Neurons Flashcards

1
Q

how is brain activity tracked

A

O2 usage in tissues

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2
Q

optogenetics

A

changes in cell function using light gated ion channels

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3
Q

blood brain barrier

A

filters most particles out of blood that reaches brain

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4
Q

what animal has giant axons

A

squid

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5
Q

nerve related diseases

A

MS, alzheimers, huntingtons, epilepsy

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6
Q

integration

A

coordination of functions via receiving and then sorting signals out

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7
Q

autocrine

A

releases smth to bind to self receptors

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8
Q

paracrine

A

signaling to nearby cells in tissue

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9
Q

endocrine

A

signaling molecules move thru system via blood. long-term, metabolism, growth, reproductive cycles = coordination of tissues

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10
Q

synaptic signaling

A

specialized APs and neurotransmitters, spec to target cell where endocrine is general

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11
Q

why are neurons important

A

instant action. needed for being predator or prey

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12
Q

signal pathway in neuron

A

synapse > dendrite > cell body > hillock (AP starts) > axon > synapse

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13
Q

glial cells in CNS purpose

A

half of brain cells, direct and connect and protect neurons

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14
Q

astrocytes

A

glial CNS cells, connect neurons to blood vessels for nutrients

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15
Q

microglia

A

glia in CNS, brain immune cells

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16
Q

oligodendrocytes

A

insulation in CNS, wrap around cells many times and can wrap many neurons

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17
Q

Schwann cells

A

insulation in PNS. only cover 1 neuron and wrap around 200+ times

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18
Q

membrane potential

A

Vm , measured in mV

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19
Q

resistance

A

Rm (ohms). low resistance inside axon and high membrane resistance is ideal for prop of AP

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20
Q

length constant

A

l, or lamba. = the time it takes for 37% of the signal to degrade (related to length the signal travels while strong, we want it to be large)

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21
Q

ohms law

A

V=IR

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22
Q

voltage

A

separation of + and - charges

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23
Q

current

A

movement of ions

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24
Q

ohms law in cell terms

A

ion flow = membrane potential/resistance

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25
Q

krogh principle application

A

squid axons use same principles as ours

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26
Q

square wave

A

the blip in current when it is applied

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27
Q

depolarization of membrane is..

A

graded until it reaches AP threshold

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28
Q

time constant

A

the delay btwn peak of stimulus and peak of the response depolarization

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29
Q

hyperpolarization

A

movement of charge further from 0

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30
Q

lambda (length constant) eq

A

k(sqrt(membrane R/internal R))

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31
Q

maximizing lambda in verts vs inverts

A

usually verts minimize int resistance somewhat but focus on maximizing membrane R. inverts minimize int resistance and dont care about membrane

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32
Q

Nernst eq

A

z(61)log(Cext/Cint)

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33
Q

the resting Vm is closest to equilibrium for..

A

whatever species is most permeable

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34
Q

goldman eq

A

shows total membrane potential, 61log(P(Cext)+…/P(Cint)..) or the int/ext for anions. with each species in the cell involved in this eq

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35
Q

how many ions cause potential change

A

literally a few out of thousands

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36
Q

action potential magnitude

A

always the same, but can show diff signal by the freq of APs

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37
Q

parts of AP

A

resting, rising phase, overshoot, falling phase, undershoot, back to resting

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38
Q

channels open in resting neuron

A

just leaky K

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39
Q

Hodgkin cycle

A

Na channels. they open at threshold (-50 mV), cause more depolarization, stay open, more open, at 40 mV the second gate closes but the first stays open until cell gets back under -50.

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40
Q

voltage gated K open/close

A

open around 40 mV, close at -70 or -80

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41
Q

channels open during rising phase

A

leaky K, voltage Na

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42
Q

channels open during overshoot

A

all 3 types

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43
Q

channels open during falling

A

just K (voltage and leaky). same for undershoot

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44
Q

tetradotoxin

A

inhibits voltage gated Na channels

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45
Q

absolute refractory period

A

during high peak, there absolutely cannot be another AP (they cannot amplify one another) because the Na inactivation gate stays closed during falling phase

46
Q

relative refractory period

A

during undershoot, sometimes another stimulus can activate Na channels before the neuron is back to resting potential. but the purpose of undershoot is to make this more difficult

47
Q

speed of AP prop

A

55 mph

48
Q

what part of neuron has graded potentials

A

dendrite

49
Q

when circumference of axon doubles

A

Rm halves, but Ri dec exponentially

50
Q

saltatory conduction

A

AP jumps thru insulation and is refreshed at nodes of Ranvier

51
Q

invert myelin

A

not same thing but crustaceans have their own version

52
Q

7 main neurotransmitters

A

norepinepherine, acetylcholine, serotonin, dopamine, GABA/glycine, glutamine

53
Q

electrical synapses

A

neurons connected by gap junction, AP travels directly thru (slows down AP a little but still fast)

54
Q

chemical synapses

A

neurotransmitters released at end of one neuron stimulate response when picked up by next neuron receptors. can be ionotropic or metabotropic

55
Q

ionotropic synapse steps

A

faster. AP activates Ca channels at synapse, the Ca activates SNARE and vesicles release NT into synapse. receptors are ion channels, and open or close having some effect (often AP at the next cell)

56
Q

metabotropic synapse steps

A

slower, AP activates Ca channels at synapse, the Ca activates SNARE and vesicles release NT into synapse. receptors are GCPRs which can have cascading effects, learning, memory, etc.

57
Q

gates at the end of axon

A

calcium gates activated by voltage at end of AP, Ca comes in and activates proteins for vesicle movement so neurtransmitters released

58
Q

vesicle proteins in axon

A

SNARE proteins. activated by Ca, deactivated (cleaved) by botulinum and also the tetanus toxin

59
Q

post synaptic potential

A

graded potential at cell body. can be EPSP (excitatory, depolarization - lets in Na+) or IPSP (inhibitory, hyperpolarization - lets in Cl-)

60
Q

types of neurotransmitter molecules

A

amino acids (glutamate, GABA/glycine) - usually ionotropic, biogenic amines (acetylcholine, norepinepherine, dopamine, serotonin) - usually longer lasting and metabotropic

61
Q

what determines cell response to neurotransmitters

A

type of receptors at synapse

62
Q

muscarine receptors

A

slow the heart rate. activated by acetylcholine but also poison mushrooms

63
Q

how does neuron integrate signals

A

summation of magnitude of inputs based on magnitude and distance from hillock.

64
Q

presynaptic inhibition

A

a synapse can exist on an axon to stop the AP from reaching its target cell

65
Q

NMJ

A

neuromuscular junction, each muscle cell has only one nerve cell controlling it (neurons can control multiple muscle cells). always nicotinic acetylcholine receptors (excitatory). junction is HUGE with LOTS of Ach released. each AP gives a response (relay signal)

66
Q

acetylcholinerase

A

destroys Ach. and the products go back to og neuron to be recycled. its inhibitors include pesticides and nerve gas (muscles stay constantly flexed). also can treat alzheimers by helping the nt stay in junction longer so a normal amount can build up

67
Q

alcohol effects

A

disrupts cell membranes so many processes are changed

68
Q

nicotinic receptors

A

acetylcholine, ionotropic EPSPs

69
Q

muscarinic receptors

A

acetylcholine, metabotropic IPSPs

70
Q

agonist

A

increases the effect of smth

71
Q

curare

A

used in poison arrows, antagonist of nicotinic receptors, leads to respiratory arrest. can be counteracted by acetylcholinerase inhibitors

72
Q

synaptic plasticity

A

mechanism of learning and memory, synapses change based on inputs

73
Q

habituation

A

decrease in response upon repeated exposure

74
Q

sensitization

A

having a reaction again and the reaction increases to something that it was accustomed to when a different stimulus is given (resets pathway)

75
Q

facilitation

A

successive PSPs increase in amplitude when presynaptic APs have a higher freq

76
Q

antifacilitation

A

successive PSPs decrease in size as freq of APs from the neuron increases

77
Q

how do facilitation and antifacilitation occur

A

change in NT release or receptors at synapse

78
Q

aplysia

A

sea hare/slug. syphon withdrawal demonstrated habituation and could be reset by an electric shock

79
Q

aplysia experiment mechanism

A

NMJ monitored with electrode when touch stimulus was given (electrode activated sensory neuron and the corresponding nmj magnitude was recorded), activation dec but unsure if it is due to receptors or NTs. when pain neuron is activated, it triggers serotonin receptors before the sensory neuron synapses and these are metabotropic GPCRs, activate vesicle proteins to put out more NT and cAMP activates a kinase that mobilizes vesicles, inactivates the K a bit, allowing Ca channels to stay open longer (more NT released). this is sensitization

80
Q

LTP

A

long term potentiation. shown in rat brain. enhancement of synaptic transmission after intense stimulation at some past time.

81
Q

hippocampus

A

part of the brain for long term memory and spatial learning.

82
Q

tetanus

A

a bombardment of APs

83
Q

nerves in the rat experiment

A

CA3 stimulates, PS is CA1

84
Q

CA1 neuron setup

A

starts with NMDA receptors blocked by Mg, and AMPA (both activated by glutamate and should let in Na). extreme stimulus (tetanus) causes depolarization, Mg leaves NMDA, NMDA lets Ca in, which activates more implantation of AMPA and other cell processes via calmodulin inc expanding the synapse. after stimulus, NMDA is blocked again but the permeability and therefore PSP has changed

85
Q

how can LTP happen

A

large stimulus like strong emotion, or repetition

86
Q

what feedback does LTP demonstrate

A

positive

87
Q

proof NMDA helps with hippocampus

A

mice (Doogie) with more NMDA were more curious and had improved spatial memory

88
Q

nervous system

A

cells designed for repeated conduction of electrical signals

89
Q

CNS

A

brain, spinal cord

90
Q

PNS

A

sensory and motor neurons

91
Q

nerve

A

bundle of neurons in PNS (afferent and efferent)

92
Q

ganglia

A

PNS grouping of cell bodies and synapses

93
Q

diff btwn CNS and PNS neurons

A

there is none

94
Q

path of info in spinal cord

A

goes in dorsal root and out ventral

95
Q

white matter

A

glial cells

96
Q

grey matter

A

neurons

97
Q

what does autonomic NS control

A

smooth muscles, exocrine glands, cardiac muscles, some endocrine glands (adrenal)

98
Q

somatic NS

A

skeletal muscles

99
Q

involuntary reflex

A

signal goes to spinal cord, must contract one muscle and relax its pair, and tell brain to be alert for this stimulus

100
Q

parasympathetic impacts

A

rest and digest - inc bile, digestion, blood vessel dilation, dec bp

101
Q

sympathetic impacts

A

fight or flight - activates adrenal, blood to muscles and lungs, bp up, vasoconstriction, pupils contract

102
Q

autonomic ganglion

A

where the signal from NS switches neurons to go to effectors, all pos and fast, nicotinic with Ach

103
Q

catecholomines

A

epinepherine, norepinepherine

104
Q

somatic synapses

A

more myelin, travels body with no synapse until destination, always Ach and nicotinic

105
Q

norepinepherine receptors in autonomic ns type

A

metabotropic with GCPRs. alpha1, alpha2, beta1 = adrenergic receptors

106
Q

beta blockers

A

block beta receptors for norepinephrine in the heart, brings down heart rate

107
Q

dopamine reuptake inhibitors

A

cocaine, meth, adderall (receptors are saturated with dopamine (usually metabotropic)>reward response/excitatory)

108
Q

serotonin reuptake inhibitors

A

depression meds (receptors are saturated with serotonin (usually metabotropic)>inhibitory)

109
Q

ketamine

A

inhibits NMDA receptor for for glutamate (excitatory)

110
Q

typical glutamate receptors

A

AMPA, NMDA