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A Intro to Neuro > Brain Rhythms & Sleep > Flashcards

Brain Rhythms & Sleep Flashcards

1
Q

Outline of topics in rhythms and EEG

A
  • Neural basis of EEG
  • Synchronization
  • Epilepsy and seizures - categories and typical neural activity
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2
Q

Outline of topics in sleep

A
  • REM, NREM, Stages
  • Effects of sleep deprivation, Fatal Familial Insomnia
  • Sleep and learning
  • Sleep and glymphatic house cleaning
  • Neural and chemical regulation of sleep
  • Dreams and ream readout
  • Sleep disorders
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3
Q

EEG in synchronized activity

A
  • In synchronized activity, signals can summate to form a low-frequency and large-amplitude EEG
  • Typically associated with a relaxed or sleeping brain
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4
Q

A low-frequency and large-amplitude EEG is typically associated with a ___ or ___ brain

A

Relaxed or sleeping

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5
Q

EEG in desynchronized activity

A
  • In desynchronized activity, the sum of the out-of-sync activity does NOT lead to a big change in amplitude of signal so there is a high-frequency and low-amplitude EEG
  • Typically associated with an active brain
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6
Q

Peter the tiny horse is tired after a semester of torturing NEUR 10 students so he decides to take a nap before the big final exam. Which of these matches how his brain waves would look on an EEG when he’s just fallen asleep?

a) Low frequency, high amplitude waves
b) Low frequency, low amplitude waves
c) High frequency, low amplitude waves
d) High frequency, high amplitude waves

A

a) Low frequency, high amplitude waves

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7
Q

What are the two ways in which large sets of neurons can produce synchronous activity?

A
  • Relying on a pacemaker: thalamus
  • Oscillator circuit
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8
Q

Explain how large sets of neurons can produce synchronous activity by relying on a pacemaker

A

Relying on a pacemaker (central clock): The thalamus often acts as a very powerful pacemaker (has specialized VG ion channels that allow for generation of very rhythmic, self-sustaining discharge patterns even without input)

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9
Q

Explain how large sets of neurons can produce synchronous activity by using an oscillator circuit

A

Oscillator circuit: relying on the collective behavior of neurons by collectively exciting or inhibiting each other

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10
Q

How is Peter’s brain generating these synchronous waves so that the EEG can read electrical changes from a whole population of neurons?

a) The waves align with his snores
b) The thalamus acts as a pacemaker
c) Inhibitory and excitatory cells in the oscillator circuit regulate rhythm
d) Interneurons that switch the sign for all neurons in a circuit
e) More than one of the above

A

Answer: E, both B and C are correct

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11
Q

Generalized tonic-clonic seizure (Grand Mal)

A
  • Sudden onset
  • Tonic phase
  • Clonic phase
  • Can have one or both of these
  • Recovery is from minutes to hours
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12
Q

Tonic phase of seizure

A

Comes first, limb stiffening (in extreme cases, you stop breathing because muscles contract so strongly)

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13
Q

Clonic phase of seizure

A

Rapid contraction of muscle

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14
Q

How long is recovery from tonic-clonic seizure?

A

Minutes to hours

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15
Q

Complex partial/focal seizures

A
  • Aura precedes the seizure (abnormal light, hallucinations (usually depends on what sensory area the lesion is in))
    ○ TEMPORAL seizures are the most common
    type
  • Van Gogh and Dostoyevsky: called
    complex partial seizures “ecstatic seizures”, may have caused euphoria and powerful feelings of being connected to a higher power, occurred in their temporal lobes
  • Has a gradual start/stop
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16
Q

Onset and end of complex partial/focal seizure

A

Gradual start/stop

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17
Q

What is the most common type of complex partial/focal seizure?

A

Temporal seizure

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18
Q

A patient comes in reporting episodes of a sensation of “ecstasy” followed by tingling in his arm and then numbness along the entire R side of his body. What are the most likely diagnosis of these episodes?

a) grand mal seizures
b) Complex partial seizures
c) Narcolepsy
d) Fatal Familial Insomnia

A

b) Complex partial seizures

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19
Q

Causes of seizures

A

There are many causes: Head trauma, tumors, stroke, Alzheimer’s, some genetic forms generally affecting ion channels (increased excitatory activity or reduced inhibitory activity), withdrawal from certain depressant drugs (ex. alcohol), convulsants (seizure-promoting agents through actions like blocking GABA channels) BUT most of the time the cause is unknown

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20
Q

Treatments for seizures

A
  • Anticonvulsive drugs (helps 2⁄3 of patients): Shifting the balance of
    excitation and inhibition i.e. block sodium channels, block glutamate
    channels, inhibit metabolism of glutamate
  • Surgical resection (extreme cases ex. poor Patient HM)
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21
Q

All of the following are treatments that one would expect to decrease brain seizures EXCEPT:

a) Increase glutamate reuptake
b) Block Na+ channels
c) Block glutamate receptors
d) Block GABA receptors

A

d) Block GABA receptors

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22
Q

Sleep cycle graph

A
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23
Q

Sleep Cycle

A
  • Body cycles between light sleep and deep sleep throughout the night (with decreasing phases of deep sleep as the night progresses)
  • About 5-7 cycles per night
  • When sleeping, you first enter NREM stage 1
  • As the night progresses, there is a general reduction in NREM sleep and increase in REM (50% of REM occurs in the last 1/3 of the night)
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24
Q

__% of REM occurs in the last __ of the night

A

50% in the last 1/3 of the night

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25
Q

When you fall asleep, what stage do you first enter?

A

NREM stage 1

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26
Q

NREM sleep

A
  • 75% of sleep
  • Increased parasympathetic activity (lower heart rate, BP, O2 usage), temperature and energy consumption of the body are lowered
  • Some muscle tone and some movement
  • 3-4 stages make up NREM sleep
  • Slow or no eye movements
  • EEG shows low frequency and high amplitude activity
  • Rate of energy use, the general viring rates of its neurons, and ‘general mental processes’ hit their lowest point of the day
  • Occasional dreams (like a snapshot)
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27
Q

REM sleep

A
  • 25% of sleep
  • Increased sympathetic activity (sometimes even higher than when awake)
  • Temperature control systems ‘quit’ so temperature continues to shift downwards, heart and respiration rates increase but become irregular
  • Very floppy muscle tone i.e. REM atonia, from inhibition of lower motor neurons → paralyzed (movement commanded but not carried out)
  • Interspersed between the stages of NREM sleep (don’t begin at REM sleep)
  • Rapid eye movements
  • “Paradoxical sleep”: The EEG looks awake (high freq and low amplitude)
  • Complex dreams
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28
Q

What accounts for REM atonia in REM sleep?

A

Inhibition of lower motor neurons

29
Q

Which of the following are true during late night sleep

a) Increase in REM sleep over NREM sleep
b) You are more likely to get sleep paralysis
c) More eye movement in your sleep
d) You will have more low frequency, high amplitude sleep compared to high frequency, low
amplitude sleep

A
30
Q

Which are some theories on why we need sleep?

a) Memory consolidation
b) To avoid the dangers of the scary dark night
c) To rest and digest
d) Clearing toxins in the brain
e) All of the above

A

e) All of the above

31
Q

Sleep deprivation in rats

A
  • Show weight loss, disruption of temperature regulation, dysregulated immune system
  • Most of these symptoms can be linked to hypothalamus→ eventually will just die in a few weeks
32
Q

Randy Gardner

A
  • At 17 years old, wanted to see how long he could stay awake
  • Stayed awake for 11 days
  • Fatigue and irritability after a few days
  • Got tremors, motor problems, nausea, memory difficulty, speech problems
  • Eventually had hallucinations while awake (entry into dream-like activity?)
  • Back to normal after a few days getting sleep
33
Q

Cool sleeping behaviors

A
  • Bottlenose dolphins sleep with only 1 hemisphere at a time
  • Blind Indus River Dolphin must keep swimming b/c of the
    environment it lives in so it gets sleep through many “microsleeps” of 4-6 seconds (add up to 7 hours in a day)
  • Sea otters hold hands when sleeping
34
Q

Short-term impacts of sleep-deprivation in humans

A

Increase in heart attacks when we lose an hour of sleep in daylight savings

35
Q

Medium-term impacts of sleep deprivation on humans

A

Experiment of people sleeping 5 hours a night vs. 8 hours a night
○ Basic physiology: Had higher heart rate, BP, cortisol (measure of stress), increased heart attack risk
○ Weight and hunger: Less leptin and more ghrelin → ate more and weight gain
○ Hormones: Women had a drop in follicular releasing hormones (lowers fertility) and men had a drop in testosterone (almost equivalent to aging 10-15 years)
○ Type II diabetes: Humans with no sign of diabetes put on a low sleep regimen had 40% lower glucose absorption and significant number became pre-diabetic

36
Q

Long-term impacts of sleep-deprivation in humans

A

Many disorders/diseases correlated with amount of sleep (elevated BP, stroke, obesity, etc)

37
Q

Sleep-replay consolidation hypothesis

A

Hypothesis:
1. Replay underlies spatial planning for navigation
2. Replay underlies or enhances memory consolidation

How did we see this:
- Tasks: Hippocampal recordings while rats ran around a track shows different place cells activated
- Finding: these same sequence of place cells were active as the rat paused and during their sleep (online vs offline) at 20x real time speed

38
Q

What is the glymphatic system?

A

Glia + lymphatic system

39
Q

What does the glymphatic system do?

A

System works to clear metabolic waste during sleep

40
Q

Mechanisms of the glymphatic system

A
  • CSF flow: during sleep, cerebrospinal fluid flows into the brain along blood vessels, surrounding neurons in a network-like system
  • Interstitial fluid exchange: CSF mixes with interstitial fluid (fluid between brain cells) to collect waste products
  • Drainage pathways: the mixed fluid and waste exchange exit the brain through perivascular spaces (channels around veins
41
Q

Implications of glymphatic system

A
  • System removes things like beta amyloid which is implicated in diseases like Alzheimer’s
  • In animals, removal of beta amyloid is impaired in Alzheimer’s
  • Also involved in disorders like ALS and Huntington’s
    Loop: old age -> less sleep -> more waste accumulation -> more toxins that harmful to neurons present ->worsening disease pathology
42
Q

Lesion of the reticular activating system while you’re asleep would put the brain into which state

a) NREM
b) REM
c) Wakefulness
d) Ecstasy

A

a) NREM

43
Q

What led to the discovery of the ascending reticular activating system?

A

Stimulation of the midline tegmentum

44
Q

Ascending reticular activating system

A
  • Stimulation of midline tegmentum led to the discovery of ascending reticular activating system
    ○ Stimulation transitioned EEG activity from NREM-like to more active and awake
    ○ Contains neurons (NE, 5-HT, ACh, histamine, hypocretin/orexin) increase their firing rates in anticipation of awakening and during various forms of arousal
    ○ General effects are depolarizing neurons, increasing their excitability, and suppression of rhythmic firing
45
Q

What is adenosine?

A

An endogenous sleep factor

46
Q

What causes the build up of adenosine?

A

Breakdown of ATP

47
Q

Adenosine in sleep and wake cycles

A
  • Levels increase while awake but decrease in sleep (opposite of melatonin)
  • The body has adenosine receptors: Binding adenosine to adenosine
    receptors tends to hyperpolarize neurons (“quieting effect” on body) and
    may affect modulatory systems involved in wakefulness (NE, 5-HT, ACh)
    ● Concentration of adenosine = how much you feel like you need to sleep
48
Q

What are the levels of adenosine and melatonin throughout the day

a) Both peak when you first wake up
b) Adenosine peaks when you first wake up and Melatonin peaks when you are about to sleep
c) Adenosine gradually increases throughout the day while melatonin gradually increases throughout the night
d) Adenosine gradually increases throughout the day while melatonin gradually increases throughout the night

A

c) Adenosine gradually increases throughout the day while melatonin gradually increases throughout the night

49
Q

Caffeine

A
  • Caffeine blocks adenosine receptors (adenosine can’t bind to adenosine receptors and increase sleep pressure) → “trick” the system to feel more awake
  • Adenosine can’t bind to adenosine receptors and cause sleep pressure
  • Peak caffeine effect is 30 minutes after ingestion
  • Half-life is pretty long (5-7 hours)
  • Does NOT affect production of adenosine so once caffeine clears out, all the accumulated adenosine comes back in and binds to receptors →
    “caffeine crash”
50
Q

Melatonin release

A
  • Melatonin release from pineal gland → increase in blood flow (especially in limbs/hands) → drop in core temperature
  • Release starts around dusk and peaks around 4AM
  • Core body temperature peaks in the afternoon and is lowest at night
  • Melatonin release and core body temp are inversely related
51
Q

When is core body temp highest and lowest?

A

Highest in afternoon and lowest at night

52
Q

How are melatonin release and core body temp related?

A

Inversely related

53
Q

Where is melatonin released from?

A

Pineal gland

54
Q

Function of melatonin

A

Its effect on blood flow and body temp do not produce sleep or circadian rhythms, but seem to relay circadian information from SCN to the rest of the body: Regulate sleep timing, not sleep production

55
Q

What type of sleep do dreams occur in and what is the evidence for this?

A
  • REM sleep
  • Measurements of brain waves and fMRI shows acitvation of area V1 and higher visual areas when you dream
  • Experiments on fMRI brain activity during dreams show more activation of higher visual areas
56
Q

Experiments on fMRI brain activity during dreams shows more activation of ___

A

Higher visual areas

57
Q

What hormones rise and fall during REM sleep?

A
  • Increase in glutamate and ACh (get active)
  • Decrease in NE and 5-HT
58
Q

Deprivation of just REM sleep

A

Deprivation of only REM sleep has no significant impacts but subjects have REM rebound after

59
Q

Which of the following is there an increase of during the dream stage of sleep

a) Norepinephrine
b) Glutamate
c) Serotonin
d) ACh

A

b) Glutamate
d) ACh

60
Q

How is brain activity different during an exam than in a relaxed state?

a) higher amplitude
b) higher frequency
c) more synchronized

A

b) higher frequency

61
Q

Atonia & REM sleep behavior disorder

A

Loss of REM atonia – move and talk in sleep (during dreams)
* Cause unknown – associated with tumors and withdrawal from alcohol and sedative drugs
* More than 90% of cases are older men
* Treated with sedatives

62
Q

Narcolepsy

A

The three principal symptoms of narcolepsy are:
1. REM sleep attacks – immediate REM sleep rather than a
progression of slow wave sleep first
2. Cataplexy – sudden atonia triggered by intense emotions
(slurred speech, muscle weakness)
3. Sleep paralysis – atonia that extends into the time awake

  • Caused by degeneration of the hypocretin neurons in the lateral hypothalamus. These are also known as orexin neurons which are
    active while awake, feeding, etc (discussed in motivation lecture). In most cases this appears to be an autoimmune disease.
  • Treated with stimulants
  • Hypocretin treatment ineffective (does not cross blood-brain barrier)
63
Q

Cataplexy in narcolepsy

A

Causes a person to become immobile and rigid, with a decreased response to stimuli and pain

64
Q

Over the course of a night’s sleep, time spent in which of the following sleep phases decreases
most dramatically

a) REM sleep
b) Light slow wave sleep
c) Deep slow wave sleep

A

c) Deep slow wave sleep

  • Deep slow wave sleep (stage 3 of NREM) occurs predominantly during the first third of the night. Its duration decreases significantly as the night progresses, and you spend less time in deep sleep during the second half of the night.
  • Light slow wave sleep (NREM stages 1 and 2) and REM sleep dominate the later parts of the night. REM sleep periods become progressively longer and more frequent as the night goes on.
65
Q

Narcolepsy is associated with loss of ___ neurons

A

hypocretin

66
Q

Narcolepsy has all of the following properties except

a) prion disease
b) cataplexy
c) REM sleep attacks

A

a) prion disease

67
Q

Adenosine is thought to promote sleep because

a) it is made in the pineal gland
b) it stimulates glutamate receptors
c) it inhibits diffuse modulatory systems
d) it enhances monoamine neurotransmission

A

c) it inhibits diffuse modulatory systems

Adenosine promotes sleep by inhibiting diffuse modulatory systems such as the noradrenergic, serotonergic, and dopaminergic systems, all of which are involved in maintaining wakefulness. By inhibiting these systems, adenosine contributes to the transition from wakefulness to sleep.

68
Q

Neurons in which diffuse modulatory system increase their activity at the onset of REM sleep

a) ACh neurons in the pons
b) NE neurons in he locus coeruleus
c) serotonin neurons in the raphe nuclei

A

a) ACh neurons in the pons

At the onset of REM sleep, there is a significant increase in the activity of acetylcholine (ACh) neurons in the pons, particularly in regions like the pedunculopontine tegmental nucleus (PPT) and the laterodorsal tegmental nucleus (LDT). These cholinergic neurons play a critical role in initiating and maintaining REM sleep by promoting the cortical activation and the characteristic rapid eye movements.

In contrast:

b) NE neurons in the locus coeruleus: These decrease their activity during REM sleep. In fact, the locus coeruleus becomes almost silent during this phase, as norepinephrine is associated with wakefulness and non-REM sleep.

c) Serotonin neurons in the raphe nuclei: These also decrease their activity during REM sleep. Like norepinephrine, serotonin is more active during wakefulness and non-REM sleep, with minimal activity during REM.

69
Q

Sleep paralysis is a symptom of what disease?

A

Narcolepsy

A Intro to Neuro (22 decks)

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