Sleep

Question 1

secondary cell death

Answer 1

damage to gray matter…causes cell death by vascular compromise

Question 2

blood flow, BBB, ischemia, edema

Answer 2

what are causes of secondary cell death?

Question 3

glutamate or asp

Answer 3

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

Question 4

NMDA

Answer 4

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

Question 5

pressure and touch

Answer 5

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

Question 6

fine touch and fine motor

Answer 6

what may not recover after cut nerve (epicritic)?

Question 7

steroids and NMDA antagonists

Answer 7

what are treatment interventions for neuronal degeneration/regeneration?

Question 8

axon reaction

Answer 8

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

Question 9

capase 3 and capase 9

Answer 9

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

Question 10

chromatolysis

Answer 10

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

Question 11

hypertrophy of glia (esp. astrocytes)

Answer 11

this can occur after nerve damage…prevents axon growth

Question 12

axon reaction, chromatolysis, retrograde cell death

Answer 12

three steps in neuronal reaction to axotomy

Question 13

NGF, BDNF

Answer 13

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

Question 14

1-3 weeks

Answer 14

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

Question 15

Bands of Bunger

Answer 15

chains of Schwann cells within a common basal laminar sheath

Question 16

Schwann cell proliferation (confined by basal lamina)

Answer 16

most significant response of removal of axonal/myelinic debris

Question 17

gliosis

Answer 17

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

Question 18

NOGOs

Answer 18

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

Question 19

semaphorins

Answer 19

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

Question 20

astrocytic glial scar

Answer 20

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

Question 21

vascular MP and resident microglia

Answer 21

what removes phagocytic debris in CNS injury?

Question 22

1-1.5 years

Answer 22

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

Question 23

collateral sprouting

Answer 23

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

Question 24

1 mm/day

Answer 24

how fast does axon growth in regeneration?

Question 25

chondroitin sulfate proteoglycans

Answer 25

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

Question 26

axonal growth ceases, synaptic transmission matures, cortical activation constrained

Answer 26

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

Question 27

long term potentiation

Answer 27

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

Question 28

VLPO

Answer 28

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

Question 29

insomnia

Answer 29

lesion of VLPO will cause this

Question 30

Berger

Answer 30

physician that first used EEG on humans

Question 31

spindle

Answer 31

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

Question 32

aminergic inhibition; cholinergic excitation

Answer 32

this decreases in REM sleep; this increases

Question 33

orexin neurons

Answer 33

lesions of these neurons cause narcolepsy

Question 34

REM sleep disorder

Answer 34

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

Question 35

cataplexy

Answer 35

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

Question 36

somnambulism

Answer 36

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

Question 37

beta

Answer 37

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

Question 38

alpha

Answer 38

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

Question 39

GABA

Answer 39

benzodiazepines inhibit this

Question 40

adenosine

Answer 40

caffeine inhibits this (to keep awake)

Question 41

theta

Answer 41

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

Question 42

delta

Answer 42

hallmark for deep sleep

Question 43

theta

Answer 43

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

Question 44

thalamus

Answer 44

central pacemaker of circadian rhythm

Question 45

90 minutes

Answer 45

how often is sleep cycle repeated?

Question 46

stage 1

Answer 46

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

Question 47

stage 2; 5-15 minutes

Answer 47

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

Question 48

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

Answer 48

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

Question 49

REM; 30-50 minutes

Answer 49

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

Question 50

30 min

Answer 50

refractory period between REM episodes

Question 51

restoration and adaptation

Answer 51

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

Question 52

diffuse modulatory NT system

Answer 52

neurons responsible for sleep and waking are part of this

Question 53

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

Answer 53

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

Question 54

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

Answer 54

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

Question 55

Ach, serotonin

Answer 55

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

Question 56

norepi

Answer 56

NT involved in REM sleep off (\*active\*)

Question 57

Ach

Answer 57

this enhances REM sleep

Question 58

thalamus (block sensory info to cortex)

Answer 58

diffuse modulatory NT system controls rhythms via this

Question 59

NE, serotonin, Ach

Answer 59

falling asleep due to decrease in these NT

Question 60

locus ceruleus and raphe neurons

Answer 60

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

Question 61

pontine-geniculo-occipital

Answer 61

waves that characterize REM sleep

Question 62

preoptic hypothalamic (GABAergic)

Answer 62

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

Question 63

HLA gene

Answer 63

gene involved in narcolepsy

Question 64

cataplexy

Answer 64

sudden REM paralysis from awakened state

Question 65

cataplexy, hypnagogic hallucinations, sleep paralysis, orexins deficiency

Answer 65

4 components of narcolepsy

Question 66

locus ceruleus and raphe neurons

Answer 66

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

Question 67

dopamine antagonists

Answer 67

treatment for restless leg syndrome

Question 68

suprachiasmatic nucleus; GABA

Answer 68

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