1
Q
Waking
Stage W
A
Alpha and Beta-activity
–> Beta activity is desynchronized
2
Q
Desynchrony
A
- reflects the fact that many different neuronal circuits are actively processing information
- occurs when a person is alert
- -> Beta-activity
3
Q
Stage 1 sleep (NREM 1)
A
Theta-activity
--> firing of neurons in the neocortex is becoming more synchronized
Transition between sleep and wakefulness
(10min)
4
Q
Stage 2 Sleep (NREM 2)
A
Theta activity
Sleep spindles: play a role in consolidation of memories
K-complexes: triggered by noises
(15 min)
5
Q
K-complexes
A
- triggered by noises/occur in response to a stimulus
- large waveforms in EEG
- forerunner of delta waves
6
Q
Sleep spindles
A
play a role in the consolidation of memories
--> short bursts of waves
7
Q
Stage 3 Sleep (NREM 3)
Slow wave sleep
A
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)
8
Q
REM-Sleep
A
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
9
Q
Functions of slow wave sleep
A
- 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
10
Q
Effects of sleep deprivation
A
- cognitive abilities are effected
- -> perceptual distortions
- -> hallucinations
- -> trouble concentrating
- one never regains all the sleep one lost
- causes increase in free radicals
11
Q
Free radicals
A
- 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
12
Q
Oxidative Stress
A
- 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
13
Q
Fatal familial insomnia
A
damage to portions of the thalamus
–> disappearance of slow wave sleep + only brief episodes of REM sleep without paralysis
14
Q
Functions of REM Sleep
A
promotes brain development
- facilitates the consolidation of nondeclaractive memories
15
Q
Rebound Phenomenon
A
After sleep deprivation
--> when permitted to sleep normally there is a higher-than normal percentage of REM sleep in the recovery night
16
Q
Nondeclarative memories
A
Memories gained through experience + practice
e.g.: learning to drive a car, recognizing a face, throw a ball
17
Q
Declarative memories
A
Memories of past episodes of ones life, memories one can talk about
Memories of the relationships between a stimuli or events
18
Q
Adenosine
A
- sleep promoting substance that accumulates during waking and is destroyed during sleep
- plays the primary role in the control of sleep
19
Q
Neural control of sleep
Procedure
A
- 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
20
Q
Role of caffeine
A
- antagonist
- blocks adenosine receptors to prevent sleepiness
- only works when there is actual sleep deprivation
21
Q
Neural control of arousal
–> What are the systems involved ?
A
Five systems of neurons are of importance for alertness and wakefulness
- -> Acetylchonergic System - -> Norodrenergic System - -> Serotonergic System - -> Histaminergic System - -> Orexinergic System
22
Q
Acetylchonergic System
A
- 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
23
Q
Norodrenergic System
A
- located in the locus coeruleus ( dorsal pons )
- stimulation causes immediate waking ( vigilance )=> high firing rate during
–> waking
24
Q
Serotonergic System
A
- located in the raphe nuclei ( reticular formation )
- stimulation causes locomotion and cortical arousal=> high firing rate during
–> wakefulness
25
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
=> control of wakefulness is shared with other neurotransmitters
26
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
27
Homoestatic control
Mainting the balance of sleep/wake at an optimal level
28
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
29
Cicardian Control
Entraining periods of sleep to particular portions of light/dark cycle
30
Preoptic Area
- suppresses the activity of the arousal neurons when active
| - -> most involved area in sleep
31
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
32
REM Flip Flop
- controls cycles of Rem Sleep and Slow wave sleep
| - REM on + off regions are interconnected by GABA neurons
33
Primary Insomnia
Difficulty falling asleep after going to bed or waking during the night
34
Secondary Insomnia
Inability to sleep due to another mental/physical condition such as pain
35
Sleep Apnea
Inability to sleep and breathe - caused by an obstruction of the airway
--> particular form of Insomnia
36
Nonpharmalogical treatment
Cognitive behavior therapy, changes in sleep hygiene, etc.
37
Pharmalogical treatment
drugs (hypnotics)
| --> Agonists at the GABAa Receptor
38
Narcolepsy
sleep at inappropriate times
39
Sleep attack
overwhelming urge to sleep caused by boring conditions
--> symptom of narcolepsy
40
Cataplexy
- Sustaining varying amounts of muscle weakness, sometimes completely paralyzed (inhibition of the motor neurons)
- caused by strong emotions
- -> symptom of narcolepsy
41
Sleep paralysis
Inability to move just before the onset of sleep, or on waking in the morning
42
Hypnagogic Hallucinations
Dreaming, while lying awake, paralyzed
| --> lucid dreaming
43
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
44
REM sleep behavior disorder
failing to exhibit paralysis during REM
| --> opposite to cataplexy
45
Cicardian Rhythm
Cycle of approximately 24h, that controls sleep/wake, physical activity and body temperature
--> located in the SCN
46
Zeitgeber
Illumination/light keeps the inner clock adjusted to 24h
--> Light synchronizes the endogenous rhythm
47
Suprachiasmatic Nucleus (SCN)
- provides the primary control over timing of sleep cycles
| - -> receives input from the visual system
48
Melanopsin
Special photoreceptor that provides information about the level of light that synchronizes cicardian rhythms
--> present in the ganglion cells
49
Ganglion cells
Neurons that transmit information from the eyes to rest of the brain
50
Pineal Gland
- controls annual rhythms
| - secretes melatonin
51
Melatonin
- secreted during the night
ex. : during longer night (winter) - more secretion
- can alter the cicardian rhythm
52
Effects of shift work and jet lag
- disparity between internal rhythm + external environment
53
Solution to jet lag and shift work
providing Zeitgebers at appropriate times
ex.: exposure to bright lights
54
Molecular Clock in mice
| Procedure
1. Proteins clock + cycle bind together and form a dimer
2. Dimer binds to DNA
- -> enhances ttranscription of the genes Period + Cryptochrome
3. Per + Cry bind together as a complex
- -> inhibits activity of the Clock/cycle dimer
- -> slows down the transcription of per + cry
4. Per + Cry proteins eventually break down
- -> inhibition of the dimer stops
5. Whole cycle starts again
Body & Behaviour
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