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Terms in this set (24)
What is the trend in hours of sleep we require as we age?
We need less and less as we get older!
What are some general complications of not getting enough sleep?
- Heart disease
- Type 2 diabetes
What are two of the major theories/roles for sleep?
1.) Learning and memory consolidation
2.) Repair and Restoration
What is the brain "circuit" associated with sleep? (Where specifically does it begin? What is the result of the circuit?)
1. Light stimuli at ganglion cells --->
2. Glutamate (excitatory) signaling to SCN (suprechiasmatic nucleus) --->
3. Pineal Gland stimulated, release of MELATONIN
4. Increase in sleepiness
What is the result of damage to the SCN (Suprachiastmatic nucleus)
The SCN is the body's biological clock. Thus, damage to the SCN will result in less consistent body rhythms that ARE NOT SYNCHRONIZED to LIGHT AND DARK.
What is the normal time period before sleep that melatonin is released? What effect does taking melatonin pills have?
2 - 3 hours before sleep. Melatonin pills can essnetially "phase-advance" your sleep if taken 2-3 hours before you want to sleep!
What is the "feedback" of melatonin on SCN?
It resets the biological clock through its effects on the receptors of SCN
What is the specific photopigment in the ganglion cells of the eyes that are associated with the retinohypothalamic path?
What is used to detect brain waves during sleep?
What brain "rythmns" are indicative of awake & activated cortex?
Beta rythmns >14Hz . High frequency, low amplification.
What brain "rythmns" are indicative of quiet, waking (daydreaming) in cortex?
Alpha rythmns: 8-13 Hz
What brain "rythmns" are associated with deep, restorative sleep? Describe their waves: ________ amplitude and _________ frequency
Highest amplitude & Lowest frequency (than any other brain rythmn)
Stage 1 sleep: what waves? how are they different than waking?
Alpha waves - higher amplitude, lower frequency than waking
Stage 2 sleep: what waves? special characteristics?
Alpha waves - with K-complexes (single, large amplitude) and sleep spindles (many low amplitude signals in fast succession)
Stage 3: characteristics?
The "lull" - waves become higher in amplitude, indicating greater cortical SYNCHRONY
Stage 4: What waves? What is significant about this stage?
Delta waves. This stage is significant in "restoration" and memory consolidation
The EEG waves of an awake individual. However, there is complete muscle paralysis. Eyes dart back and forth underneath eyelids.
Mix of brain state of excitement, yet muscular immobility - "paradoxical sleep"
What is the standard cycle of sleep?
Initially: 1, 2, 3, 4
After one hour sleeping: 4 -> 3 -> 2 -> REM (repeats every 90 minutes).
Describe the length of Stage 3 & 4 as a sleep session progresses.
Initially: stage 3 & 4 predominate
Later stages: REM predominates, stages 3 & 4 become very short
Orexin: Where is it located? What is its function? Additional importance?
Localization: Lateral hypothalamic area (LHA) and posterior hypothalamus (PH)
Function: arousal - sends excitatory projections to entire CNS.
Additional: stimulates feeding behavior
What area of the brain counters the actions of Orexin released from the lateral hypothalamic area & posterior hypothalamus? How does it do so?
The VLPN or VLPO: Ventrolateral Preoptic Nucleus
Is always active, however in ABSENCE OF EXCITATORY STIMULATION TO OREXIN nuerons such as limbic system/SCN (light!)/Energy balance:
Sends inhibitory projections to monoaminergic neurons (serotonin/dopamine/norepinephrine) and orexin neurons which MAINTAINS SLEEP STATE. Only a small amount of excitation to thalamus/cortex is present in sleep state.
What is the mechanism of maintaining the awake state?
Limbic system/SCN (light!)/Energy balance --
excitation --> Orexin -- > excitation --> monoaminergic neurons (serotonin/dopamine/norepinephrine)
Then all these happen:
1. monoaminergic neurons --> inhibition --> orexin
2. monoaminergic neurons --> inhibition --> VLPO (sleep center)
3. monoaminergic neurons --> excitation --> thalamus/cerebral cortex --> wakefulness!
Damage / no presence of Orexin neurons.
This causes mutually inhibitory circuit between monaminergic neurons and VLPO - this causes ABRUPT switches between states when one side of the "equation" outcompetes the other!
Insomina: what is it? what are causes? how can we fix the problem?
It is: impairment in ability to sleep
Causes: Anxiety/emotional problems (think: limibic stimulation to orexin). Health / drugs.
Solution: Sleeping drugs. Relieve stressor in life.
Reconditioning procedures!: no naps / strict waking
Deep breathing from diaphragm
Cognitive Behavior Therapy: changing the belief about an event can change the effect of the event!
THIS SET IS OFTEN IN FOLDERS WITH...
Memory & Learning
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