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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
Q

caudal brainstem

A

necessary for sleep

26
Q

ascending fibres of reticular formation innervate

A

cerebrum

hypothalamus, thalamus, forebrain

27
Q

descending fibres of reticular formation innervate

A

e.g. skeletal muscle

28
Q

some e.g. of nuclei in reticular formation

A

for vomiting, coughing, autonomic control

29
Q

what causes onset of SWS

A

sleep inducing peptide?

possible immune role

30
Q

onset of REM

A

phasic bursts of activity

PGO spikes

propogate from pons rostrally

dorsolateral pons (nucleus reticularis pontis oralis)

lateral geniculate nucleus of the thalamus

occipital cortex

correlate with onset of rapid eye movements and other changes of REM sleep

31
Q

hypothalamic areas and the basal forebrain implicated as responsible for falling asleep

A

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
Q

tuberomammillary nucleus

affected by what drugs

A

contains cell bodies of histaminergic neurons that innervate brainstem and promote wakefulness

antihistamines cause drowsiness

33
Q

basal forebrain

affected by what drugs

A

contains cell bodies of adenosine-releasing neurons that promote sleep

adenosine antagonists suppress sleep

34
Q

transition between SWS and REM

A

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
Q

REM on cells

A

cholinergic

36
Q

REM off cells

A

aminergic

37
Q

narcolepsy

A

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
Q

orexin/hypocretin

A

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
Q

insomnia affects

A

15%

40
Q

parasomnias affect

A

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
Q

plasticity

A

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
Q

what are most cortical areas used for

A

sensory processing and memory storage in parallel

43
Q

engram

A
44
Q

short-term/working memory

left vs right hemisphere

area of brain involved

A

retained for a few minutes

phonological loop:

verbal sketch pad

left hemisphere - language

visuospatial sketch pad:

right hemisphere

hippocampus

reverberating synapses in engram

45
Q

long-term memory

A

info is consolidated

retained for long periods

protein synthesis - to reinforce neurons that encode a memory

46
Q

short term synaptic efficiency change

A

raised NT release following a high rate of discharge

47
Q

longer term morphological changes to synapse

A

increased number of synapses following increased exocytosis

protein synthesis required

48
Q
A
49
Q

synaptic efficiency change with use

A

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
Q

morphological changes to synapse with use

A

as exocytosis increases, the membrane expands

if exocytosis > endocytosis, the bouton expands

bouton divides ⇒ increased number of synapses

51
Q

implicit (procedural) memory

A

automatic or reflexive quality

accessible only through performed tasks, or engaging skills

cerebrocerebellum involved

52
Q

explicit (declarative) memory

A

facts, general info

recalled by a deliberate act of recollection

Hippocampus and cortical tissue overlying hippocampus

53
Q

role of hippocampus

A

processing or consolidation of declarative memory

long term potentiation

54
Q

long term potentiation

requirements

A

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
Q

NMDA receptor

binding sites relating to memory

also requires ____ and ______ receptors

A

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
Q

NMDA receptor activation causes

A

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
Q

loss of hippocampus, amygdala and overlying temporal cortex

A

severe anterograde amnesia (inability to learn anything factual)

short term memories intact

high IQ

prior long term memories intact

motor learning unaffected

58
Q

hippocampus and overlying cortical tissue necessary for

A

declarative memories

59
Q

loss of brain tissue with Alzheimer’s

A

early loss in hippocampus and cerebral cortex

appearance of protein deposits - plaques and tangles

CNS (36 decks)

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