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Introduction to Physiological Psychology Psych 260 Introduction to Physiological Psychology Psych 260 Kim Sweeney [email protected] cogsci.ucsd.edu/~ksweeney/psy260.html What could possibly go wrong? n Causes of Narcolepsy – Uncertain, but appears to be influenced by a hereditary autoimmune disorder in which orexigenic neurons are attacked by immune system § When orexigenic neurons are systematically destroyed in lab rats, narcoleptic behavior results § Canine narcolepsy is caused by mutations in one of the orexin receptors 1 What can possibly go wrong? n REM Sleep Behavior Disorder – No paralysis observed during REM sleep § The result? Dreams can be acted out! – Appears to have some genetic component What can possibly go wrong? n Slow-Wave Sleep Problems: – Generally observed in children, and especially during stage 4 sleep § Bedwetting § Night terrors § Sleepwalking 2 If you don’t sleep… n Effects of sleep deprivation appear to be more cognitive than physiological – Complete lack of exercise doesn’t result in diminished need for sleep – Quadriplegics and paraplegics need sleep n However, lack of sleep can be fatal! – Research with fruit flies – Fatal familial insomnia § Lack of SWS, brief episodes of REM If you don’t sleep… n SWS appears to be crucial for brain rest n REM appears to involve mental ‘house cleaning’ – REM deprivation results in rebound § Suggests brain needs a certain amount of REM – REM time decreases over development 3 Learning is ‘development’… n Research with both humans and non- human animals suggests that sleep aids in consolidation of long-term memories n SWS and REM each play an important role Memory n Declarative memory vs non-declarative memory 4 No Sleep vs. SWS vs. SWS + REM Visual discrimination task Karni et al, 1991 Mednick et al, 2003 No sleep vs. SWS only Paired words mirror shadowing Tucker et al., 2006 5 Sleep and Memory n REM sleep appears to facilitate consolidation of non-declarative memories n SWS seems to facilitate consolidation of declarative memories Peigneux et al., 2004 6 n During SWS (but not REM sleep), same hippocampal and para- hippocampal areas were activated as when learning the route! Peigneux et al., 2004 Chemical control of sleep n Sleep is regulated: – If deprived of SWS or REM sleep, an organism will try to ‘make up’ the missed sleep. – If SWS is obtained in a nap, that amount will be ‘deducted’ from the following nights sleep. n This suggests that something ‘knows’ how much sleep we are getting! 7 Regulating mechanism n Adenosine- a neuromodulator that inhibits neural activity Astrocytes have glycogen When brain is active, glycogen is During SWS astrocytes regain glycogen used by neurons for energy Adenosine inhibits neural activity Being awake depletes glycogen Fall in glycogen level -> increase in extracellular adenosine Caffeine blocks adenosine receptors! Neurotransmitters of sleep and arousal n Acetylcholine n Norepinephrine n Serotonin n Histamine n Orexin 8 Neurotransmitters of sleep and arousal n Acetylcholine – Produced in dorsal pons and basal forebrain and then widely distributed – Acetylcholine increases arousal (greater desynchronization) – High levels of Ach found both in REM and awake states Neurotransmitters of sleep and arousal n Norepinephrine – Produced in the dorsal pons and then widely distributed – Part of the “fight or flight” system – Increases ability to pay attention to stimuli – Highest levels when awake, lower in SWS, lowest in REM 9 Activity of NE neurons in LC of DP Neurotransmitters of sleep and arousal n Serotonin – Produced in the raphe nuclei of the reticular formation and widely distributed – Higher serotonin levels associated with greater arousal. 10 Activity of serotonergic neurons in raphe nuclei The neurotransmitters of sleep n Histamine – Produced in hypothalamus and widely distributed – High when awake, low during both REM and SWS 11 The neurotransmitters of sleep n Orexin – Produced in lateral hypothalamus and broadly distributed – Promotes wakefulness NTs of sleep n Acetylcholine: arousal – Levels high during wakefulness and REM n Norepinephrine: arousal (vigilance) – Levels high when alert, low during SWS and REM n Serotonin: arousal – Levels high when awake, lowering increasingly as you head towards REM n Histamine: arousal – Levels high when awake, low during SWS and REM n Orexin: arousal – Levels high when alert, low during rest and all sleep states 12 Neural Control of SWS n Ventrolateral preoptic area – Destruction of this area produced insomnia (and eventually death) in rats Neural Control of SWS n Ventrolateral Ventrolateral preoptic preoptic area area – Receives inhibitory – Contains inhibitory inputs from: GABA-secreting neurons which project § Locus coeruleus to: § Raphe nuclei § Dorsal pons § Hypothalamus (acetylcholine) § Locus coeruleus (norepinephrine) § Raphe nuclei (serotonin) § Hypothalamus (histamine, orexin) 13 So… n Either the ventrolateral preoptic area is inhibited, or it is inhibiting. n Orexin helps tip the scale towards “awake” The REM flip-flop n REM-ON and REM-OFF neurons – During awake states, REM-OFF neurons are activated by § Orexin § Serotonin § Norepinephrine 14 The REM flip-flop n REM-ON and REM-OFF neurons – Once sleep has begun, this excitatory activity decreases… REM-OFF neuronal activity decreases too. The REM flip-flop n REM-ON and REM-OFF neurons – So REM-ON system kicks in! 15 Circadian Sleep Cycles n Circadian rhythms – “about a day” n Virtually all physiological, biochemical, and behavioral processes show some circadian rhythmicity n Zeitgebers – environmental cues that entrain circadian cycles Free-Running Cycles n Remove zeitgebers – still see circadian sleep-wake cycles? – Yup! – Free-running periods vary, but are usually constant within a subject – Most are longer than 24 hours - ~ 25 16 Jet Lag and Shift Work n Jet lag – zeitgebers are accelerated or decelerated n Shift work – zeitgebers unchanged, but sleep-wake cycle must be altered n Both produce a variety of deficits n Can the effects be prevented or minimized? 17 .
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