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CHAPTER 15. Sleep and Consciousness Sleep and Dreaming. Why do we sleep?. Why do we sleep? Long unanswered question We know consequences of NOT sleeping, but not understand why we must sleep Two major theories regarding function of sleep Restorative hypothesis

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chapter 15

CHAPTER 15

Sleep and Consciousness

Sleep and Dreaming

why do we sleep
Why do we sleep?
  • Why do we sleep?
    • Long unanswered question
    • We know consequences of NOT sleeping, but not understand why we must sleep
  • Two major theories regarding function of sleep
    • Restorative hypothesis
      • species with higher metabolic rates typically spend more time in sleep
      • sleep is restorative.
    • Adaptive hypothesis
      • Less obvious but alternative hypothesis.
      • amount of sleep an animal engages in depends
        • availability of food
        • safety considerations
        • low predator vulnerability = greater sleep time
sleep deprivation effects
Sleep deprivation effects
  • Profound deprivation effects observed in shift workers:
    • Those who work nights
    • Particularly grave yard shift
    • Typically sleep less than day shift workers
    • Fail to adjust sleep-wake cycle adequately
      • 5 days a week have reverse day/night cycle
      • Weekends revert back to regular hours
  • Result: disrupts natural biological or circadian rhythm
  • Effects include:
    • Poorer work performance
    • Higher likelihood of accidents
    • Poorer cognitive function
    • Higher stress levels
slide4

Importance of

biological rhythm

  • Circadian rhythm:
    • rhythm or cycle that is about a day in length.
    • Circa = about
    • Dia = day
    • A little longer- about 25 hours long
  • suprachiasmatic nucleus (SCN) of the hypothalamus:
    • main brain area that functions as biological clock
    • Controls circadian rhythms in mammals
  • Lesioning SCN in rats abolishes normal 24-hour rhythms
    • Sleep and activity,
    • body temperature,
    • Drinking
    • steroid secretion.
    • Functions as pacemaker: keeps time and regulates activity of other cells
slide5

The suprachiasmatic nucleus: The nuclei, indicated by the arrows, took up more radioactive 2-deoxy-glucose in the scan on the left because the rat was injected during the day; the rat on the right was injected at night.

slide6

Importance of

biological rhythm

  • zeitgebers(“time-givers”) = cues for time
    • The SCN is entrained to the solar day by these zeitgeber cues
    • Differences in light intensity across day serve as cues to the brain
  • Several studies highlight how this works:
    • SCN relies on light discrepancy to detect day/night
    • If place 3rd shift workers in light settings that mimic opposite day/night cycle, deleterious effects of 3rd shift disappear
    • Antarctic workers in Antarctic winter: moved to natural 25-hour day
  • Phase delays show easier to “go to bed later” than “go to bed earlier”
    • Explains why easier to travel west than travel east
    • More jet lag when going East!
slide7

SCN function

  • The SCN regulates pineal gland’s secretion of melatonin
    • Light resets biological clock by suppressing melatonin secretion
    • Melatonin = hormone that induces sleepiness.
      • Melatonin often used to combat jet lag
      • Also used to treat insomnia in shift workers and in individuals who are blind.
  • Light information reaches SCN via direct connection from retinas: retinohypothalamic pathway.
    • Ganglion cells in retina contain melanopsin: light-sensitive substance, or photopigment.
    • Melanopsin located in widely branching dendrites
      • Helps cells in detecting overall level of light
      • NOT contribute to image formation
      • ONLY for controlling circadian rhythm.
slide8

Ultradian rhythms

  • Animals have basic rest and activity cycle
    • 90-100 min periods throughout day
    • Alertness waxes and wans; particularly in wee morning hours and late afternoon
  • Ultradian rhythms
    • rhythms that are shorter than a day in length.
    • Important for controlling
      • Hormone production
      • urinary output
      • Alertness
      • And other functions which follow regular cycles throughout day.
slide9

neurochemical regulation of sleep

  • Adenosine provides at least one of mechanisms of sleep homeostasis.
    • During wakefulness: Adenosine accumulates in basal forebrain area.
    • inhibits arousal-producing neurons there
    • Result: drowsiness and reduced EEG activation.
  • Adenosine also active in preoptic area of the hypothalamus (POA).
    • Warming POA activates sleep-related cells
    • Warming inhibits waking-related cells in the basal forebrain
    • Warming enhances slow-wave EEG.
  • Neurons in Ventrolateralpreoptic nucleus(VPN) double rate of firing during sleep: function = inhibit neurons in arousal areas
slide11

Two critical pathways

  • Pedunculopontine and latero-dorsal tegmental nuclei (PPT/LDT)
    • Neurons from the PPT/LDT activate areas crucial for transmission to the cortex
    • Also desynchronize the EEG;
    • This pathway active during REM sleep.
  • Serves as an arousing pathway
    • activates the cortex
    • facilitates the processing of inputs from the thalamus.
    • completed by neurons from lateral hypothalamus.
slide13

Chemical control

of arousal

  • Arousal involves selective activity in LH neurons: release either hypocretin or melanocortin/melanocortin-concentrating hormone
  • Hypocretin:most active during waking
    • released by LH neurons and received by other arousal centers:
      • Basal forbrain area, particullarlytumeromammillary nucleus,
      • PPT/LDT
      • raphe nuclei and locus coeruleus
    • Help keep waking centers active
    • Not sure if initiates waking or maintains it; may prevent unintentional “switching”
  • Melanocortin or melanocortin-concentrating hormone:
    • most active during REM Sleep
    • Acts on part of PPT/LPT pathway
slide14

EEG patterns:

  • EEG: Electroencephalogram: Records overall activity of various regions of brain
  • Awake patterns: Alpha and Beta Waves:
    • when a person is awake
    • Alpha waves at 8-12 hertz (Hz): associated with relaxation
    • Beta waves: 13-30 Hz. with lower amplitude: associated with alertness, arousal
  • Why lower amplitude with awakefulness/alertness?
    • EEG = sum of all electrical potentials
    • When relaxed/asleep: firing rhythmical, symmetrical, thus increases amplitude
    • When awake: firing less rhythmical, less symmetrical,
      • varies as respond to incoming stimuli- this reduces amplitude
slide16

NON REM Sleep: Stage N1

somnolence or drowsy sleep: transition of the brain from alpha waves to theta waves

Sudden twitches and hypnic jerks (positive myoclonus) associated with the onset of sleep during N1.

may also experience hypnagogic hallucinations during this stage , which can be troublesome

Individual loses some muscle tone and most conscious awareness of the external environment.

slide17

NON REM EEG Sleep: Stage N2

characterized by sleep spindles ranging from 11 to 16 Hz (most commonly 12–14 Hz) and K-complexes.

muscular activity decreases,

conscious awareness of the external environment disappears.

This stage occupies 45% to 55% of total sleep in adults.

slide18

NON REM EEG Sleep: Stage N3

  • deep or slow-wave sleep
  • characterized by presence of a minimum of 20% delta waves ranging from 0.5 to 3 Hz
  • Individual may move around in bed, change positions
  • Parasomnias may occur during this stage:
    • night terrors
    • nocturnal enuresis
    • sleepwalking,
    • somniloquy
slide19

REM sleep

  • After stage 4: the sleeper moves rather quickly back through the stages in reverse order.
    • THEN enters REM sleep
    • Pattern is Stage 1,2,3,4,3,2,1 REM,1,2,3,4,3,2,1 etc.
  • REM, or rapid eye movement, sleep
    • So named because the eyes dart back and forth horizontally during this stage.
    • Looks much like relaxed state Alpha waves
    • Not easily aroused
    • But: respond to stimuli
  • REM = Paradoxical sleep:
    • Sleeper is more alert
    • Increased HR, BP; Sexual activation occurs
    • But show muscle paralysis or atonia
slide20

PGO waves

  • Ponto-geniculo-occipital waves or PGO waves:
    • phasic field potentials
    • begin as electrical pulses from the pons, move to LGN , end up in primary visual cortex
    • waveforms originate in these areas
  • Appearances of PGO waves most prominent right before REM
    • May be intricately involved with eye movement of wake AND sleep cycles
  • Arousal by PGO waves may account for EEG desynchrony and visual imagery observed during REM sleep.
slide21

Firing rates in arousal centers during waking and sleep

  • Activity in the locus coeruleus; (b) activity in the raphe nuclei.
  • AW, alert waking; QW, quiet waking; DRO, drowsy; SWS, slow wave sleep; Pre REM, 60 seconds before REM; Post REM, first second after REM ends.
slide22

REM Sleep

  • During a normal night of sleep: about four or five periods of REM sleep
    • REM sleep episodes quite short at beginning of the night; longer toward end
    • Many animals/some people tend to wake or experience period of light sleep for short time immediately after a bout of REM.
  • Neuronal brain activity similar to that during waking hours
    • body is paralyzed due to atonia
    • REM-sleep stage = paradoxical sleep
    • no dominating brain waves during REM sleep
    • Vividly recalled dreams mostly occur during REM sleep
slide23

Function of Rem Sleep

  • Activation-synthesis hypothesis,
    • during REM sleep : forebrain integrates neural activity generated by brain stem with information stored in memory.
    • brain uses information from memory to impose meaning on nonsensical random input.
  • Biological hypothesis: REM sleep promotes neural development during childhood.
    • excitation that spreads through the brain from the pons during REM sleep encourages differentiation
    • Also encourages maturation
    • As well as myelination in higher brain centers.
slide24

Theories of non-REM Sleep

  • Early theories of non-REM functions
    • focused on rest and restoration:
    • early data showed slow wave sleep increases following exercise- so must be restorative for body.
    • More current data suggests these EEG changes due to overheating rather than fatigue.
    • Horne (1988): slow wave sleep more related to increased brain temperature than increase in body temperature/physical exertion.
  • Horne (1992): slow wave sleep promotes cerebral recovery
    • especially in the prefrontal cortex.
    • Important areas for memory, consolidation
slide25

Sleep and learning

  • REM sleep obviously important:
    • Amount of REM increases during sleep period following learning
    • REM deprivation after learning reduces retention.
    • REM sleep increases daily with spaced trials;
      • Result = better consolidation and better learning
    • Supports ideas of spaced learning rather than cramming
  • BUT: Non-REM sleep ALSO important:
    • Evidence from both animal and human studies
    • non-REM sleep also important for learning:
      • increasing slow potentials over frontal and temporal area during Stage 1
      • Results in improved recall, word association task performance
  • Consolidation is multi-step process:
    • requires a combination of REM and slow wave sleep
    • Both important, one not necessarily more than other.
slide26

Sleep and learning

  • Ribeiro, et al., (2004): Neuronal replay strongest during non-REM sleep
    • recall and amplification of hippocampal activity that occurred during learning
    • Replaying, rehearsing and consolidating.
    • During REM, hippocampus up-regulates genes in cortex that are involved in synaptic plasticity: implements transfer of memory from hippocampus to cortex.
  • Crick and Mitchison’s (1995) reverse learning hypothesis
    • REM = period of memory erasure.
    • neural networks involved in memory must have way to purge themselves of erroneous connections
    • Simulation data show enhanced performance of computer neural networks with reverse learning,
    • Mammals without REM sleep have large brains for their body size-can’t undo learning as well.
  • Bottom Line: REM sleep allows memory consolidation and erasing what you don’t need to remember.
slide27

Sleep medications?

  • Sleep medications can alter state of consciousness by altering function of the LH neurons
  • Antihistamines: block histamine receptors in LH pathway
    • pass through blood brain barrier
    • block histamine receptors in LH/arousal pathway and thus shut down hypocretin pathways
  • Other agents enhance GABA activity in LH/arousal pathway
    • Thus are also inhibitory
    • Include:
      • Barbiturates:
      • benzodiazepines,
      • Alcohol
      • most gaseous anesthetics
  • Note: These all disrupt REM sleep and the sleep cycle
    • little to no memory consolidation/erasure
    • Poor restorative sleep