finals except life is meaningless and i hallucinated a baby in the grocery store Flashcards
what wavelengths can we see, why
400-700. because earth’s atmosphere is most transparent to these wavelengths
what are extraspectral colors
purple and white. mix of wavelengths (e.g. purple is when 2 or more wavelengths affect red and blue cones more than green cones
what are the percentages of cone
63% red, 31% green, 6% blue
what colors do rodes (rhodopsin) prefer to see
blue-green
what is a r+g ganglion cell
excited by red light and by green light, aka yellow channel
r-g, g-r ganglion cell
activated by red light, inhibited by green., and vice versa. red-green opponent channel
b-(r+g) ganglion cell
blue-yellow opponent channel
explanation for afterimages
opponent channels. if you stare at something, your cells (e.g. g-r) gradually fatigue. when you look away, only the less fatigued ones are visible (e.g. r-g)
daltonism
red-green colorblindness. red and green cone visual pigments lie on x-chromosomes. 95% of all variations in color vision.
why are women rarely color blind
women are rarely color blind because if one x-chromosome codes a faulty pigment then the other x-chromosome compensates.
how could a woman become a tetrachromat
if 2 x-chromosomes code for 2 different functional red cone pigments
reflectance
intrinsic color of a surface, the tendency to reflect certain wavelengths and absorb others
color constancy
ability to infer reflectance in different light
chevreul illusions for color and brightness
different hues and different saturations -> look redder when close to low saturation and different hues
external ear
pinna, ear canal, sealed at the end by tympanic membrane aka eardrum
middle ear
air filled space behind eardrum connected to pharynx by eustachian tube
inner ear
cochlea for hearing, vestibular apparatus for equilibrium
sound waves and molecule density
at the peak of the waves the molecules are crowded together and pressure is high. vice versa
Frequency is percieved as
pitch. low freq-> low pitch
Unit of frequency
waves/sec (hz)
human hearing range, best acurity
16-20,000hz. around 10 octaves. best hearing around 1000-3000 hz
what does loudness depend on
frequency (needs to be within hearing range) and amplitude
middle ear small bones (ossicles)
eardrum hits the malleus, moving the incus, and then the stapes, pushing the oval window. act as a lever system, these 3 bones are the smallest in the body
where does the oval window lead
cochlea
vestibular duct and tympanic duct anatomy
aka scala vestibuli, scala tympani. oval window connects with vestibular duct which communicates with tympanic duct at helicotrema, tympanic duct connects to round window. filled with perilymph (fluid similar to plasma)
cochlear duct
aka scala media, contains endolymph (similar to intracellular fluid). waves shake cochlear duct as it has auditory receptor hair cells.
organ of corti
in the cochlear duct, sits on the basilar membrane under tectorial membrane. hair cells have their little hairs against the tectorial membrane.
hair cells (number, type of cell, how they work
20,000 per cochlea (40,000 total). EPITHELIAL CELLS, NOT NEURONS. 50-100 stiff hairs called stereocilia. bend when waves in the perilymph (liquid in vestibular and tympanic duct) deforms basilar and tectorial membranes
how does a hair cell send a signal
cilia bend towards longest cilium to depolarize and release transmitter and activate a primary sensory neuron. this neuron form auditory nerve
auditory nerve
cochlear nerve, a branch of cranial nerve 8.
cilia bending away from the longest cilium causes
hyperpolarization, releasing less transmitter, doesn’t excite neuron as much
basilar membrane responding to different frequency
near oval window: stiff and thicc basilar membrane. picks up high frequency signals. near helicotrema: wibbly and thinn basilar membrane. picks up low frequency signals. brain deduces which hair cells are most active
auditory signals localization in the brain
pass through each ear to both sides of the brain (so right and left ear signals will be everywhere in the brain)
primary auditory cortex
in temporal lobe
how does brain know where the sound comes from
loudness and timing. if sound is louder in right ear? from right side. loud sounds make auditory neurons fire faster. or, if sound reaches the right side before the left.
conductive hearing loss
sound cannot be transmitted through external or middle ear. weber test (tuning fork in the middle of the head, which is louder), it is louder in the bad ear because it doesn’t have to compete with sounds through ear canal. rinne test (骨传导), tuning fork will be louder transmitted through bone
sensorineural hearing loss
damage to haircells/inner ear. mammals cannot replace. 90% of elderly hearing loss (presbycusis) is sensoineural. unaffected by rinne test. weber test is louder in good ear because 骨传导 doesn’t help
how does the vestibular apparatus sense head relative to gravity
utricle and saccule have hair cells that are activated when the head tilts relative to gravity
how does the vestbular apparatus sense head rotation
semi-circular canals are fluid filled hoops, fluid sloshes left if you turn ur head right, activating hair cells
vestibular hair cells signalling
activate primary sensory neurons of vestibular nerve, a branch of cranial nerve 8
where do cranial nerve 8 go
pass through cerebellum. or synapse in medulla, then go to cerebellum OR up through thalamus to cortex.
proprioception
awareness of the position of body parts relative to each other. e.g. you can sense how much your elbow is flexed with eyes closed.
nociception
tissue damage or the threat of it. percieved as pain or itch
4 somatic senses
touch, temperature, proprioception, nociception
somatosensory receptor cells are all
neurons
cell bodies for somatic sensation below the chin are in…
cell bodies in dorsal root ganglia
receptors for the head have cell bodies…
in the brain
where to neurons transduce touch/pressure into electrical signals
at nerve endings (tips of fibers in skin and viscera)
types of receptors in skin
free nerve endings, merkel receptors (or disks), encapsulated receptors (meissner or pacinian corpuscles).
free nerve endings
detect mechanical stimuli, temperature, chemicals
merkel recpetors
mechanoreceptor nerve endings in contact with specialized epithelial cells called merkel cells. signal contact, very sensitive to deformation of skin. more tonic than phasic (sustained signal)
encapsulated receptors
meissner and pacinian corpuscles, mechanoreceptors in connective tissue.
most receptors are phasic/tonic?
phasic. nerve ending depolarizes but returns to baseline in 3ms.
meissner corpuscles
mainly in tongue and hairless skin, erogenous zones, palms, fingertips. shaped like an egg, inside has many looping endings,l ike spring mattress. detect sideways shearing (like petting blahaj). phasic
pacinian corpuscles
nerve endings sheathed in many layers. sense tiny displacements if motion is quick. phasic, respond strongly to vibration and other quick stimuli
2 point discrimination on lips and fingertips, on calves
2-4mm on lips and fingertips, on calves 40mm
thermoreceptors
cold receptors respond max at 30 degrees, warm receptors at 45. both phasic tonic. more cold than warm receptors, few thermoreceptors in total (only 1000 beccause don’t need localization)
above 45 degrees, what happens to receptors
pain receptors activated, cold fibers briefly respond creating paradoxical cold
nociceptors respond to
mechanical, heat, chemicals. chemicals from damaged cells (K+, histamine, prostaglandins), serotonin released by platelets from injury
somatosensory afferents have 2 groups
small, large
small fiber types
c and a delta. free nerve endings, mostly. c fibers are unmyelinated, 2m/s max speed. a delta are thicker, myelinated, 30m/s max speed.
adequate stimuli for small fibers
different adequate stimuli, such as mechanical stimuli, chemicals, temperature.
large fibers
a-beta. come from merkel disks or encapsulated mechanoreceptors. myelinated, conduct at 70 m/s
large fiber projection into brain
go up spinal cord in dorsal columns, then in the medulla synapse on neurons which go to other side (ipsilateral)
small fiber projection into brain
synapse directly or via interneurons and motoneurons for reflex responses. or on dorsal horn neurons that cross the midline and run in spino thalamic tracts in the lateral part of the cord between dorsal and ventral horns
reason for large fiber’s projection into brain
feedback, especially for motor cortex as it manipulates objects. needs to travel a long way to the brain quickly.
reason for small fiber’s projection into brain
evoke simple responses to specific stimuli (withdrawing from pain, brushing away a bug, thermoregulatory and sexual responses). can be handled in spinal cord without brain input.
how somatosensory info goes from spinal cord to thalamus, cortex
signals from spinal cord go to ventroposterolateral (VPL) nucleus of thalamus. signals from head (not shown) go to the ventroposteromedial (VPM) nucleus. both go to primary somatosensory cortex
somatotopic
means neighboring places correspond to neighboring brain places.
primary somatosensory cortex (s1) is in what lobe
parietal
lateral inhibition among somatosensory fibers
lateral inhibition enhances spatial differences, you feel hot bath is most hot around the water surface. somatosensory version of chevreul illusion
TRP ION CHANNELS, types and where it is present
most nociceptors and thermoreceptors have this. trpv1 are called vanilloid receptors, respond to damaging heat, chemicals (including capsaicin). trpm8 react to cold and menthol. ALSO IN WALLS OF MOUTH
congential analgesia death expected age
20 due to injury and infection (cannot feel pain)
2 types of pain
fast and slow. respectively carried by a delta and c fibers (both small!).
nociceptive signals reaching the limbig system
emotional distress, nausea, vomiting, sweating
decending pathways blocking nociceptive cells
when ur at con and ur feet doesn’t hurt because of the adrenaline
referred pain
nociceptors from different places converge on a single ascending tract. tract send signal to brain, brain infers its from skin because internal organ dmg is rare
how do a beta gate control pain
c fibers contact secondary neurons in dorsal horn, secondaries inhibited by a beta fibers using interneurons. (e.g. rubbing sore feels better)
analgesic mechanisms
aspirin inhibits prostaglandins and inflammation, slowing transmission of pain
opioids decrease transmitter release from primary sensory neurons and postsynaptically inhibit secondary sensory neurons.
natural painkillers
endorphins, enkephalins, dynorphins
liver and gallbladder pain
below boob to shoulder
colon, stomach, small intestine, appendix. which pain on top of what
stomach above small intestine above appendix above colon
chemoreception
smell and taste. evolutionarily old, bacteria and animals without brains (me) use it
olfactory epithelium
top of nasal cavity, covering 3cm with 5 million receptor cells each for each nostril.
pigmentation of epithelium
richness is related with olfactory sensitivity. people: pale yellow. cats: dark mustard brown.
receptor neurons in epithelium
a single dendrite that extends into olfactory epithelium. branches to form nonmotile cilia, increasing the surface area of the cell (for catching more odorants).
how many odorant receptor molecules per receptor? how many types of receptor cell?
only one type of receptor molecule but a lot of that one type. 400 kinds of receptor cell (400 primary odors)
g protein coupled receptor molecules for olfaction, how does this send an action potential
odorant binds receptor, activates g-olfactory, which increases cAMP concentration, cAMP-gated cation channels open, depolarizing receptor neuron, triggering action potential that goes to olfactory bulb
how many genes for g protein coupled recptor molecules
1000 genes, making the largest known gene family in vertebrates.
how much of the g protein coupled genome expressed in humans
3-5% of genome
sensitivity of olfactory receptors
can detect a single molecule of preferred chemical, but 40 cells must react before we experience it as smell
pinocytosis occurs in what sense’s cells
olfactory receptor cells. constantly sip fluid then send it along nerves into brain
lifespan of olfactory receptor cells
short lived, degenerate after a month or 2. unusual.
how do olfactory receptor cells send signal to olfactory bulb
tiny holes in cribiform “sievelike” plate at the bottom of the cranial cavity
olfactory bulb
extension of cerebrum, under the frontal lobes in the brain.
projection from receptors to bulb is called
olfactory nerve, or cranial nerve 1
olfactory convergence
rods converge on gaglion cells, enhances sensitivity but discards spatial information
head damage can damage what sense
can damage olfaction, primary sensory neurons
olfactory bulbs projects where
directly to olfactory cortex, by passing thalamus. also limbic system, linked to motivation and emotion, so odors can bring emotional memories
olfactory cortex is in where
frontal and temporal lobes
parts of limbic system
cingulate gyrus, hippocampus, amygdala
olfaction adaptation
primarily phasic, people get used to bad smells over time
pheromones O_o
chemicals released by an animal that affects physiology or behavior of its own species. in rodents, the vomeronasal organ (VNO) processes phermonone behavior
human pheromones OwO
VNO disappears you omegaverse authors fuck you. (we do respond to some chemical signals though)
tastebud number, location
people have 5000 mainly at the top of the gongue but also on soft palate, epiglottis, upper esophagus. babies have 10,000. we also have chemoreceptors in stomach and intestines. some resemble ones on tongue.
taste bud made up of?
100 receptor EPITHELIAL cells. NOT neurons. arranged like petals, open up with a small pore (taste pore)
typical taste bud has how many types of receptor cells, what do they detect
- sweet detects sugar. umami detects glutamate (protein). bitter detects poison. salty and sour detect Na+ and H+. tongue may have receptors for fatty acids
3 types of taste receptor cells
type 1: salt. type 2: sweet, bitter, umami. type 3: sour.
taste receptor cells communicating at synapses
only type 3 cells form synapses with SENSORY neurons, activating them with serotonin. type 2 cells release atp, acting on GUSTATORY neurons and type IIs.
why do type 2 taste cells release atp
they have receptor molecules coupled to g protein called gustducin, activating signal pathways to increase intracellular Ca2+ and releasing atp.
detecting salt and sour releases atp?
no. they involve ion channels not linked to g proteins
experience of food depends on?
smell, temperature, pain, texture, crunch, appearance, cognition
taste signal to brain route
taste buds: synapse in medulla and thalamus en route to cortes. excite cranial nerves 7, 9 and 10. facial, glossopharyngeal, and vagus nerves.
hypothalamic controls __ using __ in order to __
controls feeding, plasma osmolarity, body temperature, sexual/stress responses using negative feedback (using signals from body to monitor) to maintain homeostasis or carry out rhythms
hormonal and neural influences of the hypothalamus
nuclei within hypothalamus send neural signals to each other, and to other parts of the brain. also synthesizes hormones to posterior pituitary, which is then released into blood. makes releasing hormone into hypophyseal portal system to ANTERIOR pituitary, release other anterior pituitary made hormones
lesions of what causes obesity, of what cause thin
ventromedial hypothalamus and lateral hypothalamus respectively
arcuate NPY neurons inhibit and activate
inhibit paraventricular nucleus (PVN, a satiety center), which activates sympathetic nervous system, but since arc-npy inhibits pvn, sympathetic is inhibited too. sympathetic decreases feeding, but since sympathetic is inhibited, feeding is allowed. excite lateral hypothalamus (LH, feeding center). orexin released from LH further promotes feeding and stops pvn.
arcuate nucleus of thalamus release what
release NPY, GABA, and agouti-related peptide (AgRP)
arcuate pomc neurons release what
cleave pro-opiomelanocortin (POMC) to make a melanocyte stimulating hormone (alpha MSH) which they release at the synapses.
arc-pomc neurons inhibit and activate
inhibit dorsomedial hypothalamus (dmh) and excites pvn, ventromedial hypothalamus (vmh)
pvn and vmh in arc-pomc pathway do what
promote sympathetic nervous system
dmh in arc-pomc pathway do what
inactivate sympathetic, but since dmh is inhibited, the overall is promoting sympathetic.
final outcome of arc-pomc
no feeding. sympathetic ns being active will always cause no feeding, arc-npy will inhibit arc-pomc
how does body know if you’ve reached your weight set point
leptin levels, which is released by fat cells. cells, especially ones in feeding and anorexigenic centers have receptors for leptin. so mutated leptin production and leptin reception will cause obesity.
leptin effects in feeding centers
excite pvn, thus indirectly increasing sympathetic activity and decreasing feeding. decreases arc-npy and lh to prevent feeding.
leptin effects on satiety centers
excite arc-pomc, vmh to promote sympathetic and decrease feeding. inhibit dmh as it decreases sympathetic
how does brain know when to end meal
blood glucose. excites arc-pomc, inhibits lh. sensors in walls of stomach measuring nutrients and stretch
walls of stomach sensed nutrients and stretch releases what
cholecystokinin (CCK), peptide YY (PPY), glucagon-like peptide 1 (GLP1). Act via blood to excite Arc-POMC, PVN, VMH, inhibit DMH. SAME EFFECTS AS LEPTIN.
nerve stimulated from stretch and sugar detected
vagus nerve, which excites vmh via nucleus tractus solitarius (NTS)
ghrelin released when does what
when stomach is empty by cells in stomach walls. stretch stops release. acts directly on arc-NPY and LH and inhibits PVN
dangerous appetite supressors
amphetamines, fenfluramine
rimonabant
blocks CB1 endocannabinoid receptors, moderate weight loss but nausea, depression, suicide
leptin for weight loss drug
not helpful, obesity rarely leptin deficient
cck and pyy agonists
not helpful (supposed to stimulate stretch of stomach)
liraglutide
a possible solution for obesity, GLP-1 agonist
circadian rhythms found in
bacteria, protozoa, plants, fungi, animals
human circadoan rhythms influence
behavior, alertness, mood, body temp, hormone levels
endogenous meaning
not simply reponses to environmental changes. circadian rhythms continue even when the environment is constant.
what is entraining
to have all the cells with their individual internal clocks kept in sync by master clock in brain taking in sensory signals
transcription translation feedback loop
aka TTFL, when PER protein represses transcription of per.
PER/TIM maxed out when? effects on other things
maxed out at 4 am, shutting off per, tim mRNA. lowest amount of PER/TIM at evening, maxed out per, tim mRNA because PER/TIM no longer repressing.
clk and cyc effects on per, tim
clk makes CLK, cyc makes CYC. daytime: CLK-CYC binds DNA, stimulates per, tim transcription. nighttime: PER/TIM blocks CLK-CYC from binding to DNA, repressing transcription of per/tim.
doubletime gene
makes protein DBT, binds PER, causing it to break down, so PER rise slower than they would otherwise, so they do not peak until 6 hours after per, resulting in overall cycle of 24 hours
human homologs of circadian rhythm genes and proteins
TIM > CRY. clk > clk. cyc > bmal1. dbt > ck1з. same logic present as in drosophila. CLK/BMAL1 dimer stimulates transcription of per and cry when not blocked by PER/CRY, for example.
zeitgeber, main one?
cues for cellular clock: light, temperature, feeding, exercise, social interaction. main zeitgeber: light sensed by melanopsin retinal ganglion cells which project onto master clock (suprachiasmatic nucleus aka SCN of hypothalamus)
SCN recieve light signals does what
chemical changes to break down PER/CRY. If after 4am, PER/CRY levels already falling, so clock is forward a little. If in evening, when PER/CRY are rising, clock back.
entrainment
nudging clock in synchrony, other clocks are entrained to SCN after neural signals go from SCN to other brain areas.
pineal body
projected onto from SCN via hypothalamus nuclei and sympathetic nervous system. at the back of diencephalon. secretes melatonin.
melatonin levels throughout the day acts on what
at dusk, blood levels rise 8 fold, peak at 2am, fall back to daylight levels at 8am. melatonin acts on melatonin recepts in scn to reset master clock
melatonin for jet lag
jet lag is because clock can only adjust by one hour a day. melatonin taken 30 min before target bed time for eastward travel
chronotypes
people within a species sleep at different types so not everyone is asleep (passero: 10-5am. zafferano: 4am-8am + naps. milo: 12-7am. amaryllis: no sleep schedule. nikhil: 11-6am. sylvan: 9-4am to keep early morning watch)
lateral hypothalamus on sleepiness
daylight causes scn to indirectly excite neurons in LH for orexin so arousal. without: narcolepsy. darkness means other LH cells are active, releasing neuropeptide melanin-concentrating hormone (MCH), and inducing sleep. mch and orexin inhibit each other
sleep pressure
awake? breakdown of ATP causes adenosine buildup. caffiene blocks receptors. in sleep, adenosine drops.
rem sleep
eyes move, dream, 30-40 hz brain waves, muscle tone vanishes
nonREM sleep
dreamless. stage 3 is deep, 2-4 hz brain waves.
cycle of rem sleep
first rem is after 90 minutes, rem gets longer over the night and sleep gets shallower
sleep deprivation on sleep
first catch up on nREM then more REM
human sleep compared to other primates
more rem, less time. on ground.
simple reflexes
sensory neurons make synapses with spinal cord motoneurons to make simple reflexes. simplest form of motor control, somatic reflexes using skeletal muscle
monosynaptic reflex
single synapse between afferent and efferent neurons
polysynaptic reflex
2 or more synapses. can have both in CNS.
stretch reflex
passive stretch (I.E. ELONGATION) of muscle from weight or contraction of antagonist causes active contraction. very fast and sensitive due to muscle spindle afferents (fastest afferent) and monosynaptic connection to motoneurons
stretch reflex example
hold heavy weight, muscle contracts so you don’t drop it.
stretch reflex latency
25ms for forearm, 37 for ankle
stretch reflex strongest where
postural muscles as it is for stabilizing posture
when is stretch reflex supressed
movement
how does stretch reflex go to the brain
parallel multisynaptic paths through spinal cord, branches up to somatosensory cortex as well
golgi tendon reflex
active tension on the muscle causes relaxation or reduction of tension
how does golgi tendon reflexsynapse
at the interneurons in the intermediate zone of spinal cord, inhibiting the motorneurons of the muscle that sent the signal
purpose of golgi tendon reflex
regulate level of activity complementary to stretch reflex to avoid overexertion. prevents movement, acts in concert with stretch reflex to stabilize posture. suppressed when you actually want to move
how will overactivation of biceps cause contraction of triceps and relaxation of biceps.
tricep will stretch due to overactivation of bicep, causing stretch reflex, triceps contract. overactivation of biceps will cause golgi tendon reflex and biceps relax so you can move the triceps.
flexion withdrawal reflex
noxious injury to limb causes flexion proximal (close to body) and extension distal (far from body).
where does flexion withdrawal reflex synapse
nociceptor afferents synapse on interneurons at the superficial dorsal horn. multisynaptic path to motoneurons
reciprocal inhibition
activation of one motor nucleus causes other to be inactivated, so you can move. not wanted if you want joint stiffness
patellar tendon reflex + synapsing
kick when bang leg iwth a hammer. tap on patellar tendon, stretch quads’ muscle spindle that fires, having an interneuron that causes the quad to kick
cross extension reflex + synapsing
step on lego causes contralateral extension using commissural interneurons carrying signal to contralateral spinal cord.
extensor thrust + synapsing
pressure on sole of foot activates leg extensors. mechanoreceptors project to intermediate zone interneurons and then extensor motoneurons
babinsky sign
extensor thrust (in toes) influenced by corticospinaltract. normally, toes curl down when sole stroked, otherwise, toe curls up.
vestibulo spinal reflex + synapsing
head tilted down activates otolith afferents, downhill limbs extend. otolith afferents activate lateral vestibulo-spinal tract that ipsilaterally (same side) project to extensor (antigrav) motor nuclei
vestibulospinal reflex lag
80 ms
central pattern generators
network of interneuron in spinal cord, brainstep coordinate interaction of many motor groups. reflexes can only do simple movement.
what do you need to restore postural stability after pertubation
centrally coordinated response
cpg activation order
order of relevance.
cpg role
behavioral responses, locomotion, motor control
leg step cycle programmed by? properties?
network of neurons in intermediate zone of lumbar cord. neurons are pacemakers with diffuse excitation (sometimes on/off). reciprocal inhibition, phase dependent reflection
2 half centers of cpg during swing cycle
flexor burst generator to drive flexor motor nuclei > ON. extensor burst generator to drive extensors > OFF
bipedal bird waddle vs human walking energy consumption
wading birds < human < geese, penguins
flexor burst generator connects with what
connects with flexor motor neurons to activate leg flexion and swing. vice vers
flexion phase length
fixed regardless of locomotion/speed
stance phase length
variable duration depending on speed
how is the stance phase regulated so you dont fall
sensory feedback: mechanoreceptors will feed sensory info
stance phase reflexes
stretch reflex, golgi tendon reflex, extensor thrust
why do you need sensory control for steps
to match muscle contraction with loading conditions (is the ground hard? soft? slippery?) tell you when you can swing again
e3 phase (last of stance) ends only if
leg not bearing weight, hip is extended, other land is in stance bearing weight
phases of swing phase
f and e1
arm swing modulation with walking
cpgs in cervical cord program arm motion. flexion phase synchronous with contralateral flexion in leg. phase-linked (lumbar for leg to cervical for arm) via propriospinal tracts
why do we need posture compensation in trunk and head to not fall over when walking. where are the corresponding cpgs
because we are bipedal and postural cpgs that coordinate posture are in the reticular formation
head angle during walking, how maintained
head is still despite other parts moving, using visual (slower system but vertical and motion cues), vestibular (gravity), propioceptive reflexes (a type of somatosensory).
autonomic nervous system (ans) works with what to maintain homeostasis
endocrine and behavioral state systems
ans deals with
internal organs, blood flow, smooth muscles of eye, viscera, exercise, emotion, effect of gravity, eating
preganglionic ans neuron is located in __, project onto __, release __
central nervous system (brainstem or spinal cord), project onto postganglionic neurons’ ganglia, release ACH
postganglionic axons project onto __, release__
project onto sympathetic tissue. most sympathetic release noepinephrine except ACh at skin sweat glands. most parasympathetic release Ach with the exception of NO for erections
sympathetic nervous system preganglionic neurons
preganglionic: thoracolumbar spinal cord (intermedio-lateral horn), short to sympathetic chain.
sympathetic nervous system postganglionic neurons
long, synapse and linked together in sympathetic chain
parasympathetic nervous system preganglionic neurons
long preganglionic neurons from brainstem or sacral spinal cord (several cranial motor nuclei 3, 7, 9 and 10).
parasympathetic nervous system postganglionic neurons
short postganglionic neurons from ganglia to effector organs. ganglia embedded in targed organ
sympathetic nervous system responses
fight or flight, prepare for emergency, stress, exercise, increase heart rate blood pressure, mobilize energy stores, pupil dilation, diffuse effect due to widespread and interconnected nerves. decrease gastrointestinal and urinary functions, releases epinephrine
adernal medulla and sympathetic nervous system.
sprecialized neuroendocrine tissue that acts with sympathetic, described as sympathetic ganglion. recieves signal from preganglionic sympathetic neurons and chromaffin cells release epinephrine
parasympathetic effects
quiet, relaxed states, active in rest and digest, increase gastrointestinal activities, decrease heart rate and blood pressure
para and symp. systems at rest
tonic activity, both branches active. PARA DOMINATES. complementary effects.
targets of autonomic neurons
smooth muscle, cardiac muscle glands. the synapse is a neuroeffector junction without axon terminals. the structure is called a varicosity with an axon swelling that contains vesicles filled with neurotransmitter
noepinephrine taken up by
metabolized by monoamine oxidase after remooval from synapse. can be reused also
autonomic reflexes
can be modulated, linked to sensory system for input for reflexes, negative feedback loop. e.g. cannot pee if watched,
pupilary light reflex location
at pretectal area of midbrain. too bright: parasympathetic reflex via 3rd cranial nerve to ciliary ganglion and circular iris muscles. too dark: sympathetic reflex via thoracic cord, sympathetic chain to radial muscles
pupilary light reflex but tricked
light illusions (cortical influence)
baroreflex
detect blood pressure changes using special sensors in blood vessels. signals sent to brainstem part called nucleus of solitary tract (NTS), main hub for processing info from baroreceptors. this hub then sends info to ventrolateral medulla
ventrolateral medulla 2 parts
caudal (lower) part inhibits rostral, decreases blood pressure. rostral (upper) part raises blood pressure and heart rate to increase sympathetic activity
muscle sympathetic effects
mostly influenced by noadrenergic vasoconstriction to maintain blood pressure as a part of blood pressure
how does autonomic nervous system work with endocrine and behavioral system for homeostasis
hypothalamus, pons, medulla takes in sensory info (somatosensory, visceral) to regulate blood pressure using brainstem cardiovascular center, body temperature, respiratory pattern generator in lateral medulla and pons.
periaqueductal gray effects
midbrain premotor center for autonomic behavioral brograms (fight, fear, feeding, vocalization, sex, etc). significant interaction with hypothalamus, reticular formation
how is fight stimulated in sympathetic
cardiovascular center in medulla and raphe in spinal cord depolarizes all motoneurons and decreases pain transmission in dorsal horn
reticular activating systems
global change in cns activity with diffuse modulatory system, mainly metabotropic mechanisms
cholinergic (ach) reticular activating system. originate? terminate?
sleep-wake cycle, arousal, learning, memory, sensory info through thalamus. originates from base of cerebrum, pons and midbrain. terminate at cerebrum, hippocampus, thalamus
serotenergic (serotonin) upper reticular activating system. originate? terminate?
mood, emotion, behavior, aggression, depression. originate raphe nuclei along brain stem midline, project onto most of brain
sertenergic (serotonin) lower reticular activating system. originate? terminate?
pain, locomotion, same as upper except project to spinal cord
dopaminergic (dopamine) reticular activating system. originate? terminate?
reward center. originate substantia nigra in midbrain, ventral tegmentum in midbrain. to cortex and parts of limbic system.
histaminergic (histamine) reticular activating system. originate? terminate?
sleep wake control, supports waking state. originate posterior thalamus, terminate forebrain.
skeletal muscle
striated, somatic nervous system activates it, motor neurons and muscle fibers form a muscle unit, with chemical signalling between the 2.
smallest unit of muscle
sarcomere (actin + myosin)
muscle fiber
extend length of muscle from tendon to tendons
sarcolemma
membrane of muscle cell
t-tubule system
invagination of sarcolemma into muscle fiber
sarcoplasmic reticulum
intracellular organelle to store calcium
muscle contraction
sarcomere shortening, actin and myosin sliding past each other. actin is the thin double stranded. myosin is the one that looks like 王
troponin and tropomyosin
no calcium means troponin holds myosin over tropomyosin over myosin binding sites on actin so actin cannot bind myosin and the muscle is relaxed. with calcium means calcium binds troponin, causing it to move and make tropomyosin expose myosin binding sites, and now muscle can contract
motor unit
muscle fiber of motor unit are all the same type. categories based on histochemical characteristics. muscle fibers all contract together. smoothness and precision of movement depends on number and timing of motor units activated. small motor units activated first.
crossbridge cycle
power stroke, thin and thick filaments detach (low energy)
power stroke
myosin head moves propelling thin filament (high to low energy). begins when there is calcium at the muscle
when is the crossbridge cycle ready for the next cycle
when it is high energy and atp has bound and is now hydrolyzed. the adp and phosphate remain bound to myosin, yeet phosphate when stroking.
rigor mortis is caused by
myosin binding to actin and being able to detatch due to the lack of atp after death
excitation contracting coupling for skeletal
how action potentials in sarcolemma causes contractions. motor neurons release ach, na+ entry causing muscle action potention, ap in t-tubule causes dhp (type of calcium channel) which opens RYR ca2+ channels and ca2+ arrives, binding to troponin allowing actin-myosin binding. then power stroke.
terminating contraction for skeletal
calcium leaves binding sites due to ca++ atpase in sarcoplasmic reticulum. calcium from cytosol into sarcoplasmic reticulum.
fast twitch glycolytic fibers
large amounts of tension, rapid fatigue with large diameter motor neurons
slow twitch oxidative fibers
slow contracting, many mitochondria, oxidative metabolization, fatigue resistant. small diameter motor neurons.
twitch contraction
time depends on fiber type. many twitches working together generates force. has three period: latent, period of contraction, period of relaxation.
latent period
excitation-contraction coupling. preparing to stroke
period of contraction
high ca2+, crossbridge cycling
period of relaxation
ca2+ falling, tension gradually drops to 0
summation and tetanus
increased action potential frequency, twitches fuse and add onto each other, contractile force increases. repeated stimulation causes tetanus and too much causes rapid decrease in tension.
smooth muscle location, traits
internal organs, blood vessels (vasculature, GI tracts, urinary, reproductive, respiratory tracts, pupill). no sarcomeres, ans involuntary control. wide range of lengths, layers in many directions, contractions and relaxes slower, uses less energy, sustained contracts for longer
single unit smooth muscle
in intestine and blood vessels. spontaneous activity from ANS
multi-unit smooth muscle
large airways and arteries, each fiber acts individually, heavily innervated, generally only contracts when stimulated
excitation-contraction coupling (smooth muscle)
lacks specialized receptor regions (no neuro-muscular junction) ca2+ from extracellular fluid and a bit from sarcoplasmic reticulum causes cascade ending with phosphorylation of myosin and myosin atpase
what must happen before crossbridge cycling for smooth muscles
calcium channels open in plasma membrane. calcium triggers release of calcium release from sarcoplasmic membrane, calcium binds to calmodulin. ca-calmodulin binds to mlck, phosphorylates myosin.
relaxation of smooth muscle
phosphatase yoinks phosphatase from myosin, calcium removed from cytoplasm by ca-ATPase, ca-na counter transport
cardiac muscle traits
contractile, conductile cells. striated, contractile filaments in sarcomeres. intermediate sarcoplasmic reticulum size. has gap junctions. also controlled by ans
aps for cardiac muscle
300 ms. long due to slow ca 2+ channels. can have forcceful contraction. the time is 20-50 times longer than skeletal. Na+, ca2+ permeability changed ofc lol
how to increase force for cardiac muscle
force increased by increasing muscle length (starling law)
excitation-contraction coupling for cardiac muscle
significant ca2+ from extracellular fluid, rest from sarcoplasmic reticulum (like smooth). contractile proteins can now contract. sarcoplasmic reticulum pump and Na+ Ca2+ pumps remove ca2+ from cytosol
complex/volitional movement
motor output planned and refined by motor cortex, basal ganglia, and cerebellum. irrelevant to gravity, removed from posture control. learned or eveoled
motor cortex
at precentral gyrus of central sulcus. somatotopic organization.
motor cortex neuron synapsing
most axons from motor cortex that go to spinal cord go to interneurons like stuff in the red nucleus/ direct corticospinal synapses on motoneurons (20% of descending axons.
motor field
one corticospinal axon synapses with many motor nuclei. many synapses are silent, allowing for plasticity
somatosensory inputs access to motor cortex
only some sensory input has direct access to motor cortex. cutaneous input from somatosensory association areas like touch on skin, and proprioceptive input from thalamus can access.
multiple representation.
single motor nuclei represented in columns at many loci. a cluster is a synergy. depends on personal experience. more synergies means more representation. very obvious for languages, as motor map is laid out in development
red nucleus
rubrospinal cells (contralateral, crosses midliine of spinal cord, ends up in intermediate zones) within red nucelus synergize (first region for distal limb movements).
reticulospinal and vestibulospinal tracts do not synergize as much because
not precise movements
premotor areas
project onto motor cortex, programming for higher order movements, select motor cortical synergies for a given movement. pattern generation for highly learned movements. processes sensory inputs for cueing movement phases. dorsal visual to dorsal movement, vice versa
brocas’ area is an example of
a premotor area for preparing to speak/write/type with info from wernicke’s
preparatory activity for premotor areas
motor neurons set up motor cortex which is not active during performance. it is only active during preparatory phase of movement to facilitate synergies. active all the way from warning to go cue
cingulate motor area (CMA)
genuine smile, within cingulate sulcus. emotional, motivational drive for movements
supplementary motor area (SMA)
also somatotopic, on medial wall of hemisphere. less info recieved than with motor cortex. controls bilateral coordination when there are different movements (taking bottle off tray). conscious (volitional) signals like fake smile
