Sleep Flashcards
secondary cell death
damage to gray matter…causes cell death by vascular compromise
blood flow, BBB, ischemia, edema
what are causes of secondary cell death?
glutamate or asp
excess release of these after trauma can cause excitotoxicity (in secondary cell death)
NMDA
these receptors alter the Ca permeability…aid in secondary cell death (excitotoxicity can cause upregulation of these receptors)
pressure and touch
what is usually first to recover after cut nerve (protopathic sensation)?
fine touch and fine motor
what may not recover after cut nerve (epicritic)?
steroids and NMDA antagonists
what are treatment interventions for neuronal degeneration/regeneration?
axon reaction
cytologic and biosynthetic changes in neuron after injury at level of soma
capase 3 and capase 9
these are activated in glutamate exocitotoxicity (after Ca channels are openend)…activated by Cyt c and then lead to apoptosis of cell
chromatolysis
characterized by vacuolation, enlarged nucleolus, dissolution Nissl substance, biosynhtesis structural proteins, axonal transport, membrane lipids
hypertrophy of glia (esp. astrocytes)
this can occur after nerve damage…prevents axon growth
axon reaction, chromatolysis, retrograde cell death
three steps in neuronal reaction to axotomy
NGF, BDNF
examples of chemicals that are released by target cells for neurotropism (maintenance of connections)
1-3 weeks
myelin debris is removed within this time period (usually by macrophages) in PNS
Bands of Bunger
chains of Schwann cells within a common basal laminar sheath
Schwann cell proliferation (confined by basal lamina)
most significant response of removal of axonal/myelinic debris
gliosis
after CNS injury…astrocytes become reactive and reinstate glial limiting membrane
NOGOs
molecules produced by oligodendrocytes that create barrier for regeneration in CNS (*inhibit myelin*)
semaphorins
chemical molecule that axons avoid while growing (grow away from them)…provide barrier for regrowth
astrocytic glial scar
this results from gliosis in CNS injury….forms barrier to regeneration
vascular MP and resident microglia
what removes phagocytic debris in CNS injury?
1-1.5 years
time frame that reinervation must occur to avoid target breakdown/degeneration
collateral sprouting
primary form of plasticity….degeneration leads to sprouting of adjacent fibers and formation of new synapses (*reactive synaptogenesis*)
1 mm/day
how fast does axon growth in regeneration?
chondroitin sulfate proteoglycans
example of extracellular molecule that is produced by reactive astrocytes and can impede regeneration in CNS
axonal growth ceases, synaptic transmission matures, cortical activation constrained
these can cause critical periods of plasticity to end (plasticity decrease with age)
long term potentiation
in cortical synaptic plasticity…this occurs due to precise timing of EPSP and spike activity
VLPO
theis GABAergic center in hypothalamus major player in sleep (depresses tubulomamillary secretion of histamine so fall asleep)
insomnia
lesion of VLPO will cause this
Berger
physician that first used EEG on humans
spindle
from thalamic input….bursts generated during stage 2 (synchronize thalamic and cortical input)
aminergic inhibition; cholinergic excitation
this decreases in REM sleep; this increases
orexin neurons
lesions of these neurons cause narcolepsy
REM sleep disorder
this occurs if motor system isn’t inhibited in REM cycle by glycine
cataplexy
emotional response (laughter) causes descending inhibition of muscle activity (muscles turn to mush adn fall down)
somnambulism
aka sleepwalking (*typically during stage 1 and 2*)
beta
sleep wave that is for activated cortex, fastest (>14 Hz)
alpha
sleep wave that is for quiet-awake state, 8-13 Hz
GABA
benzodiazepines inhibit this
adenosine
caffeine inhibits this (to keep awake)
theta
sleep wave that is for some sleep states, 4-7 hz
delta
hallmark for deep sleep
theta
what waves predominate in sleep (synchrony = high EEG amplitude)
thalamus
central pacemaker of circadian rhythm
90 minutes
how often is sleep cycle repeated?
stage 1
characterized by drowsiness, slow rolling movements of eyes, alpha waves become irregular and wane
stage 2; 5-15 minutes
characterized by high amplitude K complexes; sleep spindles generated by thalamic pacemaker; how long does this stage last?
stage 3; 20-40 minutes (ascends to stage 2 for 10-15, lightens, then REM)
large, slow delta waves in EEG; how long does this last in first cycle?
REM; 30-50 minutes
characterzed by fast beta rhythms, sharp and frequent eye movements; how long does this last?
30 min
refractory period between REM episodes
restoration and adaptation
what are two reasons/theories we are designed to sleep?
diffuse modulatory NT system
neurons responsible for sleep and waking are part of this
Ach (pons/midbrain junction), norepi (locus coeruleus), serotonin (raphe nuclei)
NT involved in wakefullness (these are all *activated*)
Ach (pons/midbrain junction), norepi (locus coeruleus), serotonin (raphe nuclei)
NT involved in non-REM sleep (these are all *decreased*)
Ach, serotonin
NT involved in REM sleep on (first is activated, other is inactive)
norepi
NT involved in REM sleep off (*active*)
Ach
this enhances REM sleep
thalamus (block sensory info to cortex)
diffuse modulatory NT system controls rhythms via this
NE, serotonin, Ach
falling asleep due to decrease in these NT
locus ceruleus and raphe neurons
firing of these decrease in REM sleep (while Ach increases)
pontine-geniculo-occipital
waves that characterize REM sleep
preoptic hypothalamic (GABAergic)
inhibit histamine activating cells that project to forebrain (in action of sleep)
HLA gene
gene involved in narcolepsy
cataplexy
sudden REM paralysis from awakened state
cataplexy, hypnagogic hallucinations, sleep paralysis, orexins deficiency
4 components of narcolepsy
locus ceruleus and raphe neurons
where does hypocretin/orexin project to (from lateral hypothalamus)
dopamine antagonists
treatment for restless leg syndrome
suprachiasmatic nucleus; GABA
what controls circadian rhythms (cycle depends on gene expression); what kind of neurons are these?
