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what is considered endogenous circadian rhythms?
sleep cycle
frequency of drinking and eating
body temp
secretion of hormones
urination
sensitivity to drugs
Why do we have circadian rhythms?
To keep our internal workings in phase with the outside world
if there were no external cues, the human circadian rhythm would be slightly longer than 24 hours
What are Zeitgebers?
time giver
stimulus that resets circadian rhythm
Examples of Zeitgebers
sunlight
exercise
meals
arousal
temp of environment (colder room = early wake up)
tides
travelling west
phase-delays our circadian rhythms
travelling east
phase-advances our circadian rhythms
SCN (suprachiasmatic nucleus)
main control center of circadian rhythms of sleep and temp
located above the optic chiasm and part of the hypothalamus
damage to SCN = less consistent body rhythms: animals still fall asleep and wake up but would do so at very random times of the day
SCN very active during the day, not as much at night
single cell extracted from SCN and raised in tissue culture continues to produce action potential in a rhythmic pattern
retinohypothalamic path
small branch of optic nerve
travels directly from retina to SCN
NOT A VISUAL PATHWAY - used to synchronize daily cycle
sensitive to light but not used for seeing
comes from ganglion cells that have melanopsin (photosensitive)
when light hits ganglion cells = SCN activated
slave oscillators
sub-systems of the brain that uses info from SCN to determine when to execute a behaviour
controls the rhythmic occurrence of a behaviour
hunger, physical activity
driven by SCN via hormones, proteins or neurotransmitters
what is responsible for generating the circadian rhythm?
proteins
PER and TIM
How does PER and TIM control the circadian rhythm?
increase the activity of certain kinds of SCN neurons that regulate sleep and waking
higher levels of PER and TIM = lower activity of circadian rhythm, hence lower cellular firing in SCN
Effects of external stimuli on PER and TIM
daylight degrades PER and TIM, so SCN cells are working overtime to make
reaches a substantial amount at night, SCN cells can relax now since there is enough PER and TIM
SCN and other parts of the brain
inhibits pineal gland = less melatonin during the day bc that’s when SCN is active
at night, retinohypothalamic path is not activated, so SCN is deactivated, which activates the pineal gland = increase melatonin
Coma
extended period of unconsciousness
low brain activity
little response to stimuli
result of brain injury
vegetative state
alternates between sleep and arousal but no awareness of surrounding
some autonomic (involuntary) arousal to painful stimulus
minimally conscious state
a stage higher than a vegetative state
occasional brief periods of purposeful action and limited speech comprehension
Brain death
no sign of brain activity
no response to any stimulus
legally dead
what was used to discover various stages of sleep?
EEG - allows bulk cortical activity to be recorded at diff phases of sleep
polysomnograph
combination of EEG and eye-movement records
electrodes places around the eye
electromyogram
measures muscle movement and tone
electrodes placed on the jaw
beta waves
high freq (12-30 Hz)
most common in frontal lobe - in memory and visual areas
alpha waves
not-intellectually engaged like doomscrolling
lower frequency (8-12 Hz)
higher amplitude and more synchronized than beta
theta waves
4-8 Hz
S1/non-REM stage of sleep
can still respond but is considered asleep (are you asleep? No…)
Delta waves
1-4 Hz
slow brain activity
high amplitude
Stage 1 sleep
start of sleep
most of the neurons are firing equally
slowly go from alpha → theta
Stage 2 sleep
slower theta waves
sleep spindles - 12-14 Hz, lasts at least half a second, very high freq - MEMORY consolidation
K-complex - sharp wave, temporarily inhibits neuronal firing, high amplitude, very brief
Slow wave sleep: stage 3 and 4
delta waves
slowing of heart rate, breathing rate, and brain activity
highly synchronized neuronal activity
important for protein synthesis (good memory) and release of growth hormones (build muscle mass)
if interrupted = fatigue
length decreases as the night progresses
early parts of sleep
REM sleep
rapid eye movement
theta and alpha waves
muscle atonia
vivid dreams
after an hour of sleep = first REM
length increases as the night progresses
more REM sleep in early stages of life
NREM sleep
throughout the night we alternate between NREM and REM randomly
nightmares
The reticular formation
part of the midbrain
extends from medulla to forebrain
responsible for arousal
receives input from eyes and ears
pontomesencephalon
part of RF
releases acetylcholine and glutamate, which contributes to cortical arousal
Locus coeruleus
small structure in the pons
LC axons release norepinephrine - increase wakefulness and important for fight/flight
shuts down when asleep
arouses various areas of the cortex
Hypothalamus
has neurons that release histamine - excitatory
antihistamines = sleepiness and shuts down the hypothalamus
Hypothalamus and orexin
oexin released by lateral and posterior nuclei of hypothalamus
orexin = neurotransmitter
needed to STAY awake
if someone lacked orexin = people would alternate in between brief periods of waking and sleeping
Basal forebrain and arousal
orexin is also released by cells in the basal forebrain → wakefulness and arousal
basal forebrain is anterior and dorsal to hypothalamus
cells in BF also release GABA (inhibitory) - important for sleep, decreasing temp and metabolic rate, hyperpolarizing the thalamus and cortex
other axons release ach = excitatory and increases arousal when awake but shifts sleep from NREM to REM
brain activity in REM
activity increases in the pons, limbic system (feeling emotions during sleep), and visual cortex
activity decreases in motor cortex, and the dorsolateral prefrontal cortex
associated with PGO waves originate in the pons - high amplitude
REM deprivation = high density of PGO waves
serotonin and nonadrenaline interrupts REM
sleepwalkers
awake in motor cortex, pons and medulla
occurs in stage 3 or 4
lucid dreaming
high activity in frontal and temporal cortex (important for awareness)
sleep paralysis
pons in REM = loss of muscle tone, but the rest are awake
sleep apnea
inability to breathe while sleeping for a long period of time (few seconds to a few minutes)
consequences: sleepiness during the day, impaired attention, depression
causes: genetics, old age, obesity
effects: cognitive impairment
treatment; breathing device
Narcolepsy
frequent attacks (gradual or sudden) of sleepiness
occasional cataplexy: muscle atonia triggered by strong emotions
sleep paralysis
hypnagogic hallucinations
seems to run in families, but no identified gene
caused by lack of hypothalamic cells that produce and release orexin (important to stay awake)
treatment: stimulant drugs like Ritalin = increase wakefulness by increasing dopamine and norepinephrine activity. -activates LC
Periodic limb movement disorder
repeated involuntary jerking of arms and legs
occurs during NREM
treatment: sleeping pills = inhibit motor neurons and sleeping with a weighted blanket
REM behaviour disorder
acting out dreams in REM sleep
inadequate GABA and other inhibitory neurotransmitters
all animal with SC _____
sleep
all warm-blooded animals _____
dream