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PCL200 > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

what is a hypnotic

A

drug that induces sleep

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2
Q

what is a depressant

A

a drug that reduces neuron activity (and arousal)

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3
Q

what is a stimulant

A

drug that promotes wakefulness and arousal

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4
Q

t/f we do not know if lower lifeforms such as insects sleep

A

true

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5
Q

rapid eye movements during sleep are found only in

A

mammals and birds (warm blooded vertebrates)

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6
Q

what does an EEG do

A
  • Records electrical activity in the head
  • When neurons fire an action potential, it is electricity that can be picked up by an electrode
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7
Q

can tell a person’s level of consciousness by

A

the power of their brainwaves

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8
Q

a synchronized wave is

A

usually high power

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9
Q

when these neurons all fire at the same time

A

it is a big peak and a big trough, making it a high power wave

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10
Q

we describe stages of sleep based on

A

the patterns of neural activity in the brain and features of body physiology (muscle tone, heart rate, breathing rate, body temperature)

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11
Q

beta activity

A

when you are very concentrated

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12
Q

alpha activity

A

very typical when you are awake, but are not thinking too much

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13
Q

theta activity is

A

light sleep
- Breathing rate is similar to when we are awake
- Heart rate is also similar
- Easy for us to wake up

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14
Q

sleep spindle

A
  • Important for progressing into deep sleep
  • Stage two sleep
  • Can be roused, but not as easy as theta activity
  • Could also have dreams
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15
Q

K Complex

A

important for mental housekeeping

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16
Q

delta activity

A
  • Deep sleep
  • Waves are synchronous and high power
  • Slowest frequency our brain does
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17
Q

N1 is

A

light sleep with normal breathing and heart rate (brief)

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18
Q

N2 shows

A

sleep spindles, K complexes, and some delta waves. Breathing & heart rate slow, body temp drops.

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19
Q

N3 is

A

deep sleep characterized by long stretches of delta waves

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20
Q

REM Sleep

A

skeletal muscles are paralyzed, breathing shallow and faster. EEG patterns similar to those of wake or light sleep.
- Our brains actually look awake

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21
Q

a typical sleep cycle is

A

about 90 minutes, but the length of time spent in (NREM) sleep and REM sleep varies through the night, with more NREM initially, and more REM sleep towards morning.

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22
Q

sleep time breakdown for age

A
  • Newborns: 8 hours of REM, average 16 hours of sleep per day
  • In 20’s: 2 hours of REM, average of 8 hours of sleep per day
  • In 80’s: 45 minutes of REM, average of 6.5 hours of sleep per day
23
Q

why do we sleep

A
  • Evolutionary argument does not hold
  • Brain needs sleep and rest, which is why we sleep
  • Acute sleep deprivation does not adversely affect other organs but causes cognitive impairments and increased emotionality.
24
Q

chronic insufficient sleep (less than 7 hours) is associated with

A

increased risk of diabetes, cardiovascular disease & cancer.

25
Q

fatal familial insomnia

A

neurodegenerative disease affecting the thalamus and other brain regions, caused by a mutation in the PRNP gene. Midlife onset, progressive inability to sleep is fatal.
- Use of hypnotics does not appreciably change course of illness and death occurs 6-36 months after onset.

26
Q

Rechtshaffen Experiment

A

rats deprived of sleep will die in 3-4 weeks – eat more, lose weight, cannot thermoregulate, death

27
Q

Preventing NREM sleep causes

A

a stronger “sleep pressure” and the brain subsequently spends more time than usual in NREM sleep.

28
Q

Preventing REM Sleep

A

does not create the same sleep pressure, but memory consolidation and retrieval are impaired.

29
Q

t/f there are physiological functions for both NREM and REM sleep

A

true

30
Q

what are the physiological functions for NREM sleep

A

Clear the by-products of metabolic activity – glymphatic system moves fluid 3X faster during slow-wave sleep.

31
Q

what are the physiological functions for REM sleep

A

consolidate memories and forget unimportant events

32
Q

why do we dream (5 things)

A
  • Dreams occur in both REM and NREM sleep, but the quality of the dreams are different.
  • REM dreams are more vivid, story-like, and remembered upon waking.
  • Elements of dream often touch on aspects of events or thoughts of the day.
  • The brain can review & rehearse newly learned skills & facts.
  • Nightmares may serve a function of practicing one’s reaction to worst-case scenarios.
33
Q

external and internal factors that affect sleep onset and duration

A
  • Time of day
  • Light
  • Noise
  • Environment (novelty & stress = dopamine & norepinephrine = wakefulness)
  • Release of melatonin from pineal gland
  • Body temperature
  • Accumulation of adenosine in CSF
34
Q

Increasing the firing of these neurons or increasing the synaptic levels of the neurotransmitters will promote (related to sleep)

A

wakefulness

35
Q

Decreasing the firing of these neurons will promote

A

sleep

36
Q

adenosine promotes

A

sleep

37
Q

adenosine binds to

A

adenosine receptors in the sleep area of the brain and this causes the sleep- on neurons to fire.

38
Q

to induce sleep

A

inhibit the neurons that promote wakefulness (orexin, dopamine, serotonin, norepinephrine, histamine)

39
Q

One way to promote sleep is to increase

A

GABA neurotransmission

40
Q

what two drugs increase GABA signalling

A

Benzodiazepines and Barbiturates

41
Q

example of benzos

A

diazepam, lorazepam

42
Q

example of barbiturates

A

phenobarbital

43
Q

low dose benzo

A
  • The inhibitors are inhibited.
  • Dopamine neurons are free to fire!
44
Q

high dose benzo

A
  • Both the inhibitor and the dopamine neurons are inhibited.
  • Arousal level - low
45
Q

Benzos increase GABA signalling by

A

increasing the frequency of GABA channel opening.

46
Q

natural agonist for GABA channel is

A

neurotransmitter GABA

47
Q

Benzos and GABA interaction

A
  • Benzodiazepines bind to a different site on the receptor.
  • Benzos don’t bind to the exact same site as GABA – they amplify the effects of GABA.
  • For the purposes of this class, we describe them as GABA receptor agonists
48
Q

what is the target receptor for benzos

A
  • The GABA-A receptor (the GABA-A channel)
  • They are agonists – they make the channel more likely to open.
49
Q

Which class of drugs is considered safer, benzos or barbiturates

A

Benzodiazepines are safer than barbiturates. They are less likely to cause a lethal overdose. There is also a drug that can counteract a benzodiazepine (called flumazenil), but there is no drug to counteract a barbiturate overdose.

50
Q

When these drugs bind to their receptor, does it cause the neuron to fire more or less frequently

A

They make the neuron less likely to fire. The therapeutic effects (promoting sleep) are due to the quieting effects of these drugs on neurons in the reticular activating system, the thalamus, and the cortex. The anxiolytic effects are due to quieting neurons in the amygdala.

51
Q

What are the unwanted side effects of benzodiazepines

A
  • Benzodiazepines can cause amnesia (memory loss), cognitive impairment, motor impairment (falls, car accidents), sleepiness in the morning (hangover), and stomach upset.
  • They can also cause tolerance to the drug’s effect (it no longer works to promote sleep and a higher dose is needed).
  • They can cause physical dependence, so that withdrawal symptoms occur when people stop taking the drug.
  • Withdrawal symptoms include irritability, insomnia, and anxiety.
  • They can cause addiction, where the person has a craving to take the drug.
52
Q

Which sleep-aid causes parasomnias like driving a car while asleep

A
  • Zolpidem (Ambien) can cause parasomnias (doing unusual things while asleep). These include sleepwalking, sleep-cooking, sleep-eating, sleep-conversations, sleep-showering, sleep-texting, sleep- driving, and sleep-sex. There is usually anterograde amnesia – where the person has no memory of the events.
  • Women and men metabolize Ambien differently. Women are now prescribed a lower dose than men.
53
Q

New pharmacotherapies for insomnia 1

A
  • Orexin receptor antagonist – suvorexant.
  • FDA approved for treatment of primary insomnia.
  • Decreases latency to sleep onset and latency to persistent sleep.
    Does not cause tolerance, dependence, or addiction.
54
Q
A

PCL200 (6 decks)

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