TRAVERS 1 Flashcards

1
Q

WHAT PART OF THE NEURON DOES GRADED POTENTIAL?

A

DENTDRITES

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2
Q

WHAT PART OF THE NEURON DOES ACTION POTENTIAL?

A

AXON

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3
Q

what is the exception to neurons being terminally differentiated?

A

hippocampus

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4
Q

how many percent of cns cells are neurons?

A

10%

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5
Q

what percent of cells in cns are glial cells?

A

90%

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6
Q

what is the myelinating glia in pns?

A

schwann cells
provides myelin to one axon
many schwann cells per axon

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7
Q

what is the myelinating glia in cns?

A

oligodendrocytes

contributes to many axons

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8
Q

what are microglia

A

macrophage like cell (phagocytic role)

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9
Q

what are astrocytes?

A

regulate extracellular fluid- remove k+ and neurotransmitter
provide neurons metabolically (eg glucose)
surround brain capillaries: form blood brain barriers

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10
Q

what is the structural component of axons?

A

microtubule

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11
Q

anterograde transport

A

from cell body towards terminal
motor proteins: kinesins
fast transport -organelles such as nt vesicles
slow transport- structural proteins

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12
Q

retrograde transport

A

dyneins
fast transport
from axon terminals toward cell bodies such as growth factors and viruses

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13
Q

why does damaged cns neurons no regenerate?

A

axons sprout but axons do not reach targets
scar formation prevents surviving axons from reaching targets
astrocytes make chondroitin sulfate proteoglycans that inhibit neuron growth

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14
Q

anterograde degeneration

A

distal to lesion

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15
Q

transganglionic degeneration

A

axon process heading toward cns degenerates

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16
Q

transynaptic degeneration

A

neuron contacted centrally by the axon dies

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17
Q

chromatolysis

A

associated with protein synthesis

cell body swells, eccentric nucleus

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18
Q

how does schwann cells contribute to regeneration?

A

schwann cells proliferate
produce laminin for substrate for regenerating axons
schwann cells secrete nerve growth factor
ngf transported to ganglion cell body

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19
Q

what does ngf do?

A

regulates gene expression and promotes sprouting

regulates: microtubules, microfilaments, nt production, ion channels, nt receptors

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20
Q

what is collateral sprouting?

A

most likely to occur when an axon fails to regenerate- surviving axon nearby may sprout new terminals into the area previously occupied by the other sensory cell
no evidence of collateral sprouting for teeth- soft tissue only

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21
Q

temporal summation

A

adding together of PSP from one synatic contact over time

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22
Q

spatial summation

A

adding together of PSP produced by diff synapses

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23
Q

action of drugs at synaptic junction

A
  1. increase leakage of nt from vesicle to cytoplasm, exposing it to enzyme breakdown
  2. inc transmitter release into cleft
  3. block transmitter release
  4. block transmitter reuptake
  5. block cleft enzymes that metabolize transmitter
  6. bind to receptor on postsynaptic membrane to block (antagonist) or mimic (agonist) transmitter action
  7. inhiibit or stimlate second messenger activity within post synaptic cell
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24
Q

actions of neuromodulators

A

may act postsynaptically to amplify or dampen on-going synaptic activity
may act on pre-synaptic cell to alter synthesis, release, uptake or metabolism of nt
actions involve changes in dna/protein synthesis or enzyme activity- slower in action

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25
Q

acetylcholine

A

synthesized from choline and acetyl coA by choline acetyltransferase in synaptic terminal
action stopped by diffusion and degradation by actylcholinesterase
choline reuptake by presynaptic neuron

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26
Q

neurons that release ach

A

motor neurons
neurons in nucleus basalis and pons
all pregang neurons sym and para sym
all post gang parasym neurons

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27
Q

basal forebrain and pontine nuclei

A

cognitive function

sleep regulation

28
Q

diff acetylcholine receptors

A

muscarinic and nicotinic

29
Q

muscarinic receptors

A

mainly found in cns except parasymp post gang synapse- salivary glands
binding of ach triggers g protein that open or close ion channels- depol or hyperpol

30
Q

WHAT ARE MUSCARINIC RECEPTORS BLOCKED BY?

A

ATROPINE

31
Q

nicotinic trceptors

A

relatively few in cns
ach binding opens ion channels within receptor- channel permeable to na and k
ex nmj

32
Q

what are nicotinic receptors blocked by?

A

CURARE

33
Q

myasthenia gravis

A

autoimmune disorder in which indibidual makes antibodies to nicotinic receptors
characterized by muscle weakness
treated with acetylcholnesterase inhibitors

34
Q

alzheimers disease

A

most common form of dementia
etiology unknown
many neuronal pop involved
loss of neurons in nucelus basalis leading to decrease in cholinergic activity in cortex

35
Q

what are biogenic amiens?

A

synthesized from amino acids

36
Q

what are catecholamines?

A

dopamines, norepinepherine, epinephrine

synthesized from amino acid tyrosine

37
Q

catecholamine life cycle

A

synthesis- presynaptic terminal- stored in vesicles
release- ca dependent
termination of action- presynaptic neuron reuptake and degradation

38
Q

where are biogenic amines found?

A

neurons that synthesize the ligand in very limited locations
receptors for the ligands found extensively thruout cns
receptors are almost exclusively g-protein coupled receptors

39
Q

what are biogenic amines involved in?

A

parkinsons, depression, schizophrenia

40
Q

dopamine

A

found in areas of midbrain and brainstem

41
Q

dopamine receptor subtypes

A

all g-protein coupled
two main groups: d1 and d2
d1- activate adenylate cyclase
d2- inhibit adenylate cyclase- hyperpolarization

42
Q

what do drugs do to dopamine receptors?

A

block d2 receptors

43
Q

ventral tegmental area and dopamine

A

associated with reward and addiction”

cocaine and amphetamine prolong dopamine action at synapse

44
Q

substantia nigra and dopamine

A

associated with motor system

loss of dopamine assciated with parkinson’s disease

45
Q

tardive dyskinesia

A
pt receive dopamine blocking drugs
involuntary movements delayed onset
inc incidence with advanced age
rhythmic oral movements-involuntary, repetitive body movements
d2 receptors
46
Q

epinephrine

A

epinephrine requires presence of additional enzymes for synthesis from norepinephrine

47
Q

norepinephrine neurons

A

sympathetic post ganglionc neurons and some cns

48
Q

epinephrine

A

adrenal gland as circulating hormone- not much in cns

49
Q

noradrenergic receptors

A

g-protein coupled
alpha receptors: a1- excittory- intracellular release of ca
a2- inhibitory via opening k channels or blocking ca
beta receptors- open ca channels
NE can have very diff effect on tissue depending on receptor

50
Q

locus ceruleus and ne

A

attention/sleep

51
Q

other brainstem and ne

A

autonomic and homeostatic functions

52
Q

serotonin

A

synthesized from tryptophan
found in several discrete cns populations
involved in many functions ranging from sensorimotor systems to cognitive function

53
Q

serotonin receptors

A

16 receptor subtypes
most are g-protein coupled
5-gt synapses target of mood altering drugs

54
Q

rostral raphe nuclei and serotonin

A

sleep, mood, homeostatic function

55
Q

caudal raphe nuclei and serotonin

A

sensori-motor function

56
Q

amino acid neurotransmitters

A

excitatory aa such as glutamate and aspartate

binds to ionotropic and metabotropic receptors

57
Q

ionotropic recept

A

ampa
kainate
nmda
receptors with channels permeable to na, k, ca

58
Q

metabotropic receptors

A

g-protein receptor

59
Q

nmda receptor

A

n-methyl-d-aspartate
involved in functions that last- memory formation, chronic pain
excitotoxicity- excessive excitation- cell death (epulepsy trauma, stroke)
neuron death from ca reaching toxic levels
synaptic mechanism of long term potentiation

60
Q

gaba

A

major inhibitory nt in cns

modified form of glutamate

61
Q

gaba receptors

A

gaba a- ionotropic receptor- opens cl- channel

gaba b- metabotropic receptor- opens k+ chammels

62
Q

huntington chorea

A

form of motor spasticity

linked to gaba deficits

63
Q

glycine

A
inhibitory nt (mostly spinal cord)
receptor opens cl- channels
blocked by strychnine
64
Q

peptides

A

formed by peptide link between2 or more amino acids
over 90 id
often co-released with other nt- synthesized in soma and must be transported to be released
functions as neuromodulator
actions can last long time
action termiantaed by proteolysis and diffusiion

65
Q

nitric oxide

A

gas
synthesis- l-arginine to no by nitric oxide synthase (nos)
not stored in vesicles
freely difusible across membrane (requires no synapse)
can modulate nt release
plays role in numerous brain functions
role in injuries: excitotoxicity

66
Q

atp

A

usually excitatory

usually co-released with classical nt