Front 30

Friedreich's Ataxia

Back 30

- 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

Front 31

Spinocerebellar Atrophies (SCA)

Back 31

- 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

Front 32

02 radicals and aging

Back 32

- 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

Front 33

GH, IGF-I

Back 33

brain trophins

Front 34

Early alzheimers

Back 34

- Short Term Memory Loss
- Amygdala, hippocampus, entorhinal cortex (olfactory bulbs, too)

Front 35

middle alzheimers

Back 35

- Memory, Confusion, Lethargy,
Errors in Judgment
- Widespread areas of cortex, sparing motor and sensory

Front 36

late alzheimers

Back 36

- Vegetative State, Loss of Control of Body Functions
- all brain areas

Front 37

amalyoid plaques

Back 37

- 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

Front 38

neruofibrillary tangle

Back 38

- come last, can kill neurons
- They are IC and EC groups of neurofilaments w/ protein Tau in abnormal paired helical arrangements

Front 39

familial mutations leading to AD

Back 39

- chrom 21 (2%) -> insoluble amyloid plaques containing the A-beta
- chrom 1 (50%) -> Mutations in presenilins 1 or 2

Front 40

sporatic AD

Back 40

- 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

Front 41

AD treatment

Back 41

- none
- Anticholinesterases may spare some neurons
- One NMDA antagonist approved
- Statins may reduce cance

Front 42

nuronal turnover in humans

Back 42

- only been shown in granule cells of the hippocampus
- depression may be linked to less ability to regenerate

Front 43

regrowth of axons

Back 43

- 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

Front 44

schwann cell

Back 44

- 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

Front 45

oligodendrocytes

Back 45

- myelinating cell of the CNS
- up to 50 myelin segments each
- attacked in MS

Front 46

astrocytes

Back 46

- 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

Front 47

ependymal cells

Back 47

- 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

Front 48

microglia

Back 48

- in CNS, can sense and respond to changes in nearby neurons
- major site of HIV infection and replication in brain

Front 49

glial cells and K

Back 49

- very permeable to K, buffer against high []'s

Front 50

Glutamate-Glutamine Shuttle

Back 50

Glutamate->Glutamine in glial cells, the other way around in neruons

Front 51

d-serine and glial cells

Back 51

- 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)

Front 52

GTPgS and glial cells

Back 52

inject this into glial cells and 50% decline in post syn current

Front 53

Ca and glial cells

Back 53

- 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)

Front 54

Catecholamines

Back 54

- dop, NE and Epi
- synthesized from Tyrosine

Front 55

Indoleamine

Back 55

- seretonin
- synthesized from tryptophan
- originates in the raphe nuclei and projects broadly to cortex, thalamus, hypo, hippo cerebellum, and SC
- target of prozac

Front 56

Imadazoleamine

Back 56

- 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

Front 57

Enzymatic NT Degradation

Back 57

COMT (post) and MAO (pre)

Front 58

Active NT uptake

Back 58

(DAT, NET, SERT)

Front 59

Nigrostriatal dopaminic projection

Back 59

- from the substantia nigra to the striatum (caudate-putamen)
- Neurons in this pathway are lost in Parkinson's disease.

Front 60

Mesolimbic dopaminic projection

Back 60

— originates in the ventral tegmental portion of the midbrain
- projects to the limbic system, including the amygdala, nucleus accumbens, hippocampus, and cingulate

Front 61

Mesocortical dopaminic projection

Back 61

- 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

Front 62

Noradrenergic system

Back 62

- broad projections from locus coeruleus to cortex, thalamus, hypo, hippo, SC and cerebellum
- implicated in arousal, attention, and feeding

Front 63

drugs that cause Dopaminergic
Activation

Back 63

- nicotine
- opiods
- caffiene
- sex
- cocaine

Front 64

Amphetamines and cocaine

Back 64

alter catecholamine levels by blocking reuptake of monaminergic transmitters such as DA and NE

Front 65

MAO inhibitors

Back 65

block breakdown of monoamines (phenelzine) - Rarely used now due to side effects

Front 66

Tricyclic antidepressants

Back 66

inhibit uptake of DA, NE, and serotonin by DAT, NET, and SERT. (desipramine)

Front 67

SSRIs

Back 67

- selectively block serotonin reuptake (fluoxetine/Prozac)
- Current first line treatment; effective in half to 2/3 of patients

Front 68

Schizophrenia

Back 68

- 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)

Front 69

1st generation antipsychotics

Back 69

- Dopamine receptor antagonist
- extrapyramidal SEs
- (haloperidol/Haldol)

Front 70

2nd generation antipsychotics

Back 70

- Dopamine receptor antagonist w/ activity against other R’s such as serotonin
- fewer extrapyramidal SEs
- (Clozapine)

Front 71

Reticular Formation

Back 71

- 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)

Front 72

Slow-wave sleep

Back 72

depends on the integrity of the raphe nuclei in the medulla, which are rich in serotonin

Front 73

REM sleep

Back 73

depends on the integrity of neurons in the locus coeruleus of the pons, which are rich in noradrenalin - particularly motor inhibition

Front 74

Motor inhibition

Back 74

- 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

Front 75

narcolepsy gene

Back 75

- 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

Front 76

Spinal Nucleus V - Overview

Back 76

V, VII, IX, X - sensory

Front 77

Solitary Nuc Overview

Back 77

VII, IX, X - sensory

Front 78

Nuc. Ambiguus Overview

Back 78

IX, X, XI - Motor

Front 79

Spinal Nucleus V - in depth

Back 79

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)

Front 80

Corneal Reflex

Back 80

- 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

Front 81

Solitary nucleus - in depth

Back 81

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)

Front 82

Dorsal Vagal Motor Nucleus

Back 82

(X) - Parasympathetic preganglionics to gut, respiratory structures and heart

Front 83

Nucleus ambiguus - in depth

Back 83

Motoneurons to muscles of pharynx and larynx
(IX, X, XI)

Front 84

Gag Reflex

Back 84

- Sensory input from (IX) to solitary nucleus.
- Motor output is via nucleus ambiguus (and sometimes phrenic nucleus).

Front 85

Edinger-Westphal nucleus

Back 85

parasympathetic preganglionic output for pupillary constriction (III)

Front 86

Some axons in VII, IX, X

Back 86

parasympathetic preganglionic output controlling tears, saliva, and mucus

Front 87

Nuc. VIII Outputs:

Back 87

- MLF to EOM nuc
- VST
- VP of Thalamus
- Vestibulocerebellum

Front 88

Voluntary Control of lateral gaze

Back 88

Frontal Eye Field.
PPRF
Nucleus of VI and III

Front 89

Vestibulat control of lateral gaze

Back 89

Vestibular nuclei
PPRF
Nucleus of VI and III

Front 90

Lateral Pontine deficit

Back 90

- 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)

Front 91

Medial Pontine deficits

Back 91

- 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)

Front 92

Lateral Medullary deficits

Back 92

- 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)

Front 93

medial Medullary deficits

Back 93

- anterior spinal art infarct
- light touch, bi (medial lemniscus)
- upper motor neuron syndrome, bi (pyramids)
- Difficulty moving tongue, slurred speech (hypoglossal nucleus and nerve)