Mar 31 Fri Rhythms, Sleep, Dreaming

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Mar 31 - FriRhythms, Sleep, Dreaming
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• Cells of the suprachiasmatic nucleus are
  internally controlled at a free running rhythm of
  25 hours
• SCN cells respond to external environmental
  signals to entrain activities to the external
  light-dark cycle (fine-tuned to a 24 hour cycle
  by environment)
• Entrainment via light stimulating photopigment
  cells in the retina (circadian photopigment cells
  release melanopsin)
• Message travels over retino-hypothalamic tract
  and provides info about external light-dark
  conditions
• SCN then controls the production of many
  compounds part of path is to the pineal gland
  which rhythmically releases melatonin (evening,
  more melatonin then sleep and decreased body
  temperature in daylight release is inhibited)

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• The suprachiasmatic nucleus (SCN) known to be an
  endogenous circadian controller based on
• Transplant studies
• Explant studies cells fire in dish
• Isolation studies SCN in place, but disconneted
  show role of chemical signals
• Gene knock-out knock-in studies

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• Neurons in suprachiasmatic nucleus
• Rhythmic metabolic pattern (more active in day)
• Neuronal activity greater during light period
• Dissect from surrounding cells, these neurons
  still show rhythm (so coming from within)
• Rhythm is genetically specified (shown for many
  generations precluded from influence of
  zeitgebers also transplantation studies)

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Rhythms

• Circadian rhythms
• Ultradian rhythms period less than a day occur
  more often than once a day
• a 90 minute cycle that repeats through the day
  and night
• variations in activity level and cognitive
  performance show a 90 minute rhythm
• Infradian rhythms occur less often than
  once/day period length is more than a day, less
  than a year (menstrual cycle)
• Circannual around a year seasonal rhythms
  (migration hibernation)

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• Sleep-wake cycle is a 24 hr rhythm.
• During sleep, there is an ultradian rhythm, a 90
  minute rhythm of different stages of sleep.
• Measuring stages of sleep
• EEG electrical activity of brain
• EMG electrical activity of muscles (neck)
• EOG electrical activity of ocular muscles (eye
  movements)

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• Controllers of Sleep
• Circadian signals from the Suprachiasmatic
  nucleus
• Homeostatic signals from sleep promoting
  chemicals - somnogens

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• Neural control of the 90 minute sleep cycle
• Sleep initiation
• VLPO ventrolateral pre-optic area of the
  hypothalamus responds to endogenous rhythm
  signals from SCN
• Basal forebrain responds to sleep promoting
  chemicals, somnogens
• Adenosine accumulates during wakefulness and
  acts as a sleep-inducer

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• Neural control of the 90 minute sleep cycle
• Sleep initiation
• VLPO
• Basal forebrain
• 2. Sleep divided into slow wave sleep (NREM) and
  REM sleep
• Slow wave sleep divided into 4 stages based on
  electrophysiology and depth of sleep (difficulty
  of awakening).
• Across stages 1-4, the EEG becomes slower
  compared to waking EEG and sleep becomes deeper.
  Energy metabolism decreases across stages 1-4
  reduced glucose and oxygen use.

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Pattern in the night

• After the 4 stages of slow wave sleep occur,
  pattern changes and reverses
• 4-6 cycles of 1,2,3,4,3,2, REM
• each cycle 90 minutes in length
• REM period gets longer each time
• last REM of night lasts about 60 min out of 90 in
  cycle
• early in night, more slow wave sleep later, more
  REM

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• Neural control of the 90 minute sleep cycle
• Sleep initiation
• VLPO
• Basal forebrain
• 2. Sleep divided into slow wave sleep (NREM) and
  REM sleep
• Pons controls sleep stages.
• REM-on acetylcholine triggers excitation
• REM-off Norepinephrine and Serotonin trigger
  inhibition
• (many other important neurotransmitters)

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• Neural control of the 90 minute sleep cycle
• Sleep initiation
• 2. Sleep divided into slow wave sleep (NREM) and
  REM sleep Pons
• 3. NREM sleep stages 1-4
• Thalamus and connections from thalamus to cortex
  are inhibited
• Thalamus cannot send sensory input to cortex
• But neurons within cortex (cortical
  neuron-to-cortical neuron connections) are firing
  almost as much as during wakefulness
• Cortical excitation coming from within cortical
  circuits not from external inputs
• Dreams are about daily routines boring reduced
  sensory content

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• 4. REM sleep - Rapid Eye Movement (REM)
• stages go from 1,2,3,4,3,2, REM
• paradoxical sleep EEG looks similar to waking
  but muscles do not move
• eyes move heart rate, breathing, and blood
  pressure increase
• Most dreaming occurs
• EEG activation due to increase in firing rates of
  neurons in reticular activating system of
  brainstem, thalamus, and some areas of cortex
• Some of the excited neurons are oculomotor
  neurons - cause eye movements
• Absence of ability to move muscles, muscle
  atonia, due to inhibition from reticular
  activating system

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• 4. REM sleep - Rapid Eye Movement (REM)
• EEG activation due to increase in firing rates of
  neurons in reticular activating system of
  brainstem, thalamus, and limbic and paralimbic
  areas of cortex
• But prefrontal areas of cortex (executive control
  centers) are not very activated
• Active thalamus provides high sensory input to
  dreams
• High visual imagery like visual hallucinations
  cholinergic stimulation. During waking,
  cholinergic system less in control than are NE
  and SE
• Dreams show emotional (limbic) and instinctual
  drive (paralimbic) content
• Dreams are illogical, lack continuity, and
  bizarre (no executive control/ thought
  prefrontal cortex not active)

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Formal psychological features of dreaming are
determined by the specific regional activation
patterns and neurochemistry during sleep. Hobson
and Pace-Schott, 2002
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• Wakefulness
• Several brain arousal systems facilitate
  wakefulness.
• Brainstem reticular activating system
  structures in core of pons and medulla that
  project to hypothalamus and basal forebrain
  inhibit sleep control centers and activate basal
  forebrain
• Hypothalamic arousal systems

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Brainstem reticular activating system is at core
of pons and medulla.
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• 2. The Hypothalamic Arousal Systems
• a. Posterior hypothalamus uses Serotonin,
  Norepinephrine, and Histamine to modulate
  multiple areas and promote wakefulness in
  forebrain
• b. Lateral hypothalamus uses Orexin to
  stabilize wake state and prevent switching from
  wake to sleep at the wrong time
• (Narcoleptics have reduced of Orexin-producing
  neurons and reduced levels of Orexin in CSF)
• During sleep, there is a progressive decrease
  across stages in output from SE, NE, and
  histamine neurons to point of being shut off
  during REM. This leaves the forebrain
  unmodulated by these waking factors and instead
  influenced more by Acetylcholine. This precludes
  waking consciousness.

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