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CNS > Unit 12 - Sleep, Learning and Memory > Flashcards

Unit 12 - Sleep, Learning and Memory Flashcards

1
Q

EEG

A

record of electrical potential changes in the brain

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2
Q

electrical waves when alert

A

β rhythm

13-60 Hz - high freq

5-10 uV - low amp

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3
Q

electrical waves when inattentive

A

α rhythm

8-13 Hz - low freq

30-50 uV - high amp

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4
Q

electrical waves when asleep/under anaesthesia

A

θ rhythm - 4-7 Hz, large amplitude

δ rhythm - 0.5-4 Hz, large amplitude

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5
Q

stage 1 of slow wave sleep

A

rhythm slows to 4-6 Hz and amplitude increases

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6
Q

stage 2 of slow wave sleep

A

more irregular and slower (1-5 Hz) waves of larger amplitude

sleep spindles (α-like) - internal trigger

K complexes - external stimulus e.g. alarm

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7
Q

stage 3 of slow wave sleep

A

slow waves - 1-2 Hz

occasional sleep spindles and K complexes

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8
Q

stage 4 of slow wave sleep

A

sleep spindles are rare

no K complexes

highest amp with lowest freq

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9
Q

sleep spindles

A

α like

internal trigger

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10
Q

K complexes

A

external stimulus

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11
Q

time between stage 1 and 4

A

30-45 minutes

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12
Q

when does first REM occur

A

90 minutes after falling asleep

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13
Q

REM rhythm

A

faster desynchronised rhythm of low amp (like awake)

lasts for 20 mins

occurs every 90 mins

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14
Q

EEG of different stages of sleep

A
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15
Q

when is there more stage 4 sleep

A

early in the night

as it is difficult to wake when in stage 4

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16
Q

sleep cycle - young child vs elderly adult

A

YOUNG CHILD

Lots more slow wave with the baby

Synthesis of proteins - growth and repair

GH in stage 4 - secretion

Baby has a lot of REM

REM - mind maintenance - neurogenesis

ELDERLY ADULT

Lots of REM

Lots of awakenings

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17
Q

proportion of REM to non-REM sleep

A
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18
Q

REM - effect on body

A

pronounced loss of muscle tone

sharp fluctuations in HR, BP and resp

rapid eye movement

raised brain temp (vs SWS)

penile erection

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19
Q

Parasomnia/REM behaviour disorder

A

no paralysis in REM

act out their dreams

associated with Parkinson’s

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20
Q

SWS - effect on body

A

substantial muscle tone

frequent body movement

HR, BP and respiration are maintained at regular rate

brain temp goes down

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21
Q

function of REM

what happens with deprivation

A

rebound increase - we need to compensate if we have lost some

DEPRIVATION:

subtle emotional and personality disturbances

abnormalities in sensory processing, sexuality and feeding behaviour

* mind maintenance

* necessary for consolidation of memories

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22
Q

function of SWS

A

rebound increase

hormones that stimulate protein synthesis released

stage 4 SWS is increased after exercise

immune system stimulation

body maintenance

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23
Q

reticular formation

where is it found

what is its role

A

network of neurons in the brainstem

can influence arousal (reticular activating system)

rostral brainstem - necessary for wakefulness

caudal brainstem - necessary for sleep

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24
Q

rostral brainstem

A

necessary for wakefulness

25
caudal brainstem
necessary for sleep
26
ascending fibres of reticular formation innervate
cerebrum hypothalamus, thalamus, forebrain
27
descending fibres of reticular formation innervate
e.g. skeletal muscle
28
some e.g. of nuclei in reticular formation
for vomiting, coughing, autonomic control
29
what causes onset of SWS
sleep inducing peptide? possible immune role
30
onset of REM
phasic bursts of activity PGO spikes propogate from pons rostrally dorsolateral **_p_**ons (nucleus reticularis pontis oralis) lateral **_g_**eniculate nucleus of the thalamus **_o_**ccipital cortex correlate with onset of rapid eye movements and other changes of REM sleep
31
hypothalamic areas and the basal forebrain implicated as responsible for falling asleep
e.g. ventrolateral preoptic area (VLPO) contains cell bodies of GABAergic neurons that innervate parts of the brainstem lesions of VLPO cause insomnia benzodiazepines promote sleep onset
32
tuberomammillary nucleus affected by what drugs
contains cell bodies of histaminergic neurons that innervate brainstem and promote wakefulness antihistamines cause drowsiness
33
basal forebrain affected by what drugs
contains cell bodies of adenosine-releasing neurons that promote sleep adenosine antagonists suppress sleep
34
transition between SWS and REM
***balance between brainstem nuclei*** **_cholinergic_** - ACh induces REM laterodorsal tegmental nucleus pedunculopontine tegmental nucleus active in REM (PGO spikes) REM "on" cells **_aminergic_** - dorsal raphe nucleus (serotonin) locus ceruleus (NA) quiescent in REM, active in SWS \< wakefulness REM "off" cells
35
REM on cells
cholinergic
36
REM off cells
aminergic
37
narcolepsy
irresistible sleep episodes excessive daytime sleepiness cataplexy - reduction in tone - sleep paralysis rapid onset of REM sleep onset in adolescence imbalance of cholinergic/aminergic activity in brainstem
38
orexin/hypocretin
peptide released by hypothalamic neurons axons terminate in areas such as brainstem and cerebrum regulates cholinergic and aminergic neurons in brainstem role in sleep/wakefulness, vigilance, hunger promotes wakefulness reduced levels of hypocretin/orexin in CSF of human narcoleptics in dogs there is an orexin receptor mutation - rare for humans to survive with such a mutation ? autoimmune disease in humans
39
insomnia affects
15%
40
parasomnias affect
10% - more common in children as they have more stage 4 sleep excessive sleepiness (infection - trypanosomiasis) - 2% narcolepsy - 0.05% somnambulism - 2.5% (sleep walking) sleep talking - 6% bedwetting - 3% REM behavioural disorder confusional arousals - half asleep, half consciously aware - night terror attacks (children) - incubus (adults)
41
plasticity
underpins ability to learn changes in function, connectivity and synaptic efficiency of neurons memories are stored through the cerebral cortex lesions after learning interfered with ability to remember
42
what are most cortical areas used for
sensory processing and memory storage in parallel
43
engram
44
short-term/working memory left vs right hemisphere area of brain involved
retained for a few minutes **phonological loop:** verbal sketch pad left hemisphere - language **visuospatial sketch pad:** right hemisphere hippocampus reverberating synapses in engram
45
long-term memory
info is consolidated retained for long periods protein synthesis - to reinforce neurons that encode a memory
46
short term synaptic efficiency change
raised NT release following a high rate of discharge
47
longer term morphological changes to synapse
increased number of synapses following increased exocytosis protein synthesis required
48
49
synaptic efficiency change with use
high rate of discharge ⇒ Na+ entry Ca2+ entry activation and translocation of CAMKII → phosphorylation of synapsin I: binds vesicles and cytoskeleton when dephosphorylated (holds vesicle away from membrane) vesicle release
50
morphological changes to synapse with use
as exocytosis increases, the membrane expands if exocytosis \> endocytosis, the bouton expands bouton divides ⇒ increased number of synapses
51
implicit (procedural) memory
automatic or reflexive quality accessible only through performed tasks, or engaging skills cerebrocerebellum involved
52
explicit (declarative) memory
facts, general info recalled by a deliberate act of recollection Hippocampus and cortical tissue overlying hippocampus
53
role of hippocampus
processing or consolidation of declarative memory long term potentiation
54
long term potentiation requirements
brief high freq stimulation of a neural pathway can cause a long-lasting increase in the strength of synaptic response can last for a long time duration of potentiation depends on strength and repetition of stimulation **LTP is only produced when presynaptic stimulation causing NT release is coupled with postsynaptic depolarisation** hippocampus and NMDA receptor involved
55
NMDA receptor binding sites relating to memory also requires ____ and ______ receptors
ionotropic glutamate receptor - glutamate and glycine binding sites Mg2+ blocks ion channel at rest more difficult to open than other glu ionotropic receptors ⇒ AMPA and kainate receptors NT binding, coupled with postsynaptic depolarisation (to remove Mg2+ from channel) is necessary for Ca2+ entry through the channel AMPA and kainate receptors facilitate the postsynaptic depolarisation
56
NMDA receptor activation causes
Ca2+ entry triggering a variet of enzyme cascades which lead to synaptic plasticity and protein synthesis inhibition of Ca2+ entry blocks LTP NMDA antagonists inhibit LTP and some types of learning
57
loss of hippocampus, amygdala and overlying temporal cortex
severe anterograde amnesia (inability to learn anything factual) short term memories intact high IQ prior long term memories intact motor learning unaffected
58
hippocampus and overlying cortical tissue necessary for
declarative memories
59
loss of brain tissue with Alzheimer's
early loss in hippocampus and cerebral cortex appearance of protein deposits - plaques and tangles

CNS (36 decks)

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