Problem 6 Flashcards
Waking
Stage W
Alpha and Beta-activity
–> Beta activity is desynchronized
Desynchrony
- reflects the fact that many different neuronal circuits are actively processing information
- occurs when a person is alert
- -> Beta-activity
Stage 1 sleep (NREM 1)
Theta-activity
--> firing of neurons in the neocortex is becoming more synchronized
Transition between sleep and wakefulness
(10min)
Stage 2 Sleep (NREM 2)
Theta activity
Sleep spindles: play a role in consolidation of memories
K-complexes: triggered by noises
(15 min)
K-complexes
- triggered by noises/occur in response to a stimulus
- large waveforms in EEG
- forerunner of delta waves
Sleep spindles
play a role in the consolidation of memories
--> short bursts of waves
Stage 3 Sleep (NREM 3)
Slow wave sleep
Delta-activity
deepest stage of sleep
- -> only loud noises can cause people to wake up - -> when woken up, people are groggy and confused
(60 min)
REM-Sleep
Theta and Beta-activity
person is paralyzed at this stage, because spinal and motor neurons are strongly inhibited
–> one does not react to loud noises, just meaningful stimuli (e.g. name)
when woken up, people are alert and attentive
Functions of slow wave sleep
- brain rests
- Recovery
- -> regions that had highest waves (most active) during wakefulness, have the highest waves during slow wave
- low metabolic rate
- -> permits restorative mechanisms to destroy free radicals
- facilitates the consolidation of declarative memories
Effects of sleep deprivation
- cognitive abilities are effected
- -> perceptual distortions
- -> hallucinations
- -> trouble concentrating
- one never regains all the sleep one lost
- causes increase in free radicals
Free radicals
- unstable molecules that can damage the cells in the body
- -> form when atoms or molecules gain or lose electrons
- accumulate during waking
- contain at least one unpaired electron
Oxidative Stress
- When the body uses oxygen it produces free radicals as a by - product
- Free radicals then bind with the oxygen molecules which results in them splitting into single atoms
–> this causes oxidative stress
Fatal familial insomnia
damage to portions of the thalamus
–> disappearance of slow wave sleep + only brief episodes of REM sleep without paralysis
Functions of REM Sleep
promotes brain development
- facilitates the consolidation of nondeclaractive memories
Rebound Phenomenon
After sleep deprivation
--> when permitted to sleep normally there is a higher-than normal percentage of REM sleep in the recovery night
Nondeclarative memories
Memories gained through experience + practice
e.g.: learning to drive a car, recognizing a face, throw a ball
Declarative memories
Memories of past episodes of ones life, memories one can talk about
Memories of the relationships between a stimuli or events
Adenosine
- sleep promoting substance that accumulates during waking and is destroyed during sleep
- plays the primary role in the control of sleep
Neural control of sleep
Procedure
- Prolonged wakefulness results in a decrease of glycogen
- -> fuel for neurons, produced by astrocytes
- Increase of extracellular adenosine
- -> inhibitory effect on neural activity
- Accumulation of adenosine promotes sleep
- During slow wave
- -> neurons rest
- -> adenosine decreases
- -> Astrocytes renew the stock of glycogen
Role of caffeine
- antagonist
- blocks adenosine receptors to prevent sleepiness
- only works when there is actual sleep deprivation
Neural control of arousal
–> What are the systems involved ?
Five systems of neurons are of importance for alertness and wakefulness
- -> Acetylchonergic System - -> Norodrenergic System - -> Serotonergic System - -> Histaminergic System - -> Orexinergic System
Acetylchonergic System
- 2 groups of ACh neurons are located in pons + basal forebrain
- 1 group is located in the medial septum
- -> controls the activity of the hippocampus
- -> REM - -> waking
Norodrenergic System
- located in the locus coeruleus ( dorsal pons )
- stimulation causes immediate waking ( vigilance )=> high firing rate during
–> waking
Serotonergic System
- located in the raphe nuclei ( reticular formation )
- stimulation causes locomotion and cortical arousal=> high firing rate during
–> wakefulness
Histaminergic System
- located in the tuberomammilary nucleus ( TMN ) of the thalamus
- axons project amongst other regions to cerebral cortex and basal forebrain
- -> increase of cortical arousal due to the release of ACh
Orexinergic System
- located in the lateral hypothalamus
- axons project to all of the regions where the other systems for alertness are located
–> has an excitatory effect on all of the other regions, thus causes the release of their neurotransmitters
=> high firing rate during wakefulness
Homoestatic control
Mainting the balance of sleep/wake at an optimal level
Allostatic control
reactions to stressful events, that serve to override homoestatic control
ex.: in case of danger one is more alert/high attentive even if one is sleep deprived
Cicardian Control
Entraining periods of sleep to particular portions of light/dark cycle
Preoptic Area
- suppresses the activity of the arousal neurons when active
- -> most involved area in sleep
Flip Flop circuit
refers to reciprocal inhibiton - determines when we wake and when we sleep
- -> on: sleep neurons are active, inhibit wakefulness neurons - -> off: wakefulness neurons are active, inhibit sleep neurons
=> mutually inhibitory, impossible that they’re active at the same time
REM Flip Flop
- controls cycles of Rem Sleep and Slow wave sleep
- REM on + off regions are interconnected by GABA neurons
Primary Insomnia
Difficulty falling asleep after going to bed or waking during the night
Secondary Insomnia
Inability to sleep due to another mental/physical condition such as pain
Sleep Apnea
Inability to sleep and breathe - caused by an obstruction of the airway
--> particular form of Insomnia
Nonpharmalogical treatment
Cognitive behavior therapy, changes in sleep hygiene, etc.
Pharmalogical treatment
drugs (hypnotics)
–> Agonists at the GABAa Receptor
Narcolepsy
sleep at inappropriate times
Sleep attack
overwhelming urge to sleep caused by boring conditions
--> symptom of narcolepsy
Cataplexy
- Sustaining varying amounts of muscle weakness, sometimes completely paralyzed (inhibition of the motor neurons)
- caused by strong emotions
- -> symptom of narcolepsy
Sleep paralysis
Inability to move just before the onset of sleep, or on waking in the morning
Hypnagogic Hallucinations
Dreaming, while lying awake, paralyzed
–> lucid dreaming
Physiological basis of Narcolepsy
- caused by a mutation of orexin-B receptor
- -> destruction or complete loss of orexin neurons
- disorder that causes immune system to attack and destroy orexin secreting neurons
REM sleep behavior disorder
failing to exhibit paralysis during REM
–> opposite to cataplexy
Cicardian Rhythm
Cycle of approximately 24h, that controls sleep/wake, physical activity and body temperature
--> located in the SCN
Zeitgeber
Illumination/light keeps the inner clock adjusted to 24h
--> Light synchronizes the endogenous rhythm
Suprachiasmatic Nucleus (SCN)
- provides the primary control over timing of sleep cycles
- -> receives input from the visual system
Melanopsin
Special photoreceptor that provides information about the level of light that synchronizes cicardian rhythms
--> present in the ganglion cells
Ganglion cells
Neurons that transmit information from the eyes to rest of the brain
Pineal Gland
- controls annual rhythms
- secretes melatonin
Melatonin
- secreted during the night
ex. : during longer night (winter) - more secretion - can alter the cicardian rhythm
Effects of shift work and jet lag
- disparity between internal rhythm + external environment
Solution to jet lag and shift work
providing Zeitgebers at appropriate times
ex.: exposure to bright lights
Molecular Clock in mice
Procedure
- Proteins clock + cycle bind together and form a dimer
- Dimer binds to DNA
- -> enhances ttranscription of the genes Period + Cryptochrome
- Per + Cry bind together as a complex
- -> inhibits activity of the Clock/cycle dimer
- -> slows down the transcription of per + cry
- Per + Cry proteins eventually break down
- -> inhibition of the dimer stops
- Whole cycle starts again
