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Neuroanatomy > Sleep > Flashcards

Sleep Flashcards

1
Q

secondary cell death

A

damage to gray matter…causes cell death by vascular compromise

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2
Q

blood flow, BBB, ischemia, edema

A

what are causes of secondary cell death?

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3
Q

glutamate or asp

A

excess release of these after trauma can cause excitotoxicity (in secondary cell death)

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4
Q

NMDA

A

these receptors alter the Ca permeability…aid in secondary cell death (excitotoxicity can cause upregulation of these receptors)

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5
Q

pressure and touch

A

what is usually first to recover after cut nerve (protopathic sensation)?

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6
Q

fine touch and fine motor

A

what may not recover after cut nerve (epicritic)?

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7
Q

steroids and NMDA antagonists

A

what are treatment interventions for neuronal degeneration/regeneration?

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8
Q

axon reaction

A

cytologic and biosynthetic changes in neuron after injury at level of soma

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9
Q

capase 3 and capase 9

A

these are activated in glutamate exocitotoxicity (after Ca channels are openend)…activated by Cyt c and then lead to apoptosis of cell

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10
Q

chromatolysis

A

characterized by vacuolation, enlarged nucleolus, dissolution Nissl substance, biosynhtesis structural proteins, axonal transport, membrane lipids

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11
Q

hypertrophy of glia (esp. astrocytes)

A

this can occur after nerve damage…prevents axon growth

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12
Q

axon reaction, chromatolysis, retrograde cell death

A

three steps in neuronal reaction to axotomy

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13
Q

NGF, BDNF

A

examples of chemicals that are released by target cells for neurotropism (maintenance of connections)

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14
Q

1-3 weeks

A

myelin debris is removed within this time period (usually by macrophages) in PNS

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15
Q

Bands of Bunger

A

chains of Schwann cells within a common basal laminar sheath

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16
Q

Schwann cell proliferation (confined by basal lamina)

A

most significant response of removal of axonal/myelinic debris

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17
Q

gliosis

A

after CNS injury…astrocytes become reactive and reinstate glial limiting membrane

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18
Q

NOGOs

A

molecules produced by oligodendrocytes that create barrier for regeneration in CNS (*inhibit myelin*)

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19
Q

semaphorins

A

chemical molecule that axons avoid while growing (grow away from them)…provide barrier for regrowth

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20
Q

astrocytic glial scar

A

this results from gliosis in CNS injury….forms barrier to regeneration

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21
Q

vascular MP and resident microglia

A

what removes phagocytic debris in CNS injury?

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22
Q

1-1.5 years

A

time frame that reinervation must occur to avoid target breakdown/degeneration

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23
Q

collateral sprouting

A

primary form of plasticity….degeneration leads to sprouting of adjacent fibers and formation of new synapses (*reactive synaptogenesis*)

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24
Q

1 mm/day

A

how fast does axon growth in regeneration?

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25
Q

chondroitin sulfate proteoglycans

A

example of extracellular molecule that is produced by reactive astrocytes and can impede regeneration in CNS

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26
Q

axonal growth ceases, synaptic transmission matures, cortical activation constrained

A

these can cause critical periods of plasticity to end (plasticity decrease with age)

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27
Q

long term potentiation

A

in cortical synaptic plasticity…this occurs due to precise timing of EPSP and spike activity

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28
Q

VLPO

A

theis GABAergic center in hypothalamus major player in sleep (depresses tubulomamillary secretion of histamine so fall asleep)

29
Q

insomnia

A

lesion of VLPO will cause this

30
Q

Berger

A

physician that first used EEG on humans

31
Q

spindle

A

from thalamic input….bursts generated during stage 2 (synchronize thalamic and cortical input)

32
Q

aminergic inhibition; cholinergic excitation

A

this decreases in REM sleep; this increases

33
Q

orexin neurons

A

lesions of these neurons cause narcolepsy

34
Q

REM sleep disorder

A

this occurs if motor system isn’t inhibited in REM cycle by glycine

35
Q

cataplexy

A

emotional response (laughter) causes descending inhibition of muscle activity (muscles turn to mush adn fall down)

36
Q

somnambulism

A

aka sleepwalking (*typically during stage 1 and 2*)

37
Q

beta

A

sleep wave that is for activated cortex, fastest (>14 Hz)

38
Q

alpha

A

sleep wave that is for quiet-awake state, 8-13 Hz

39
Q

GABA

A

benzodiazepines inhibit this

40
Q

adenosine

A

caffeine inhibits this (to keep awake)

41
Q

theta

A

sleep wave that is for some sleep states, 4-7 hz

42
Q

delta

A

hallmark for deep sleep

43
Q

theta

A

what waves predominate in sleep (synchrony = high EEG amplitude)

44
Q

thalamus

A

central pacemaker of circadian rhythm

45
Q

90 minutes

A

how often is sleep cycle repeated?

46
Q

stage 1

A

characterized by drowsiness, slow rolling movements of eyes, alpha waves become irregular and wane

47
Q

stage 2; 5-15 minutes

A

characterized by high amplitude K complexes; sleep spindles generated by thalamic pacemaker; how long does this stage last?

48
Q

stage 3; 20-40 minutes (ascends to stage 2 for 10-15, lightens, then REM)

A

large, slow delta waves in EEG; how long does this last in first cycle?

49
Q

REM; 30-50 minutes

A

characterzed by fast beta rhythms, sharp and frequent eye movements; how long does this last?

50
Q

30 min

A

refractory period between REM episodes

51
Q

restoration and adaptation

A

what are two reasons/theories we are designed to sleep?

52
Q

diffuse modulatory NT system

A

neurons responsible for sleep and waking are part of this

53
Q

Ach (pons/midbrain junction), norepi (locus coeruleus), serotonin (raphe nuclei)

A

NT involved in wakefullness (these are all *activated*)

54
Q

Ach (pons/midbrain junction), norepi (locus coeruleus), serotonin (raphe nuclei)

A

NT involved in non-REM sleep (these are all *decreased*)

55
Q

Ach, serotonin

A

NT involved in REM sleep on (first is activated, other is inactive)

56
Q

norepi

A

NT involved in REM sleep off (*active*)

57
Q

Ach

A

this enhances REM sleep

58
Q

thalamus (block sensory info to cortex)

A

diffuse modulatory NT system controls rhythms via this

59
Q

NE, serotonin, Ach

A

falling asleep due to decrease in these NT

60
Q

locus ceruleus and raphe neurons

A

firing of these decrease in REM sleep (while Ach increases)

61
Q

pontine-geniculo-occipital

A

waves that characterize REM sleep

62
Q

preoptic hypothalamic (GABAergic)

A

inhibit histamine activating cells that project to forebrain (in action of sleep)

63
Q

HLA gene

A

gene involved in narcolepsy

64
Q

cataplexy

A

sudden REM paralysis from awakened state

65
Q

cataplexy, hypnagogic hallucinations, sleep paralysis, orexins deficiency

A

4 components of narcolepsy

66
Q

locus ceruleus and raphe neurons

A

where does hypocretin/orexin project to (from lateral hypothalamus)

67
Q

dopamine antagonists

A

treatment for restless leg syndrome

68
Q

suprachiasmatic nucleus; GABA

A

what controls circadian rhythms (cycle depends on gene expression); what kind of neurons are these?

Neuroanatomy (10 decks)

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