Chapter 19: Brain Rhythms and Sleep Flashcards by Apphia Trillo

(): changes in physiological functions
according to brain clock

Circadian rhythms

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measurement of generalized activity in the cerebral cortex
helps diagnose neurological conditions (e.g. epilepsy, sleeping disorders) ++ research

electroencephalogram (EEG)

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amplitude of EEG signal = measure of () of underlying neurons (particularly dendrite excitation)

synchronous activity

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Recording of miniscule magnetic signals generated by neural activity (one billionth of the magnetic field generated by the Earth, power lines, etc.)

magnetoencephalography (MEG)

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compare MEG, EEG, fMRI, PET

MEG has better localization of neural activity vs EEG
MEG has low (or no) spatial resolution (images); c.f. fMRI and PET
EEG + MEG = fast neuron activity
fMRI + PET = changes in blood flow or metabolism

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EEG rhythms often correlate with particular states of ()

behavior

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categorization of EEG rhythms is primarily based on ()

frequency

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EEG Rhythms

(low, high) synchrony, (low, high) amplitude: alertness and waking OR dream state of sleep

low synchrony, low amplitude

neurons aren’t in sync -> involved in diff aspects of cognitive task

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(low, high) synchrony, (low, high) amplitude: deep, non-dreaming sleep OR coma/drugged states

high synchrony, high amplitude

neurons aren’t engaged in info processing

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2 ways that rhythms can be set in neuronal activity

neurons may take cues from a central clock (pacemaker)
neurons share or distribute the timing function via mutual inhibition or activation

in mammalian brain, both methods coordinate synchronous activity

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() can serve as massive cortical input as a pacemaker

thalamus

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hypothesis on brain rhythm function

sleep rhythms as the brain’s way of ()

disconnecting cortex from sensory input

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hypothesis on brain rhythm function

walter freeman: () coordinate activity of nervous system regions

neural rhythms

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() seizure: entire cerebral cortex, complete behavior disruption, consciousness loss

generalized

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tonic-clonic seizure: () driven by tonic (ongoing) or clonic (rhythmic) patterns

muscle groups

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() seizure: < 30 seconds of generalized 3 Hz EEG waves with subtle motor signs

absence

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() seizure: circumscribed cortex area, abnormal sensation or aura

partial

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partial seizures in the temporal lobe result in:

deja vu, hallucinations

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readily reversible state of reduced responsiveness to, and interation with, the environment

sleep

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() sleep: EEG similar to awake state, only eye nd respiratory muscles move, vivid dreams, high O2 consumption, active sympathetic division

rapid eye movement (REM)

an active, hallucinating brain in a paralyzed body

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() sleep: slow, large amplitude EEG -> sensory inputs can’t reach cortex, low movement and muscle tension, active parasympathetic NS, low body temp and energy consumption

non-REM (slow wave)

an idling brain in a movable body

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body during REM sleep

():body paralzyed except eye and respiratory muscles

REM atonia

almost complete loss of skeletal muscle tone

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describe the 4 stages in a sleep cycle

stage 1: transitional sleep
stage 2: slightly deeer sleep (thalamus-driven sleep spindles)
stages 3-4: deep sleep (slow, low-amplitude)

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compare the first sleep cylce to the later sleep cycles when sleeping

first cycle: stage 1: a few min; stages 2-3: 5-20 min each; stage 4: 20-40 min

later cycles: REM sleep duration increases; non-REM sleep (esp stages 3-4) decreases.

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What is the proper length of sleep? – ()

whatever amount that allows you maintain a reasonable level of alertness during the day

Early teenagers (high school students) have a similar demand for sleep as preadolescents, but fall asleep late due to changes in (1); yet, earlier start of the school day causes (2)

1. circadian timing mechanisms 2. chronic sleep deprivation

All mammals, birds, and reptiles appear to sleep, although only mammals and some birds have a () phase

REM

Sleep mainly for the (1); Sleep deprivation -> (2)

1. brain 2. cognitive impairment

explain sleep in the bottlenose dolphin

~2 h of non-REM sleep on just one side, then 1 h awake on both sides, 2 h of non-REM sleep on the other side, and so on (total 12 h per night)

Two main categories of theories of sleep function

1. restoration - sleep to rest and recover 2. adaptation - avoid trouble, conserve energy

# restoration during sleep 1. () - cells repair and regrow; no sleep -> loss of immune function 2. () - glymphatic (waste clearance) system clears out toxic byproducts; plasticity

1. cellular restoration 2. brain functions

REM sleep deprivation causes () even though REM deprivation does not cause major harm during the day time

REM rebound - sending more time in REM sleep when left to sleep undisturbed

# dream function accdg to Freud dream function -> disguised (): unconscious way to express sexual and aggressive fantasies

wish fulfillment

# dreams accdg to Hobson and McCarley (): Pons, via thalamus, activates various areas of the cortex, and the cortex tries to synthesize the disparate images into a sensible whole ## Footnote explains weirdness, but not recurring dreams

activation-synthesis hypothesis

relationship beteween sleep and memory

- intense learning increases REM sleep duration - REM deprivation prevents performance improvement

Sleep-wake cycle continues without sensory inputs -> Sleep is an ()

active process

() may induce prolonged sleep or prolonged wakefulness

Brainstem lesions

Critical neurons for control of sleep-wake cycle are part of the () systems

diffuse modulatory neurotransmitter

# Critical neurons for control of sleep-wake cycle () neurons: enhance and fire during waking state

NE, 5-HT

# Critical neurons for control of sleep-wake cycle () neurons: some enhance REM events, others are active during waking state

cholinergic

elaborate on how diffuse modultory systems can block sensory input to cortex

DMS can control rhythmic behavior of thalamus -> thalamus acts as pacemaker and influences cortical EEG; sleep rhythms of thalamus block sensory input

sleep also involves activity in () (e.g., inhibition of motor neurons during dreaming)

descending branches of diffuse modulatory systems

# Moruzzi's research relationship of brain stem and sleep

1. lesions in midline of brain stem -> state similar to non-REM sleep 2. electrical stim of midline tegmentum (midbrain) changes cortical EEG from slow, rhythmic (non-REM) to alert and aroused state

# Moruzzi's research if this region is stimulated, cortical EEG from slow, rhythmic (non-REM) to alert and aroused state

ascending reticular activating system

Neurons that increase firing rates in anticipation of awakening and during arousal: (5) -> synapse directly on the entire thalamus, cerebral cortex, and many other brain regions ## Footnote General effects: depolarization, excitability, and suppression of rhythmic firing

1. NE (locus coeruleus) 2. 5- HT (raphe N) 3. ACh (brain stem & basal forebrain) 4. histamine (midbrain) 5. hypocretin (hypothalamus) neurons

loss of hypocretin neurons leads to sleep disorder:

narcolepsy

stages of non-REM sleep

1. EEG sleep spindles 2. spindles disappear 3. slow, delta rhythms

role of thalamic neurons in non-REM sleep

- sleep spindles generated by inherent rhythmicity of thalamic neurons - delta rhythms occur when thalamic neuron MP becomes much more negative than during sleep spindles

synchronization of activity during spindle or delta rhythms is due to () within the thalamus and between the thalamus and cortex

neural interconnections

# REM sleep: PET Images 3 main things in PET images during REM sleep

1. highly active extrastriate cortex 2. high limbic activation 3. low frontal activity

# REM sleep: PET images high activity of extastriate cortex thought to be (internally/externally) generated

internally

emotional components of dreams thought to be caused by ()

high limbic activation

low frontal activity during REM sleep implies:

no high-level integration or interpretation of info from extrastriate cortex ## Footnote buzz of uninterpreted visual imagery

# control of REM sleep by brain stem neurons 1. LC and raphe N: activity (increases/decreases) 2. Pons cholinergi neurons (increases/decreases)

1. decreases 2. increases

brain stem neuron activity during REm sleep also inhibits ()

spinal motor neurons

() arises from the disruption of the bain stem systems that normally mediate REM atonia

REM sleep behavior disorder ## Footnote act out (i.e. move their bodies) during REM accdg to some dreams

# sleep promoting factors () - released by neurons (gradual increase during waking period); may have inhibitory effects on diffuse modulatory systems

adenosine

# sleep promoting factors (): increased during waking; abundant in wake- promoting ACh neurons; triggers release of adenosine

Nitric acid (NO)

# sleep promoting factors (): produced by bacteria; facilitates non-REM sleep

Muramyl dipeptide

# sleep promoting factors (): synthesized in brain, stimulates immune system, induces fatigue and sleepiness

Interleukin-1

# sleep promoting factors (): released at night, inhibited during daylight; helps initiate and maintain sleep—used to treat symptoms of jet lag and insomnia

Melatonin

# Gene expression during sleep and waking 0.5% of genes showed differences of expression levels when awake or asleep. – Genes that increased in awake rats: (1) – Genes that increased in sleeping rats: genes that contribute to ()

1. immediate early genes, mitochondrial genes & cellular stress genes 2. protein synthesis and plasticity mechanisms ## Footnote these changes are specific to brain

Narcolepsy involves direct transition from ()

waking state to REM sleep

# narcolepsy symptoms excessive daytime sleepiness

sleep attack

# narcolepsy symptoms waking to REM atonia with consciousness; often caused by strong emotions

cataplexy

group of unusual behaviors before falling asleep, during sleep, or in the time between sleep and wakefulness

parasomnia ## Footnote e.g. dream enactment (REM behavior disorder), sleep walking, bed-wetting, sleep paralysis

- daily cycles of light and dark -> but behaviors continue even if daylight and darkness cycles are removed - behavior of most animals is coordinated to cycle

circadian rhythms

collective term for environmental time cues

zeitgebers

(): Mammals completely deprived of zeitgebers settle into rhythm of activity and rest but drift out of phase with 12-hour day/light cycle

Free-run

primary zeitgeber for mature mammals

light-dark cycle

() of SCN -> shift of circadian rhythm in a predictable way

Electrical stimulation

() of SCN -> abolishes circadian rhythmicity of physical activity, sleeping and waking, and feeding and drinking

Bilateral removal

() to SCN necessary to entrain sleep cycles to night

Retinal input

specialized photopigment of photoreceptor that synapses directly onto SCN neurons to reset circadian clock (light-sensitive ganglion cells)

melanopsin

other term for light-sensitive ganglion cells

intrinsically photosensitive retinal ganglion cells

SCN output axons to parts of the hypothalamus, midbrain, diencephalons; use (1) as primary neurotransmitter; SCN neurons may also release () rhythmically

1. GABA 2. vasopressin

clock that functions even without APs -> molecular cycle based on ()

gene expression (of clock genes)

examples of clock genes

period (per), cryptochrome, clock