Bio - Module 7

• Sleep


  A behaviour - a change in consciousness
• Sleep research


  • Most done in sleep labs
  • Measures EEG (brain waves)
  • EMG (muscles)
  • EOG (eyes)
  • Heart rate
  • Respiration
  • Skin conductance
• EEG


  Measures summed electrical activity - "brain waves"
• Synchronized neural activity


  Produces large, clear waves in EEG data
• Desynchronized neural activity


  Produces small, chaotic waves without clear patterns in EEG data
• Sleep stages


  • Wakefulness stage (stage W)
  • Non-REM sleep stage 1
  • Non-REM sleep stage 2
  • Non-REM sleep stage 3
  • REM sleep stage (Stage R)
• Alpha waves


  Regular, medium-frequency waves of 8–12 Hz associated with resting wakefulness
• Beta waves


  Irregular, mostly low-amplitude desynchronized waves of 13–30 Hz associated with increased alertness and attention
• Theta waves


  More synchronized neural activity of 3.5-7.5 Hz, experienced hypnic jerks, lasts about 10 mins
• Sleep spindles


  Periods of theta activity in stage 2 NREM sleep
• K complexes


  Periods of theta activity in stage 2 NREM sleep
• Delta waves


  High amplitude, synchronized activity < 3.5Hz, characteristic of slow wave sleep
• REM sleep


  Abrupt change in EEG, becoming desynchronized, rapid eye movements, paralysis, dreams, easily awoken by meaningful stimuli
• Brain activity during sleep is not the same as unconsciousness
• Brain activity during REM sleep

  • Increased blood flow in extrastriate cortex (visual)
  • Decreased blood flow in striate (primary) visual cortex and prefrontal cortex (PFC)
  • Lucid dreaming may involve active PFC, awareness that your are dreaming
• Brain activity during slow-wave sleep

  • Generally decreased blood flow throughout the brain, but localized increases in visual and auditory cortexes
• Sleep is universal across species
• Sleep deprivation


  • Negatively impacts cognition, especially attention control
  • Related to negative health outcomes like diabetes, hypertension, stroke, and depression
• After sleep deprivation, some sleep hours can be regained over following nights, but not all
• Fatal familial insomnia

  • is an inherited neurological disorder that causes progressive insomnia and is eventually fatal
  • declines cognitive function, ANS and endocrine system impacted
  • decrease K complexes, sleep spindles (Stage 2)
  • over time, no SWS is observed on EEG and only occasional bursts of REM observed (muscles aren't paralysed)
• Increased neural activity


  Increases slow-wave sleep
• Declarative memory


  Explicit memory of facts and events
• Nondeclarative memory


  Implicit memory of procedural skills
• REM sleep


  Helps consolidate nondeclarative memory
• Slow-wave sleep


  Helps consolidate declarative memory
• The brain rehearses information learned during wakefulness during slow-wave sleep
• Thoughts related to a task during slow-wave sleep are associated with better performance on that task
• Wamsley and colleagues (2010)

  • Asked people to complete a virtual reality navigation task, then woke participants from SWS during their afternoon nap. Participants who had thoughts relating to the task upon waking performed better on a subsequent navigation task.
• Even though people often don't say they are dreaming during SWS, we can see that the brain rehearses previously acquired information during this stage.
• Adenosine, a type of neuromodulator, has been found to promote sleep.
• Sleep Regulation: Adenosine


  1. Astrocytes store glycogen

  2. Increased brain activity converts glycogen into neuron fuel

  3. Staying awake decreases glycogen levels

  4. Glycogen decrease increases extracellular adenosine

  5. Extracellular adenosine inhibits neural activity and encourages sleep

  6. During SWS, astrocytes can replenish glycogen levels
• Adenosine triphosphate (ATP) is related to glycogen, neuron fuel, and adenosine.
• Neurotransmitters important for wakefulness

  • Acetylcholine
  • Norepinephrine
  • Serotonin
  • Histamine
  • Orexin
• Acetylcholine (ACh)


  Some ACh neurons produce activation and cortical desynchrony when stimulated, other ACh neurons control activity of the hippocampus. High levels of ACh during waking and REM sleep, low levels during SWS.
• Norepinephrine (NE)


  Pathways originating from the locus coeruleus (LC) of the pons project widely throughout the brain and release NE to modulate wakefulness. NE neural activity is high during wakefulness, low during SWS and almost non-existent during REM. Important for vigilance.
• Serotonin (5-HT)


  1. HT neurons are most active when awake, less active during SWS, and largely inactive during REM. Most 5-HT neurons are in the raphe nuclei of the reticular formation and project widely.
  2. Activating raphe nuclei causes movement and cortical arousal while PCPA (stops 5-HT production) reduces cortical arousal
• Histamine


  Histamine neurons are found in the tuberomammillary nucleus (TMN) of hypothalamus. High activation during waking, low activation during SWS and REM sleep. Histamine neurons send messages to the cortex and ACh neurons to increase arousal. They also send messages to ACh neurons in the basal forebrain and pons which increase the release of cortical ACh and indirectly increase arousal
• Orexin (hypocretin)


  Orexin is a peptide neurotransmitter. Orexin neuron cell bodies are found in the lateral hypothalamus. These neurons send excitatory messages to almost every part of the brain to increase alertness/wakefulness. High firing rate during alert/active waking, low rate during SWS and REM sleep. Damages orexin neurons = narcolepsy (a sleep disorder)
• Neural Control of Sleep/Waking Transitions

  1. Preoptic area of hypothalamus is crucial for controlling arousal neurons

  2. Preoptic sleep neurons send inhibitory GABA messages to arousal neurons

  3. Arousal neurons also send inhibitory messages to preoptic sleep neurons

  4. This forms a flip-flop circuit with mutual inhibition between sleep and arousal neurons

  5. Flip-flop changes happen quickly, allowing for clear transitions between sleep and wakefulness

  6. Orexin neurons stabilise the flip-flop circuit by exciting arousal neurons
• What Activates Orexin Neurons?

  1. Receive excitatory messages from brain regions controlling circadian rhythms

  2. Receive excitatory messages from brain regions indicating hunger

  3. Receive inhibitory messages from ventrolateral preoptic area (vlPOA) driven by adenosine accumulation