neuro unit two complete set

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

hormones

chemicals released by glands that travel through blood stream to act on target tissues

endocrine glands

release products INSIDE blood stream

exocrine glands

release products outside of bloodstream (sometimes outside of body) ie blood and sweat

peptide hormones

short string of amino acides (vasopressin (pair bonding)

amine hormones

modified version of a singular amino acid, aka monoamine hormones, ie epinephrine

steroid hormones

come from cholesterol, made from four rings of carbon atoms

where are hormones made?

PERIPHERAL SYSTEM: endocrine glands- adrenal and thyroid glands, gonads (testicles and ovaries) CENTRAL SYSTEM: neurohormones are produced by neuroendocrine cells (hypothalamus)

How do protein and amine hormones influence tissues?

protein and amine hormones bind onto specific receptors on the surface of a cell and activate chemical signals- second messengers- inside of the cell

how do steroid hormones impact the cells

steroid hormones cross the cell membrane and bind to receptors inside of the cell- steroid-receptor complex binds to specific regions of DNA and controls the expression of specific processes, slower than peptide/ amine hormones

pituitary gland

“master gland” releases important hormones and regulates other endocrine glands- two parts, anterior and posterior

pituitary stalk

connects the pituitary gland to the thalamuis

neuroendocrine cells

found in the pituitary, release hormones into the bloodstream

posterior pituitary gland

releases oxytocin and vasopressin into the bloodstream (social and parental behavior, mating/bonding) produce in neuroendocrine cells in the supraoptic and paraventricular nuclei of the hypothalamus, when AP in these cells reached terminal, neurohormones released right into thalamus

anterior pituitary

contains neuroendocrine cells that make and release TROPIC HORMONES: hormones that affect the release of other endocrine glands- hypotha;klamus regs the release of tropic hormones from the anterior pituitary using RELEASING HORMONES- axons of neuroendocrine cells that produce these hormones meet at MEDIAN EMINENCE-

tropic hormones

hormones that affect the release of other endocrine glands

Median eminence

contains blood vessels that form the HYPOTHALAMIC PITUITARY PORTAL SYSTEM- hypothalamic neurons make releasing hormones, which travel to the anterior pituitary, triggering the release of tropic hormones into circulation

how is cortisol released into the body

In response to stress or waking up rhythm, hypothalamus synthesizes and releases CRH (corticotropin releasing hormone) into the pituitary gland, which signals it to release the tropic hormone ACTH (adrenocorticotropic hormone) which travels through the bloodstream to the adrenal glands on top of the kidneys which release cortisol

how are sex hormones released in the body

the hypothalamus produces the releasing hormone GnRH (gonadotropin releasing hormone) which travels to the anterior pituitary triggering the release of the tropic hormones LH and FSH which travel to the gonads (testes+ovaries) and trigger the release of sex hormones testosterone and progesterone

differences between male and female brains

male brain is 8-10% heavier, sexually dimorphic nucleus of the preoptic area (SNDPOA)=2.5x larger in males, 2.2x more cells, interstitial nucleus of the hypothalamus (INAH) 2 and 3 cell groups have larger volume in men compared to women

role of hormones in sex diferentiation

genes effect gonad development- XY have SRY (sex determining region y for production of testosterone) X X do not, gonadal hormones initiate sexual diff of brain (masc or non masc brain) environmental factors can impact gene and hormone expression

Who are transgender male to female womens’ brains most similar to?

BIOLOGICAL WOMEN- environmental factors in pregnant women can alter the expression of SRY, leaving brain structure of MTF women most biologically similar to ppl AFAB

retina

layer of neurons at the back of the eye- sensory transduction occurs here

cornea

bends light entering eye (refraction)

lens

changes shape to focus light on the retina, ciliary muscles change the shape of the lens through the process of accommodation- causes nearer or further images to come into focus

photoreceptors

sensory neurons that detect light- two types, rods and cones

rods

photoreceptors that pick up low levels of light- night vision/ low illumination, rhodopsin is the photopigment receptor

cones

do not work in low light, but process color, pigment receptor is photopsin

bipolar cells

receive input from photoreceptors and then synapse onto ganglion cells whose axons form the optic nervegang

ganglion cells

synapse with bipolar cells, axons form the optic nerve, carry AP out of eye and into the brain

horizontal cells

contact photoreceptors and bipolar cells, can contribute to lateral inhibition and edge enhancement

amacrine cells

similar to horizontal cells, but lie between the bipolar and ganglion cells

What do all cell types with the exception of ganglion cells produce in the eye

graded potentials (ganglion cells produce APs)

scotopic system

rods, works in dim light and is insensitive to color, info from many receptors converge on individual ganglion cells

Photopic system

cones, requires more light, sensitive to different wavelengths and allows for color vision

visual acuity

measure of how much detail we can see- sharopest in center of visual field fo

fovea

central region of retina, contains high density of smaller, tightly packed cones with high acuity

where are rods located on the eye

periphery- none in the fovea

optic disk

where blood vessels and optic nerve leave the eye

blind spot

part of the eye that is sightless bc its where the optic disk is and there are no photoreceptors on the optic disk

what is the pathway from the eye to brain

light enters the eye, it is focused and refracted by the cornea and lens, it then hits the back of the retina where it is processed by rods and cones whose graded potentials communicate info to bipolar cells → ganglion cells → some/ all of optic nerve crosses midline at optic chiasm, then called the optic tract Lateral Geniculate nucleus in the thalamus- axons of LGN neurons form optic radiations, end in→ v1 (also called striate cortex)

what is cortical magnification

smaller portion of the retina is magnified and processed in a proportionately larger area of v1 → greater processing of details arriving at the fovea

what is blindsight

the inability to consciously perceive visual cues, but still discriminate based on them- when v1 pathway is damaged, there is sometimes primitive visual processing thru the thalamus sending visual info to be processed not externally (not thru v1)

what do photoreceptors do in response to light?

they HYPERPOLARIZE and release less glutamate (only system to do this)

on center bipolar cells

turning ON a light excites this cell because it receives LESS glutamate- bc glutamate is inhibitory, turning on a light hyperpolarizes the photoreceptor causing it to reduce or stop its release of glutamate, resulting in it releasing glutamate in response to the cessation of constant inhibition, then causing the synapsed ganglion cell to fire an AP

off center bipolar cell

turning OFF the light excites this cell because glutamate is excitatory and leads to depolarization (bc there is no light on, steady stream of glutamate flowing from photoreceptors, which would inhibit an on center bipolar cell, but excites an off center bipolar cell, BECAUSE IN THIS INSTANCE GLUTAMATE IS EXCITATORY

ganglion cells

synapse onto both oncenter and off center bipolar cells and are ALWAYS EXCITED BY GLUTAMATE

Summarize what happens to both on and off center bipolar neurons when it is DARK

Because no light is being shown, photoreceptors are depolarized and constantly releasing glutamate, on center bipolar cells are inhibited by the glutamate release and hyperpolarize, sending little to no glutamate to ganglion cells (NO ACTIVATION). Off center bipolar cells are excited by glutamate and depolarize, releasing glutamate onto ganglion cells= activation