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biological rhythms
regular fluctuations in any living process- light is important to many of these rhythms
ultradian rhythms
repeat more than once a day (regular activity, feeding, hormone release)
infradian rhythms
repeat less than once a day (reproductive cycles)
circadian rhythms
have a span of about 24 hours, generated by an endogenous (internal/biological) clock that is highly accurate, only off by few minutes every day
what happened in Jean-Jacques deMairans experiment?
Observed the opening and closing of a heliotrope plant both when exposed to sun and when left in a dark cabinet- the leaves opened and closed regardless of the presence of light
how do ppl study internal clocks in animals?
FREE RUNNNING EXPERIMENTs in which the animal maintains its own schedule without human interference- the period of time when an animal will run on the wheel won’t be exactly 24 hours. but will be very close
phase shift
a shifting of a biological rhythm in response to a stimulus (like light)
entrainment
the process of shifting a biological rhythm to a stimulus
zeitgeber
the environmental cue that an animal syncs its internal clock to (sound, light, temp)
where is the biological clock locatesd
the suprachiasmatic nucleus (SCN) in the hypothalamus, above the optic chiasm (where the optic nerves cross the midline and become optic tracts) lesions of the SCN eliminate circadian rhythms of drinking, locomotion, and hormone secretion, in vitro SCN cells with show rhythm (daily periods of higher and lower activity) for days or weeks outside of the organism they were taken from
how do transplant studies prove that the SCN produces the circadian rhythm
Hamsters with 24 hour circadian rhythms had their SCN lesioned- in constant dim light setting showed no rhythm. Then got transplant from hamsters with 20 hour circ rhythms and began to display rhythm again, but instead of 24 hour previous, 20 hour transplant rhythm
pineal gland
in birds and amphibians is sensitive to light, thinner skull layer and photoreceptors in gland so is able to detect, releases melatonin in the absence of light- in mammals, rather than direct stim, must travel thru pathways for scn to get info
retinohypothalamic pathway
from eye to SCN, how circadian system interacts with light. Pathway contains retinal ganglion cells that project to the SCN- do not use rhodopsin or photopsin, use melanopsin, special light sensitive photopigment. SCN then activates/ deactivates pineal gland

molecular basis of SCN
SCN cells in mammals make two proteins: Clock anc Clye, which bind together to form a CLOCK AND CYCLE DIMER, dimer binds to DNA and promotes transcription of two genes: period (per) and cryptochrome (cry)*** important to regulating the circadian rhythm
How does the clock-cycle dimer and per cry protein cycle work
Clock and Cycle Dimers facilitate the transcription of per and cry genes, which then create per and cry proteins and also excite the SCN neurons, causing steady firing of AP’s. downstream these lead to wakefulness (melatonin suppression). When Per and Cry proteins accumulate, they bind to each other and inhibit the activity of the CC dimer, suppressing its excitatory influence and slowing its transcription of per and cry genes (thus stopping production of per and cry, then ceasing inhibition of clock and cycle, starting the cycle over again) CYCLE TAKES ABOUT 24 HOURS
how does the body determine the time of day
per and cry complex levels (fluctuate to impact wakefulness and sleepyness)
How does light impact the Clock-cycle per-cry shenanigans
Retinal ganglion cells detect light with melanopsin, flood cell w glutamate in presence of light, excitatory, leads to increased activation of SCN as well as increased transcription of the per gene via clock and cycle dimers, molecular clock becomes entrained to the photo (light) period and resets biological clock (why best way to combat jet lag is to go outside and stare at sun)
peripheral clocks
other organs outside of SCN can adapt to own internal/ external clocks , SCN is supposed to conduct them (like an orchestra)- cardiovascular clock, kidney clock w filtration and excretion ratesw
what can be induced by loss of sync between internal rhythms and external stimuli
diseases like cardiovasular damage
what happens when central and peripheral models fall out of sync
can contribute to the progression of disorders like cancer (shift work that changes is considered a high risk carcinogen bc body’s clock is being thrown off)
que quiere decir la orchestra model
the SCN is the conductor of peripheral clocks like melatonin, cortisol, body temp, and HR/ BP, without conductor, orchestra would play like shart

why is blue light before bedtime bad
light suppresses melatonin, melanopsin esp activated by short wavelengths like blue light (screens), can cause circadian delay or advancement by exciting the SCN artificially and REALLY effectively cir
circadian advancement
screen/blue light early in morning (activates SCN artificially early)
circadian delay
light in early evening artificially excites SCN again, and delays sleep part of circadian rhythm (melatonin production)
electroencephalogram (EEG)
electrodes all over scalp, track overall electrical current fluctuations in brain
electro-oculogram (EOG)
tracks eye movements in sleep
electromyogram
large muscle movements
what are the two distinct classes of sleep
REM- Small amplitude, fast EEG waves, complete muscle relaxation and rapid eye movements, NON-REM-Can be divided into 3 stages, has very different EEG waves
what does the brain activity of an awake person look like
BETA WAVES-mix of low amp waves with many fast frequencies
what is stage one sleep
starts with presleep alpha rhythm, which occurs during relaxation and drowsiness, time spent in alpha rhythm will decrease and waves of smaller amplitude and irregular frequency will start THETA WAVES, VERTEX SPIKES- sharp waves will appear, HR will drop, breathing will slow, muscles relax, eyes roll slowly, lasts several minutes

stage two sleep
waves of 12-14 hz will occur in bursts, called SLEEP SPINDLES- K COMPLEXES ALSO APPEAR- sharp negative EEG potentials

Stage 3 sleep (slow wave)
large amp, very slow waves called DELTA WAVES appear, occur at frequency of one wave per sec

REM sleep/ paradoxical sleep
small amplitude, high frequency activity, like an awake person except for presence of SAWTOOTH WAVES eyes move rapidly under closed lids, muscles relaxed, also called paradoxical sleep, mind looks awake but body is very asleep
Beta waves
person is awake
alpha waves
person is drowsy/ relaxed (nodding off in class)
theta waves
stage 1 sleep plus vertex spikes
K complexes and sleep spindles
stage two sleep
delta waves
stage ¾ sleep, deep sleep
fast, random wave +sawtooth waves
REM sleep
vertex spikes
stage one sleep plus theta waves
what happens in a typical night of young adult sleep (7-8) hours
around half is stage two sleep, 20% is REM sleep, cycles last from 90-110 mins, cycles in the first portion of night have more stage 3/ slow wave sleep (Growth hormone release), later cycles have less/ none SWS, more REM (memory consolidation)
impacts of sleep deprivation
irritability, difficulty concentrating, disorientation, prolonged hallucinations, compromises immune system which can lead to bacterial infections
fatal familial insomnia
inherited sleep disorder- person loses ability to sleep in midlife, leads to death within 7-24 months
what are the biological functions of sleep
restores body by restoring materials used up during day, like proteins (growth hormone released during slow wave sleep, essential for cell life repair and activation of the immune system) Sleep needed for immune system function, also helps with memory consolidation, sleep between learning and recall improves retention, consolidates declarative memory tasks, also “washes” you brain with CSF as blood vessels constrict, clears away dead cell material which is later peed out
4 neural systems underlie sleep
FOREBRAIN SYSTEM-arousal and slow wave sleep , BRAINSTEM SYSTEM-activates forebrain to wakefulness , PONTINE SYSTEM-REM sleep , HYPOTHALAMIC SYSTEM-coordinates other systems
basal forebrain
stims arousal and wakefulness in forebrain, going to sleep requires cholinergic neurons to be suppressed
reticular formation
wakes the forebrain up, targeting this will wake up sleeping animals, lesions of this area will produce persistent sleep

parts of brain active during REM sleep
Pontine Tegmentum (part of pons) and Locus Coeruleus

ACh neurons in the pontine tegmentum project to
TECTUM (rapid eye movements), LATERAL GENICULATE NUCLEUS (PGO Waves 2 v1, cause vibrant, intense dreams, MEDULLA NUCLEI: muscular paralysis, BASAL FOREBRAIN AREA: cortical activation
hypothalamus
contains several parts of brain known as sleep systems- Ventrolateral preoptic area (vlPOA) contains majority of GABAergic sleep neurons → receives input from the forebrain to induce slow wave sleep, inhibits reticular formation and orexin neurons in the hypothalamus → additionally contains OREXIN neurons, receives input from the SCN and promotes arousal in retic form , basal forebrain, and pons
how are the reticular formation and basal forebrain connected
reticular formation excites the basal forebrain which creates continuous wakefulness (like jumpstarting a car, retic form= jump starter, basal forebrain= engine that is now running)
narcolepsy
frequent, intense sleep attacks, go straight to REM sleep, may have CATAPLEXY, sudden loss of muscle tone without loss of consciousness, can be triggered by sudden intense emotional stimulus, DUE TO LOSS/ DAMAGE OF OREXIN NEURONS
Sudden Infant Death Syndrome
developmental defects of serotonin produce lesions in rostral reticular formation (waking) and medulla (breathing)- both have 5ht receptors involved in regulating breathing and waking, when disrupted, lead to insufficient arousal following life threatening co2 levels → baby suffocates because 5ht receptors required to detect suffocation and wake the baby do ont work