sleep Flashcards
what is a circadian rhythm?
24hr cycle in physiological process of living beings; internally generated & externally moderated
3 main measures of sleep
EEG, EOG,EMG
4 stages of sleep
stage 1: low voltage high frequency
by stage 4: voltage increase but frequency decrease
IS A CYCLE so people travel through them repeatedly
alpha waves
weaker bursts of eeg waves
delta waves
largest and slowest
REM sleep
what increases?
o2 consumption, cerebral firing & blood flow
Muscle contraction
Range of ANS functions i.e. blood pressure
REM and dreaming arguments
FOR: Desseilles et al. 2001 (80% of awakenings during REM can report dream)
BUT:
- Mcnamara et al 2010 (review of REM & dreams)
- Siegel 2011 “ (ALSO says about REM & health/memory)
- Oudiette et al 2012 (antidepressants reduce REM but not dreaming)
- Solms, (1997) lesions can affect dreams but not REM
Hobson & Mcarley 1989 theory
activation synthesis theory:
- various waves activate regions (pons)
- cerebral cortex tries to make sense
- we dont act out our dreams bc of muscle atonia
Recoperation theories of sleep
- awake disrupts homestasis
- need sleep to restore
- also conserves energy: smaller animals sleep more
- BUT isnt affected by sport
Ecological Niche
we’ve adapted this way to avoid preds at night time (Siegel 2009)
memory consolidation: FOR (4)
SWS: NREM
Dikelmann & born (2010): sleep helps remember material
NREM: seems to aid consolidation: ESP DECLARATIVE MEMORY (facts) Marshal et al. 2006
REM: “ REM may aid consolidation of NON DEC memory (unconscious)
4) PATTERNS of neuro activity occur during SWS; brain rehearsing? (Dikelmann & born 2010) & (Euston et al 2007)
memory consolidation: AGAINST
No correlation between species and time spent asleep and learning capacity - we sleep less than some species but are more intelligent (Siegel, 2001)
NO correlation between time in REM sleep and !) (Borrow et al 1980)
what is the problem with interpreting results from sleep deprivation studies?
May be confoudning variables i.e. stress is often the cause of sleep loss - reason for seeing what we are seeing?
Sleep deprivation & humans
Durmer & Dinges (2005) - moderate deprivation -moderate effects
deprivation on complex cognition
less consistent results - seems that a substantial amount of deprivation is needed for a consistent disruption (Drummond et al 2004) (alexander & home, 2006)
ONLY SOME COG FUNCTIONS ARE SUSCEPTIBLE
executive functioning: creative thinking > logical deduction (Nilsson et al 2005)
Rechtshaffen & Bergmann (1995)
sleep deprivation on animals: carousel
Limitations with
Rechtshaffen & Bergmann (1995)
- humans and rats have been kept awake longer than that before w.out dying
Siegel (2009) & Rial et al. (2007) - it is prob stress that killing them: all have enlarged adrenal gland (HPA axis)
REM sleep & deprivation: 2 main effects
1) REM rebound - more REM in following few nights (Brunner et al, 1990)
2) more deprivation the more likely REM will occur (i.e. frequency)
~~ REM must be separate from SWS
Sleep recovery
SWS sleep becomes more efficient DOESNT INCREASE SLEEP ( Elmenhorst et al 2008)
Evidence in support of the efficient SWS
- waking ppts in REM doesnt interfere with their performance during the day but SWS interruption does (Nykamp et al. 1998)
- if sleep time is reduced, then time in SWS stays the same but REM time decreases
reticular formation WHAT
In the brain stem (in the little bulge at front)
intricate network of neurons extending from spinal cord to thalamus
reticular formation & sleep
Bremer 1936: severed cat brains
disconnect forebrain & sensory input coming in
Cutting the forebrain off - contin sleep
cutting lower than Pons - no effect
~~~ reticular formation affects wakefulness
Sleep nuclei
reticular REM:controls REM sleep
each site (nuclei) –> controls a particular characteristic of REM sleep
TOGETHER THEY MAKE UP REM SLEEP when all activated
2 main elements of a biological clock
1) FREE RUNNING: maintains own cycle & doesnt need input from external cues - not totally in line with outside world tho
2) ENTRAINMENT: we can train our bio clock to be in synchro with an external stimulus
name for a stimulus that trains our biological clock
Zeitgeber
where is the biological clock
suprachiasmatic nucleus (tiny pair of neuron clusters in the hypothamalmus
lesions to this area cause disruption to circadian cycles i.e. sleep - waking cycle - EVIDENCE
1) Ralph & menaker (1990) hamster experiment
2) the nuclei displays cycles that are entrained by light /dark cycle
suprachaismatic nucleus may not be the only biological clock though - evidence (3)
1) bilateral lesions can leave SOME circadian rhythms unaffected
2) bilateral SCN lesions dont elimainate ability of all enviro stimuli to entrain circadian rhythms (i.e. can be others that are entrained)
3) other tissue cells display free running circadian rhythms when maintained in tissue culture
neural mechanisms of environment
~ how does light/dark entrain the sleep wake cycle
Morin & allen (2006):
~ cutting optic tracts BEFORE chaism - eliminates pathway (after, DOES NOT)
1) Retinohypothalamic tracts leave the chaism & project to the SCN (biological clock)
2) this pathway leads to pineal gland (& other areas)
3) pineal gland secretes MELATONIN
Melatonin
If light is present: melatonin secretion is inhibited
if darkness: melatonin is released –> melatonin involved with decrease in temp –> leading to sleep?
