Unit 12 - Sleep, Learning and Memory Flashcards
EEG
record of electrical potential changes in the brain
electrical waves when alert
β rhythm
13-60 Hz - high freq
5-10 uV - low amp
electrical waves when inattentive
α rhythm
8-13 Hz - low freq
30-50 uV - high amp
electrical waves when asleep/under anaesthesia
θ rhythm - 4-7 Hz, large amplitude
δ rhythm - 0.5-4 Hz, large amplitude
stage 1 of slow wave sleep
rhythm slows to 4-6 Hz and amplitude increases
stage 2 of slow wave sleep
more irregular and slower (1-5 Hz) waves of larger amplitude
sleep spindles (α-like) - internal trigger
K complexes - external stimulus e.g. alarm
stage 3 of slow wave sleep
slow waves - 1-2 Hz
occasional sleep spindles and K complexes
stage 4 of slow wave sleep
sleep spindles are rare
no K complexes
highest amp with lowest freq
sleep spindles
α like
internal trigger
K complexes
external stimulus
time between stage 1 and 4
30-45 minutes
when does first REM occur
90 minutes after falling asleep
REM rhythm
faster desynchronised rhythm of low amp (like awake)
lasts for 20 mins
occurs every 90 mins
EEG of different stages of sleep
when is there more stage 4 sleep
early in the night
as it is difficult to wake when in stage 4
sleep cycle - young child vs elderly adult
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
proportion of REM to non-REM sleep
REM - effect on body
pronounced loss of muscle tone
sharp fluctuations in HR, BP and resp
rapid eye movement
raised brain temp (vs SWS)
penile erection
Parasomnia/REM behaviour disorder
no paralysis in REM
act out their dreams
associated with Parkinson’s
SWS - effect on body
substantial muscle tone
frequent body movement
HR, BP and respiration are maintained at regular rate
brain temp goes down
function of REM
what happens with deprivation
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
function of SWS
rebound increase
hormones that stimulate protein synthesis released
stage 4 SWS is increased after exercise
immune system stimulation
body maintenance
reticular formation
where is it found
what is its role
network of neurons in the brainstem
can influence arousal (reticular activating system)
rostral brainstem - necessary for wakefulness
caudal brainstem - necessary for sleep
rostral brainstem
necessary for wakefulness
caudal brainstem
necessary for sleep
ascending fibres of reticular formation innervate
cerebrum
hypothalamus, thalamus, forebrain
descending fibres of reticular formation innervate
e.g. skeletal muscle
some e.g. of nuclei in reticular formation
for vomiting, coughing, autonomic control
what causes onset of SWS
sleep inducing peptide?
possible immune role
onset of REM
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
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
tuberomammillary nucleus
affected by what drugs
contains cell bodies of histaminergic neurons that innervate brainstem and promote wakefulness
antihistamines cause drowsiness
basal forebrain
affected by what drugs
contains cell bodies of adenosine-releasing neurons that promote sleep
adenosine antagonists suppress sleep
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
REM on cells
cholinergic
REM off cells
aminergic
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
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
insomnia affects
15%
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)
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
what are most cortical areas used for
sensory processing and memory storage in parallel
engram
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
long-term memory
info is consolidated
retained for long periods
protein synthesis - to reinforce neurons that encode a memory
short term synaptic efficiency change
raised NT release following a high rate of discharge
longer term morphological changes to synapse
increased number of synapses following increased exocytosis
protein synthesis required
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
morphological changes to synapse with use
as exocytosis increases, the membrane expands
if exocytosis > endocytosis, the bouton expands
bouton divides ⇒ increased number of synapses
implicit (procedural) memory
automatic or reflexive quality
accessible only through performed tasks, or engaging skills
cerebrocerebellum involved
explicit (declarative) memory
facts, general info
recalled by a deliberate act of recollection
Hippocampus and cortical tissue overlying hippocampus
role of hippocampus
processing or consolidation of declarative memory
long term potentiation
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
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
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
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
hippocampus and overlying cortical tissue necessary for
declarative memories
loss of brain tissue with Alzheimer’s
early loss in hippocampus and cerebral cortex
appearance of protein deposits - plaques and tangles
