Sleep

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Sleep Dreaming

• Keith Clements

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Aims

• To review the structure of sleep
• To outline the brain mechanisms controlling sleep
• To discuss theories of sleep and dreaming,
  including the relationship between sleep and
  memory consolidation.

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Stages of sleep

•         Identified by EEG (Aserinsky Kleitman,
  1953)
•         5 stages with distinct EEG
  characteristics
•         90 minute cycle throughout the night
•         Distinction between SWS and REM sleep
• REM accompanied by muscular paralysis
•         The ratio of REM to SWS sleep changes
  over the lifespan

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Dreaming

• Once thought to occur only in REM sleep
• Dement Kleitman (1957)
• 80 report dreams from REM
• 20 from non-REM
• REM non-REM dreams differ (Hobson et al., 2000)
• REM Longer, more vivid, more movement,
  emotionally charged, less related to waking life.
• SWS Thoughts Concerns

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Other species

• All vertebrates show periods of inactivity
• All mammals except dolphins the spiny anteater
  show SWS REM.
• Birds also show both.
• Sleep amounts vary across species

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Brain Mechanisms

• Sleep initially thought to start due to loss of
  sensory input
• Later work emphasized the reticular formation as
  a system regulating arousal and alertness.  
• Bremer (1930) showed that cutting through the
  brainstem at different points indicated that
  structures in the pons are involved in sleep
  staging. Sections through the midbrain produced
  permanent slow-wave sleep.

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Basal Forebrain

• Von Economos observations of Encephalitis
  Lethargica focussed attention on the hypothalamus
  and basal forebrain.
• Release of GABA by forebrain neurons triggers SWS
  (Gallopin et al., 2000).
• Narcolepsy and the hypothalamus
• Narcolepsy result from damage to part of the
  hypothalamus.
• Loss of hypothalamic neurons secreting hypocretin
  causes narcolepsy (Lin et al. 1999).
• Hypothalamic neurons send axons to the basal
  forebrain and pons. May trigger sleep.

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The reticular formation

• The reticular formation, running through the
  pons, was viewed as a a system regulating arousal
  and alertness.
• Several systems located in the brainstem are
  known to be involved in regulating aspects of
  sleep

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Monoamine systems

• Locus Coeruleus (in the Pons)
• Origin of Noradrenergic fibres, diffuse
  projection.
• Recording reveals activity during wakefulness
• Many stimulants increase Noradrenergic activity
• May suppress REM sleep
• Raphe (In the Pons Medulla)
• Origin of serotoninergic fibres
• Recording reveals activity during wakefulness
• Destruction produces temporary insomnia
  (especially REM)
• Suppresses REM

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REM sleep

• Cholinergic neurons in the Pons appear to be
  involved in REM sleep
• ACh Antagonists produce drowsiness
• Nicotine is a stimulant
• Release of ACh by ascending fibres correlates
  with activity
• Mcarley Hobson (1975) proposed that NREM/REM
  switching was triggered by reciprocal inhibition
  between cholinergic aminergic systems.

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Brain imaging studies

• During slow wave sleep brain activity falls (e.g.
  Maquet et al, 1992, report 40 reduction in
  glucose utilization in stages 3 4)
• In REM activation is localised to brainstem,
  limbic and paralimbic areas. Executive areas of
  frontal cortex are not activated (Maquet et al,
  1996 Nofzinger et al, 1997 Braun et al, 1997)

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Why do we sleep?

• Explanations include
• To conserve energy
• To avoid predators
• Meddis (1975)
• To restore the body
• Growth hormone secretion peaks during sleep.
• SWS increases after intense exercise (Shapiro et
  al 1981), but may reflect raised temperature
  (Horne Moore, 1984).
• To aid learning
• Sleep deprivation has clearer effects on
  procedural, than declarative learning.

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Sleep Memory Consolidation

• Stickgold (2005)
• Three procedural tasks (visual discrimination,
  motor sequence learning motor adaptation) all
  show improvement after sleep.
• Improvement correlates with specific sleep stages
  (SWS for all three, but also late REM for visual
  discrimination).
• Sleep deprivation may also affect types of
  learning dependent on the hippocampus.

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Why do we dream?

• Neural exercise?
• Hobson (1989) Activation-synthesis theory
• Endogenous stimulation?
• Memory Consolidation?
• Drugs which reduce REM dont affect learning.
• Animal studies (e.g. Maquet, 2001) suggest
  hippocampal activity during sleep recreates that
  during waking, but not specific to REM sleep.

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References

• Chapter 6 in Wickens (2005) or chapter 14 in
  Pinel (2009) cover sleep.
• Stickgold R. (2005). Sleep-dependent memory
  consolidation. Nature, 437, 1272-1278 (27 October
  2005)
• Further Reading
• See articles by Hobson, Pace-Schott Stickgold
  and by Vertes Eastman in Behavioral Brain
  Sciences (2000), 23(6).