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physiology except 10 times harder thanks to my stupid fucking depression > finals except life is meaningless and i hallucinated a baby in the grocery store > Flashcards

finals except life is meaningless and i hallucinated a baby in the grocery store Flashcards

1
Q

what wavelengths can we see, why

A

400-700. because earth’s atmosphere is most transparent to these wavelengths

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2
Q

what are extraspectral colors

A

purple and white. mix of wavelengths (e.g. purple is when 2 or more wavelengths affect red and blue cones more than green cones

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3
Q

what are the percentages of cone

A

63% red, 31% green, 6% blue

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4
Q

what colors do rodes (rhodopsin) prefer to see

A

blue-green

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5
Q

what is a r+g ganglion cell

A

excited by red light and by green light, aka yellow channel

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6
Q

r-g, g-r ganglion cell

A

activated by red light, inhibited by green., and vice versa. red-green opponent channel

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7
Q

b-(r+g) ganglion cell

A

blue-yellow opponent channel

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8
Q

explanation for afterimages

A

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)

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9
Q

daltonism

A

red-green colorblindness. red and green cone visual pigments lie on x-chromosomes. 95% of all variations in color vision.

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10
Q

why are women rarely color blind

A

women are rarely color blind because if one x-chromosome codes a faulty pigment then the other x-chromosome compensates.

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11
Q

how could a woman become a tetrachromat

A

if 2 x-chromosomes code for 2 different functional red cone pigments

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12
Q

reflectance

A

intrinsic color of a surface, the tendency to reflect certain wavelengths and absorb others

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13
Q

color constancy

A

ability to infer reflectance in different light

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14
Q

chevreul illusions for color and brightness

A

different hues and different saturations -> look redder when close to low saturation and different hues

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15
Q

external ear

A

pinna, ear canal, sealed at the end by tympanic membrane aka eardrum

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16
Q

middle ear

A

air filled space behind eardrum connected to pharynx by eustachian tube

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17
Q

inner ear

A

cochlea for hearing, vestibular apparatus for equilibrium

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18
Q

sound waves and molecule density

A

at the peak of the waves the molecules are crowded together and pressure is high. vice versa

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19
Q

Frequency is percieved as

A

pitch. low freq-> low pitch

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20
Q

Unit of frequency

A

waves/sec (hz)

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21
Q

human hearing range, best acurity

A

16-20,000hz. around 10 octaves. best hearing around 1000-3000 hz

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22
Q

what does loudness depend on

A

frequency (needs to be within hearing range) and amplitude

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23
Q

middle ear small bones (ossicles)

A

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

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24
Q

where does the oval window lead

A

cochlea

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25
Q

vestibular duct and tympanic duct anatomy

A

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)

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26
Q

cochlear duct

A

aka scala media, contains endolymph (similar to intracellular fluid). waves shake cochlear duct as it has auditory receptor hair cells.

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27
Q

organ of corti

A

in the cochlear duct, sits on the basilar membrane under tectorial membrane. hair cells have their little hairs against the tectorial membrane.

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28
Q

hair cells (number, type of cell, how they work

A

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

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29
Q

how does a hair cell send a signal

A

cilia bend towards longest cilium to depolarize and release transmitter and activate a primary sensory neuron. this neuron form auditory nerve

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30
Q

auditory nerve

A

cochlear nerve, a branch of cranial nerve 8.

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31
Q

cilia bending away from the longest cilium causes

A

hyperpolarization, releasing less transmitter, doesn’t excite neuron as much

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32
Q

basilar membrane responding to different frequency

A

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

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33
Q

auditory signals localization in the brain

A

pass through each ear to both sides of the brain (so right and left ear signals will be everywhere in the brain)

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34
Q

primary auditory cortex

A

in temporal lobe

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35
Q

how does brain know where the sound comes from

A

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.

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36
Q

conductive hearing loss

A

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

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37
Q

sensorineural hearing loss

A

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

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38
Q

how does the vestibular apparatus sense head relative to gravity

A

utricle and saccule have hair cells that are activated when the head tilts relative to gravity

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39
Q

how does the vestbular apparatus sense head rotation

A

semi-circular canals are fluid filled hoops, fluid sloshes left if you turn ur head right, activating hair cells

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40
Q

vestibular hair cells signalling

A

activate primary sensory neurons of vestibular nerve, a branch of cranial nerve 8

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41
Q

where do cranial nerve 8 go

A

pass through cerebellum. or synapse in medulla, then go to cerebellum OR up through thalamus to cortex.

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42
Q

proprioception

A

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.

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43
Q

nociception

A

tissue damage or the threat of it. percieved as pain or itch

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44
Q

4 somatic senses

A

touch, temperature, proprioception, nociception

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45
Q

somatosensory receptor cells are all

A

neurons

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46
Q

cell bodies for somatic sensation below the chin are in…

A

cell bodies in dorsal root ganglia

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47
Q

receptors for the head have cell bodies…

A

in the brain

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48
Q

where to neurons transduce touch/pressure into electrical signals

A

at nerve endings (tips of fibers in skin and viscera)

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49
Q

types of receptors in skin

A

free nerve endings, merkel receptors (or disks), encapsulated receptors (meissner or pacinian corpuscles).

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50
Q

free nerve endings

A

detect mechanical stimuli, temperature, chemicals

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51
Q

merkel recpetors

A

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)

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52
Q

encapsulated receptors

A

meissner and pacinian corpuscles, mechanoreceptors in connective tissue.

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53
Q

most receptors are phasic/tonic?

A

phasic. nerve ending depolarizes but returns to baseline in 3ms.

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54
Q

meissner corpuscles

A

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

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55
Q

pacinian corpuscles

A

nerve endings sheathed in many layers. sense tiny displacements if motion is quick. phasic, respond strongly to vibration and other quick stimuli

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56
Q

2 point discrimination on lips and fingertips, on calves

A

2-4mm on lips and fingertips, on calves 40mm

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57
Q

thermoreceptors

A

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)

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58
Q

above 45 degrees, what happens to receptors

A

pain receptors activated, cold fibers briefly respond creating paradoxical cold

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59
Q

nociceptors respond to

A

mechanical, heat, chemicals. chemicals from damaged cells (K+, histamine, prostaglandins), serotonin released by platelets from injury

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60
Q

somatosensory afferents have 2 groups

A

small, large

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61
Q

small fiber types

A

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.

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62
Q

adequate stimuli for small fibers

A

different adequate stimuli, such as mechanical stimuli, chemicals, temperature.

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63
Q

large fibers

A

a-beta. come from merkel disks or encapsulated mechanoreceptors. myelinated, conduct at 70 m/s

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64
Q

large fiber projection into brain

A

go up spinal cord in dorsal columns, then in the medulla synapse on neurons which go to other side (ipsilateral)

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65
Q

small fiber projection into brain

A

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

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66
Q

reason for large fiber’s projection into brain

A

feedback, especially for motor cortex as it manipulates objects. needs to travel a long way to the brain quickly.

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67
Q

reason for small fiber’s projection into brain

A

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.

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68
Q

how somatosensory info goes from spinal cord to thalamus, cortex

A

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

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69
Q

somatotopic

A

means neighboring places correspond to neighboring brain places.

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70
Q

primary somatosensory cortex (s1) is in what lobe

A

parietal

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71
Q

lateral inhibition among somatosensory fibers

A

lateral inhibition enhances spatial differences, you feel hot bath is most hot around the water surface. somatosensory version of chevreul illusion

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72
Q

TRP ION CHANNELS, types and where it is present

A

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

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73
Q

congential analgesia death expected age

A

20 due to injury and infection (cannot feel pain)

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74
Q

2 types of pain

A

fast and slow. respectively carried by a delta and c fibers (both small!).

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75
Q

nociceptive signals reaching the limbig system

A

emotional distress, nausea, vomiting, sweating

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76
Q

decending pathways blocking nociceptive cells

A

when ur at con and ur feet doesn’t hurt because of the adrenaline

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77
Q

referred pain

A

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

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78
Q

how do a beta gate control pain

A

c fibers contact secondary neurons in dorsal horn, secondaries inhibited by a beta fibers using interneurons. (e.g. rubbing sore feels better)

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79
Q

analgesic mechanisms

A

aspirin inhibits prostaglandins and inflammation, slowing transmission of pain
opioids decrease transmitter release from primary sensory neurons and postsynaptically inhibit secondary sensory neurons.

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80
Q

natural painkillers

A

endorphins, enkephalins, dynorphins

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81
Q

liver and gallbladder pain

A

below boob to shoulder

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82
Q

colon, stomach, small intestine, appendix. which pain on top of what

A

stomach above small intestine above appendix above colon

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83
Q

chemoreception

A

smell and taste. evolutionarily old, bacteria and animals without brains (me) use it

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84
Q

olfactory epithelium

A

top of nasal cavity, covering 3cm with 5 million receptor cells each for each nostril.

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85
Q

pigmentation of epithelium

A

richness is related with olfactory sensitivity. people: pale yellow. cats: dark mustard brown.

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86
Q

receptor neurons in epithelium

A

a single dendrite that extends into olfactory epithelium. branches to form nonmotile cilia, increasing the surface area of the cell (for catching more odorants).

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87
Q

how many odorant receptor molecules per receptor? how many types of receptor cell?

A

only one type of receptor molecule but a lot of that one type. 400 kinds of receptor cell (400 primary odors)

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88
Q

g protein coupled receptor molecules for olfaction, how does this send an action potential

A

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

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89
Q

how many genes for g protein coupled recptor molecules

A

1000 genes, making the largest known gene family in vertebrates.

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90
Q

how much of the g protein coupled genome expressed in humans

A

3-5% of genome

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91
Q

sensitivity of olfactory receptors

A

can detect a single molecule of preferred chemical, but 40 cells must react before we experience it as smell

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92
Q

pinocytosis occurs in what sense’s cells

A

olfactory receptor cells. constantly sip fluid then send it along nerves into brain

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93
Q

lifespan of olfactory receptor cells

A

short lived, degenerate after a month or 2. unusual.

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94
Q

how do olfactory receptor cells send signal to olfactory bulb

A

tiny holes in cribiform “sievelike” plate at the bottom of the cranial cavity

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95
Q

olfactory bulb

A

extension of cerebrum, under the frontal lobes in the brain.

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96
Q

projection from receptors to bulb is called

A

olfactory nerve, or cranial nerve 1

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97
Q

olfactory convergence

A

rods converge on gaglion cells, enhances sensitivity but discards spatial information

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98
Q

head damage can damage what sense

A

can damage olfaction, primary sensory neurons

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99
Q

olfactory bulbs projects where

A

directly to olfactory cortex, by passing thalamus. also limbic system, linked to motivation and emotion, so odors can bring emotional memories

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100
Q

olfactory cortex is in where

A

frontal and temporal lobes

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101
Q

parts of limbic system

A

cingulate gyrus, hippocampus, amygdala

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102
Q

olfaction adaptation

A

primarily phasic, people get used to bad smells over time

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103
Q

pheromones O_o

A

chemicals released by an animal that affects physiology or behavior of its own species. in rodents, the vomeronasal organ (VNO) processes phermonone behavior

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104
Q

human pheromones OwO

A

VNO disappears you omegaverse authors fuck you. (we do respond to some chemical signals though)

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105
Q

tastebud number, location

A

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.

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106
Q

taste bud made up of?

A

100 receptor EPITHELIAL cells. NOT neurons. arranged like petals, open up with a small pore (taste pore)

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107
Q

typical taste bud has how many types of receptor cells, what do they detect

A
  1. sweet detects sugar. umami detects glutamate (protein). bitter detects poison. salty and sour detect Na+ and H+. tongue may have receptors for fatty acids
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108
Q

3 types of taste receptor cells

A

type 1: salt. type 2: sweet, bitter, umami. type 3: sour.

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109
Q

taste receptor cells communicating at synapses

A

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.

110
Q

why do type 2 taste cells release atp

A

they have receptor molecules coupled to g protein called gustducin, activating signal pathways to increase intracellular Ca2+ and releasing atp.

111
Q

detecting salt and sour releases atp?

A

no. they involve ion channels not linked to g proteins

112
Q

experience of food depends on?

A

smell, temperature, pain, texture, crunch, appearance, cognition

113
Q

taste signal to brain route

A

taste buds: synapse in medulla and thalamus en route to cortes. excite cranial nerves 7, 9 and 10. facial, glossopharyngeal, and vagus nerves.

114
Q

hypothalamic controls __ using __ in order to __

A

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

115
Q

hormonal and neural influences of the hypothalamus

A

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

116
Q

lesions of what causes obesity, of what cause thin

A

ventromedial hypothalamus and lateral hypothalamus respectively

117
Q

arcuate NPY neurons inhibit and activate

A

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.

118
Q

arcuate nucleus of thalamus release what

A

release NPY, GABA, and agouti-related peptide (AgRP)

119
Q

arcuate pomc neurons release what

A

cleave pro-opiomelanocortin (POMC) to make a melanocyte stimulating hormone (alpha MSH) which they release at the synapses.

120
Q

arc-pomc neurons inhibit and activate

A

inhibit dorsomedial hypothalamus (dmh) and excites pvn, ventromedial hypothalamus (vmh)

121
Q

pvn and vmh in arc-pomc pathway do what

A

promote sympathetic nervous system

122
Q

dmh in arc-pomc pathway do what

A

inactivate sympathetic, but since dmh is inhibited, the overall is promoting sympathetic.

123
Q

final outcome of arc-pomc

A

no feeding. sympathetic ns being active will always cause no feeding, arc-npy will inhibit arc-pomc

124
Q

how does body know if you’ve reached your weight set point

A

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.

125
Q

leptin effects in feeding centers

A

excite pvn, thus indirectly increasing sympathetic activity and decreasing feeding. decreases arc-npy and lh to prevent feeding.

126
Q

leptin effects on satiety centers

A

excite arc-pomc, vmh to promote sympathetic and decrease feeding. inhibit dmh as it decreases sympathetic

127
Q

how does brain know when to end meal

A

blood glucose. excites arc-pomc, inhibits lh. sensors in walls of stomach measuring nutrients and stretch

128
Q

walls of stomach sensed nutrients and stretch releases what

A

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.

129
Q

nerve stimulated from stretch and sugar detected

A

vagus nerve, which excites vmh via nucleus tractus solitarius (NTS)

130
Q

ghrelin released when does what

A

when stomach is empty by cells in stomach walls. stretch stops release. acts directly on arc-NPY and LH and inhibits PVN

131
Q

dangerous appetite supressors

A

amphetamines, fenfluramine

132
Q

rimonabant

A

blocks CB1 endocannabinoid receptors, moderate weight loss but nausea, depression, suicide

133
Q

leptin for weight loss drug

A

not helpful, obesity rarely leptin deficient

134
Q

cck and pyy agonists

A

not helpful (supposed to stimulate stretch of stomach)

135
Q

liraglutide

A

a possible solution for obesity, GLP-1 agonist

136
Q

circadian rhythms found in

A

bacteria, protozoa, plants, fungi, animals

137
Q

human circadoan rhythms influence

A

behavior, alertness, mood, body temp, hormone levels

138
Q

endogenous meaning

A

not simply reponses to environmental changes. circadian rhythms continue even when the environment is constant.

139
Q

what is entraining

A

to have all the cells with their individual internal clocks kept in sync by master clock in brain taking in sensory signals

140
Q

transcription translation feedback loop

A

aka TTFL, when PER protein represses transcription of per.

141
Q

PER/TIM maxed out when? effects on other things

A

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.

142
Q

clk and cyc effects on per, tim

A

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.

143
Q

doubletime gene

A

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

144
Q

human homologs of circadian rhythm genes and proteins

A

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.

145
Q

zeitgeber, main one?

A

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)

146
Q

SCN recieve light signals does what

A

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.

147
Q

entrainment

A

nudging clock in synchrony, other clocks are entrained to SCN after neural signals go from SCN to other brain areas.

148
Q

pineal body

A

projected onto from SCN via hypothalamus nuclei and sympathetic nervous system. at the back of diencephalon. secretes melatonin.

149
Q

melatonin levels throughout the day acts on what

A

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

150
Q

melatonin for jet lag

A

jet lag is because clock can only adjust by one hour a day. melatonin taken 30 min before target bed time for eastward travel

151
Q

chronotypes

A

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)

152
Q

lateral hypothalamus on sleepiness

A

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

153
Q

sleep pressure

A

awake? breakdown of ATP causes adenosine buildup. caffiene blocks receptors. in sleep, adenosine drops.

154
Q

rem sleep

A

eyes move, dream, 30-40 hz brain waves, muscle tone vanishes

155
Q

nonREM sleep

A

dreamless. stage 3 is deep, 2-4 hz brain waves.

156
Q

cycle of rem sleep

A

first rem is after 90 minutes, rem gets longer over the night and sleep gets shallower

157
Q

sleep deprivation on sleep

A

first catch up on nREM then more REM

158
Q

human sleep compared to other primates

A

more rem, less time. on ground.

159
Q

simple reflexes

A

sensory neurons make synapses with spinal cord motoneurons to make simple reflexes. simplest form of motor control, somatic reflexes using skeletal muscle

160
Q

monosynaptic reflex

A

single synapse between afferent and efferent neurons

161
Q

polysynaptic reflex

A

2 or more synapses. can have both in CNS.

162
Q

stretch reflex

A

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

163
Q

stretch reflex example

A

hold heavy weight, muscle contracts so you don’t drop it.

164
Q

stretch reflex latency

A

25ms for forearm, 37 for ankle

165
Q

stretch reflex strongest where

A

postural muscles as it is for stabilizing posture

166
Q

when is stretch reflex supressed

A

movement

167
Q

how does stretch reflex go to the brain

A

parallel multisynaptic paths through spinal cord, branches up to somatosensory cortex as well

168
Q

golgi tendon reflex

A

active tension on the muscle causes relaxation or reduction of tension

169
Q

how does golgi tendon reflexsynapse

A

at the interneurons in the intermediate zone of spinal cord, inhibiting the motorneurons of the muscle that sent the signal

170
Q

purpose of golgi tendon reflex

A

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

171
Q

how will overactivation of biceps cause contraction of triceps and relaxation of biceps.

A

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.

172
Q

flexion withdrawal reflex

A

noxious injury to limb causes flexion proximal (close to body) and extension distal (far from body).

173
Q

where does flexion withdrawal reflex synapse

A

nociceptor afferents synapse on interneurons at the superficial dorsal horn. multisynaptic path to motoneurons

174
Q

reciprocal inhibition

A

activation of one motor nucleus causes other to be inactivated, so you can move. not wanted if you want joint stiffness

175
Q

patellar tendon reflex + synapsing

A

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

176
Q

cross extension reflex + synapsing

A

step on lego causes contralateral extension using commissural interneurons carrying signal to contralateral spinal cord.

177
Q

extensor thrust + synapsing

A

pressure on sole of foot activates leg extensors. mechanoreceptors project to intermediate zone interneurons and then extensor motoneurons

178
Q

babinsky sign

A

extensor thrust (in toes) influenced by corticospinaltract. normally, toes curl down when sole stroked, otherwise, toe curls up.

179
Q

vestibulo spinal reflex + synapsing

A

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

180
Q

vestibulospinal reflex lag

A

80 ms

181
Q

central pattern generators

A

network of interneuron in spinal cord, brainstep coordinate interaction of many motor groups. reflexes can only do simple movement.

182
Q

what do you need to restore postural stability after pertubation

A

centrally coordinated response

183
Q

cpg activation order

A

order of relevance.

184
Q

cpg role

A

behavioral responses, locomotion, motor control

185
Q

leg step cycle programmed by? properties?

A

network of neurons in intermediate zone of lumbar cord. neurons are pacemakers with diffuse excitation (sometimes on/off). reciprocal inhibition, phase dependent reflection

186
Q

2 half centers of cpg during swing cycle

A

flexor burst generator to drive flexor motor nuclei > ON. extensor burst generator to drive extensors > OFF

187
Q

bipedal bird waddle vs human walking energy consumption

A

wading birds < human < geese, penguins

188
Q

flexor burst generator connects with what

A

connects with flexor motor neurons to activate leg flexion and swing. vice vers

189
Q

flexion phase length

A

fixed regardless of locomotion/speed

190
Q

stance phase length

A

variable duration depending on speed

191
Q

how is the stance phase regulated so you dont fall

A

sensory feedback: mechanoreceptors will feed sensory info

192
Q

stance phase reflexes

A

stretch reflex, golgi tendon reflex, extensor thrust

193
Q

why do you need sensory control for steps

A

to match muscle contraction with loading conditions (is the ground hard? soft? slippery?) tell you when you can swing again

194
Q

e3 phase (last of stance) ends only if

A

leg not bearing weight, hip is extended, other land is in stance bearing weight

195
Q

phases of swing phase

A

f and e1

196
Q

arm swing modulation with walking

A

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

197
Q

why do we need posture compensation in trunk and head to not fall over when walking. where are the corresponding cpgs

A

because we are bipedal and postural cpgs that coordinate posture are in the reticular formation

198
Q

head angle during walking, how maintained

A

head is still despite other parts moving, using visual (slower system but vertical and motion cues), vestibular (gravity), propioceptive reflexes (a type of somatosensory).

199
Q

autonomic nervous system (ans) works with what to maintain homeostasis

A

endocrine and behavioral state systems

200
Q

ans deals with

A

internal organs, blood flow, smooth muscles of eye, viscera, exercise, emotion, effect of gravity, eating

201
Q

preganglionic ans neuron is located in __, project onto __, release __

A

central nervous system (brainstem or spinal cord), project onto postganglionic neurons’ ganglia, release ACH

202
Q

postganglionic axons project onto __, release__

A

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

203
Q

sympathetic nervous system preganglionic neurons

A

preganglionic: thoracolumbar spinal cord (intermedio-lateral horn), short to sympathetic chain.

204
Q

sympathetic nervous system postganglionic neurons

A

long, synapse and linked together in sympathetic chain

205
Q

parasympathetic nervous system preganglionic neurons

A

long preganglionic neurons from brainstem or sacral spinal cord (several cranial motor nuclei 3, 7, 9 and 10).

206
Q

parasympathetic nervous system postganglionic neurons

A

short postganglionic neurons from ganglia to effector organs. ganglia embedded in targed organ

207
Q

sympathetic nervous system responses

A

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

208
Q

adernal medulla and sympathetic nervous system.

A

sprecialized neuroendocrine tissue that acts with sympathetic, described as sympathetic ganglion. recieves signal from preganglionic sympathetic neurons and chromaffin cells release epinephrine

209
Q

parasympathetic effects

A

quiet, relaxed states, active in rest and digest, increase gastrointestinal activities, decrease heart rate and blood pressure

210
Q

para and symp. systems at rest

A

tonic activity, both branches active. PARA DOMINATES. complementary effects.

211
Q

targets of autonomic neurons

A

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

212
Q

noepinephrine taken up by

A

metabolized by monoamine oxidase after remooval from synapse. can be reused also

213
Q

autonomic reflexes

A

can be modulated, linked to sensory system for input for reflexes, negative feedback loop. e.g. cannot pee if watched,

214
Q

pupilary light reflex location

A

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

215
Q

pupilary light reflex but tricked

A

light illusions (cortical influence)

216
Q

baroreflex

A

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

217
Q

ventrolateral medulla 2 parts

A

caudal (lower) part inhibits rostral, decreases blood pressure. rostral (upper) part raises blood pressure and heart rate to increase sympathetic activity

218
Q

muscle sympathetic effects

A

mostly influenced by noadrenergic vasoconstriction to maintain blood pressure as a part of blood pressure

219
Q

how does autonomic nervous system work with endocrine and behavioral system for homeostasis

A

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.

220
Q

periaqueductal gray effects

A

midbrain premotor center for autonomic behavioral brograms (fight, fear, feeding, vocalization, sex, etc). significant interaction with hypothalamus, reticular formation

221
Q

how is fight stimulated in sympathetic

A

cardiovascular center in medulla and raphe in spinal cord depolarizes all motoneurons and decreases pain transmission in dorsal horn

222
Q

reticular activating systems

A

global change in cns activity with diffuse modulatory system, mainly metabotropic mechanisms

223
Q

cholinergic (ach) reticular activating system. originate? terminate?

A

sleep-wake cycle, arousal, learning, memory, sensory info through thalamus. originates from base of cerebrum, pons and midbrain. terminate at cerebrum, hippocampus, thalamus

224
Q

serotenergic (serotonin) upper reticular activating system. originate? terminate?

A

mood, emotion, behavior, aggression, depression. originate raphe nuclei along brain stem midline, project onto most of brain

225
Q

sertenergic (serotonin) lower reticular activating system. originate? terminate?

A

pain, locomotion, same as upper except project to spinal cord

226
Q

dopaminergic (dopamine) reticular activating system. originate? terminate?

A

reward center. originate substantia nigra in midbrain, ventral tegmentum in midbrain. to cortex and parts of limbic system.

227
Q

histaminergic (histamine) reticular activating system. originate? terminate?

A

sleep wake control, supports waking state. originate posterior thalamus, terminate forebrain.

228
Q

skeletal muscle

A

striated, somatic nervous system activates it, motor neurons and muscle fibers form a muscle unit, with chemical signalling between the 2.

229
Q

smallest unit of muscle

A

sarcomere (actin + myosin)

230
Q

muscle fiber

A

extend length of muscle from tendon to tendons

231
Q

sarcolemma

A

membrane of muscle cell

232
Q

t-tubule system

A

invagination of sarcolemma into muscle fiber

233
Q

sarcoplasmic reticulum

A

intracellular organelle to store calcium

234
Q

muscle contraction

A

sarcomere shortening, actin and myosin sliding past each other. actin is the thin double stranded. myosin is the one that looks like 王

235
Q

troponin and tropomyosin

A

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

236
Q

motor unit

A

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.

237
Q

crossbridge cycle

A

power stroke, thin and thick filaments detach (low energy)

238
Q

power stroke

A

myosin head moves propelling thin filament (high to low energy). begins when there is calcium at the muscle

239
Q

when is the crossbridge cycle ready for the next cycle

A

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.

240
Q

rigor mortis is caused by

A

myosin binding to actin and being able to detatch due to the lack of atp after death

241
Q

excitation contracting coupling for skeletal

A

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.

242
Q

terminating contraction for skeletal

A

calcium leaves binding sites due to ca++ atpase in sarcoplasmic reticulum. calcium from cytosol into sarcoplasmic reticulum.

243
Q

fast twitch glycolytic fibers

A

large amounts of tension, rapid fatigue with large diameter motor neurons

244
Q

slow twitch oxidative fibers

A

slow contracting, many mitochondria, oxidative metabolization, fatigue resistant. small diameter motor neurons.

245
Q

twitch contraction

A

time depends on fiber type. many twitches working together generates force. has three period: latent, period of contraction, period of relaxation.

246
Q

latent period

A

excitation-contraction coupling. preparing to stroke

247
Q

period of contraction

A

high ca2+, crossbridge cycling

248
Q

period of relaxation

A

ca2+ falling, tension gradually drops to 0

249
Q

summation and tetanus

A

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.

250
Q

smooth muscle location, traits

A

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

251
Q

single unit smooth muscle

A

in intestine and blood vessels. spontaneous activity from ANS

252
Q

multi-unit smooth muscle

A

large airways and arteries, each fiber acts individually, heavily innervated, generally only contracts when stimulated

253
Q

excitation-contraction coupling (smooth muscle)

A

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

254
Q

what must happen before crossbridge cycling for smooth muscles

A

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.

255
Q

relaxation of smooth muscle

A

phosphatase yoinks phosphatase from myosin, calcium removed from cytoplasm by ca-ATPase, ca-na counter transport

256
Q

cardiac muscle traits

A

contractile, conductile cells. striated, contractile filaments in sarcomeres. intermediate sarcoplasmic reticulum size. has gap junctions. also controlled by ans

257
Q

aps for cardiac muscle

A

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

258
Q

how to increase force for cardiac muscle

A

force increased by increasing muscle length (starling law)

259
Q

excitation-contraction coupling for cardiac muscle

A

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

260
Q

complex/volitional movement

A

motor output planned and refined by motor cortex, basal ganglia, and cerebellum. irrelevant to gravity, removed from posture control. learned or eveoled

261
Q

motor cortex

A

at precentral gyrus of central sulcus. somatotopic organization.

262
Q

motor cortex neuron synapsing

A

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.

263
Q

motor field

A

one corticospinal axon synapses with many motor nuclei. many synapses are silent, allowing for plasticity

264
Q

somatosensory inputs access to motor cortex

A

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.

265
Q

multiple representation.

A

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

266
Q

red nucleus

A

rubrospinal cells (contralateral, crosses midliine of spinal cord, ends up in intermediate zones) within red nucelus synergize (first region for distal limb movements).

267
Q

reticulospinal and vestibulospinal tracts do not synergize as much because

A

not precise movements

268
Q

premotor areas

A

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

269
Q

brocas’ area is an example of

A

a premotor area for preparing to speak/write/type with info from wernicke’s

270
Q

preparatory activity for premotor areas

A

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

271
Q

cingulate motor area (CMA)

A

genuine smile, within cingulate sulcus. emotional, motivational drive for movements

272
Q

supplementary motor area (SMA)

A

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

physiology except 10 times harder thanks to my stupid fucking depression (3 decks)

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