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28 Cards in this Set

  • Front
  • Back
In the waking state, what does the thalamus do? x3
1. Cortical activation
2. Sleep spindles
3. EEG synchronization
What provides the sleep/wake switch?
What provides the REM/SWS switch?
What provides the circadian clock in our brains?
Suprachiasmatic nucleus
In Sleep/Wake, where do the following NT's come from?

- Histamine
- Dopamine
- Serotonin
- Norepinephrine
TMN Tuberomammillary nucleus

VTA Ventral Tegmental Area

Raphe's nucleus

Locus Ceruleus
Hypocretins are made where?
Lateral hypothalamus
What does hypocretin system do?
Maintains/reinforces alertness

by increasing activity of all major ascending arousal systems.
T/F - Hypocretin receptors (Hcrt-1 and Hcrt-2) are always excitatory.
Where is the major sleep promoting area of the brain, and how does it promote sleep?
VLPO of the anterior hypothalamus

uses GABA to inhibit all major wake-promoting regions.
What are the major wake promoting regions? x4
Suprachiasmatic nucleus
REM sleep is controlled by a subpopulation of _________ neurons in the __________ . These are called " ________ " neurons.


What does it mean that the REM sleep system is of "dual projections."
Cholinergic REM-on neurons activate the thalamocortical system , leading to fast EEG resembling waking state EEG.

REM-on neurons also descend to activate neurons in the medial medulla to inhibit motor neurons using Glycine and GABA.
What are the key differences between REM sleep and wakefulness.x2
1. Complete absence of activity in the wakefulness-promoting aminergic pathway during REM sleep.

2. Loss of muscle tone (atonia) during REM sleep.
Aminergic neurons can be found where?
Brainstem and posterior hypothalamus
Modafinil does what?

Give example of Modafinil.
Block reuptake of dopamine (wakefulness promoting) and NE (inhibits sleep promotion), thus promoting wakefulness by hitting that shit on both sides.

T/F - Alerting agents improve and normalize sleepiness.
False - Improving sleep yes, but not normalize.
Use of alerting agents such as amphetamines and methylphenidate leads to what? x2

Rebound hypersomnolence
Mechanism of Benzodiazepines.
Binds to BZD1, BZD2, and BZD3 nonspecifically.
Mechanism of Nonbenzodiazepines (Z drugs).
Preferential binding to BZD-1
Which BZD receptor is primary for sedative and hypnotic effects?
What do hypnotic drugs do to sleep stages.
Decrease stage 1, 3, and 4

Increase stage 2

Decrease percentage and density of REM sleep, while increasing REM latency.
What are the clinical implications of hypnotic short half-life?
Rebound Insomnia
Anterograde Amnesia
What are the clinical implications of hypnotic long half-life?
Daytime Sedation
Contraindications for hypnotic use. x3
Sleep Apnea

EtOH excessive

Potential for alertness during sleep periods.
When would you recommend Flurazepam (Dalmane)?
For patients who need early morning awakening, and needing to deal with anxiety.
Which sleep med has a potential for amnesia, anxiety, and rebound insomnia?

a.) Flurazepam
b.) Zolpidem
c.) Zaleplon
d.) none of the above
c.) Zaleplon (Sonata)

is the shortest half life hypnotic. May cause all these symptoms including headache, weakness, drowsiness, and dizziness.
What are the treatment strategies x2 for transient insomnia?
1.) use lowest effective dose of BZD

2.) half life matches the desired duration
Zolpidem (Ambien) binds to which receptor?
BZ1 mostly