Chapter 19: Brain Rhythms and Sleep Flashcards
(): changes in physiological functions
according to brain clock
Circadian rhythms
- measurement of generalized activity in the cerebral cortex
- helps diagnose neurological conditions (e.g. epilepsy, sleeping disorders) ++ research
electroencephalogram (EEG)
amplitude of EEG signal = measure of () of underlying neurons (particularly dendrite excitation)
synchronous activity
Recording of miniscule magnetic signals generated by neural activity (one billionth of the magnetic field generated by the Earth, power lines, etc.)
magnetoencephalography (MEG)
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
EEG rhythms often correlate with particular states of ()
behavior
categorization of EEG rhythms is primarily based on ()
frequency
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
(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
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
() can serve as massive cortical input as a pacemaker
thalamus
hypothesis on brain rhythm function
sleep rhythms as the brain’s way of ()
disconnecting cortex from sensory input
hypothesis on brain rhythm function
walter freeman: () coordinate activity of nervous system regions
neural rhythms
() seizure: entire cerebral cortex, complete behavior disruption, consciousness loss
generalized
tonic-clonic seizure: () driven by tonic (ongoing) or clonic (rhythmic) patterns
muscle groups
() seizure: < 30 seconds of generalized 3 Hz EEG waves with subtle motor signs
absence
() seizure: circumscribed cortex area, abnormal sensation or aura
partial
partial seizures in the temporal lobe result in:
deja vu, hallucinations
readily reversible state of reduced responsiveness to, and interation with, the environment
sleep
() 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
() 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
body during REM sleep
():body paralzyed except eye and respiratory muscles
REM atonia
almost complete loss of skeletal muscle tone
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)
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.
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)
- circadian timing mechanisms
- 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)
- brain
- 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
- restoration - sleep to rest and recover
- adaptation - avoid trouble, conserve energy
restoration during sleep
- () - cells repair and regrow; no sleep -> loss of immune function
- () - glymphatic (waste clearance) system clears out toxic byproducts; plasticity
- cellular restoration
- 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
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
- lesions in midline of brain stem -> state similar to non-REM sleep
- 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
General effects: depolarization, excitability, and suppression of rhythmic firing
- NE (locus coeruleus)
- 5- HT (raphe N)
- ACh (brain stem & basal forebrain)
- histamine (midbrain)
- hypocretin (hypothalamus) neurons
loss of hypocretin neurons leads to sleep disorder:
narcolepsy
stages of non-REM sleep
- EEG sleep spindles
- spindles disappear
- 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
- highly active extrastriate cortex
- high limbic activation
- 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
buzz of uninterpreted visual imagery
control of REM sleep by brain stem neurons
- LC and raphe N: activity (increases/decreases)
- Pons cholinergi neurons (increases/decreases)
- decreases
- 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
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 ()
- immediate early genes, mitochondrial genes & cellular stress genes
- protein synthesis and plasticity mechanisms
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
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
- GABA
- vasopressin
clock that functions even without APs -> molecular cycle based on ()
gene expression (of clock genes)
examples of clock genes
period (per), cryptochrome, clock
