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Physiology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

endogenous vs exogenous

A 
endogenous = made in the body (Ach) 
exogenous = made outside the body (nicotine and muscarine)
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2
Q

acetylcholine neuron/receptor name

A

cholinergic neuron and receptor

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3
Q

epinephrine neuron/receptor name

A

adrenergic neuron and receptor

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4
Q

dopamine neuron/receptor name

A

dopaminergic neuron, D1, D2 … receptor

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5
Q

serotonin neuron/receptor name

A

serotonergic neuron, 5HT receptor

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6
Q

glycine neuron/receptor name

A

glycinergic neuron and receptor

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7
Q

GABA neuron/receptor name

A

GABAinergic neuron and GABA receptors

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8
Q

glutamate neuron/receptor name

A

glutamergic neuron, NMDA and AMPA receptors

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9
Q

acetylcholinesterase

A

on postsynaptic neuron, breaks down Ach to be reused in presynaptic neuron

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10
Q

where Ach used and where excitatory/inhibitory

A 
excitatory = somatic motor neuron, autonomic motor neuron, CNS  
inhibitory = autonomic motor neuron
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11
Q

nicotinic receptors - mechanism, naming, where found

A

nonspecific LGIC but inward flow of Na+ dominates because down electrical and concentration gradient vs K+ going down concentration but against electrical , always excitatory, found in autonomic ganglia and skeletal muscle

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12
Q

muscarinic receptors - mechanism

A

GPCR, based on G protein type and channel that is open or closed effect may be different

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13
Q

M3/M5 - location, mechanism, effect

A

GI, smooth muscle, gland Ca2+ channel opens and muscle contraction

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14
Q

M2 - location, mechanism, effect

A

heart, K+ channel opens causing hyperpolarization, inhibition of intrinsic heart rate

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15
Q

botulinum toxin - effect and mechanism

A

flaccid paralysis, SNARE complex frozen and cant change conformation, no Ach released

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16
Q

curare - effect and mechanism

A

nicotinic antagonist, flaccid paralysis

17
Q

A-bungarotoxin

A

nicotinic and muscarinic antagonist

18
Q

saxitoxin

A

blocks Na+ VGIC so no action potential generated

19
Q

tetrodotoxin

A

blocks Na+ VGIC so no action potential generated

20
Q

strychnine

A

blocks glycine receptor (so no inhibition)

21
Q

spastic vs flaccid paralysis

A

spastic = eternally contracted because too much Ach vs flaccid = no contraction at all because no Ach

22
Q

GABA and glycine location

A

GABA = brain
glycine = spine
both inhibition by Cl-

23
Q

ex of glycine in UMN and LMN

A

UMN –> releases glycine –> inhibition of Ach release by LMN –> no skeletal muscle stimulation

24
Q

monoamines - list them

A
  • catelochamines = tyrosine –> dopamine, epinephrine, norepinephrine
  • tryptophan –> serotonin
  • histidine –> histamine
25
Q

presynaptic reuptake receptors

A

on presynaptic neuron, takes up NT so it doesnt remain in synaptic cleft and cause over stimulation

26
Q

monoamine oxidase MAO

A

found in presynaptic neuron, breaks down NT

27
Q

MAO inhibitors

A

prevents MAO from breaking down NT so more NT in synaptic cleft

28
Q

MAO receptor mechanisms

A

mostly LGIC but sometimes GCPR with cAMP secondary messenger

29
Q

GPCR with cAMP

A

NT –> receptor –> G protein dissociation –> adenylate cyclase –> ATP to cAMP –> protein kinase activated –> other proteins phosphorylated

30
Q

serotonin - function and where found

A

found raphe nuclei, role in mood, cerebral circulation, behavior, appetite, libido

31
Q

SSRI - mechanism and uses

A

serotonin reuptake inhibitor, increases amount of serotonin by preventing reuptake, treats depression, anxiety, migraine

32
Q

nigrostriatal system - function, start and end, relation to parkinsons

A
  • initiate movemetn adn complex coordinated movement
  • death of neurons in this system causes Parkinsons
  • substantial nigra to corpus striatum
33
Q

mesolimbic dopamine system - start and end (many), relation to schizophrenia and Parkinsonian side effects

A
  • VTA –> nucleus accumbens, amygdala, hippocampus, prefrontal cortex, frontal cortex
  • schizophrenia = overactive mesolimbic system, hallunciatiosn
  • treated by decreasing dopamine which affects nigrostrial and causes Parkinsonian side effect
34
Q

VTA receptors and relation to drugs

A

VTA receptors for Ach and GABA, means can be stimulated by nictoine, opiods, cannabinoids etc and explains addiction from drugs

35
Q

cocaine and amphetamines

A

neurotransmitter reuptake inhibitors - cocaine triple reuptake inhibitor of serotonin, dopamine and norepinephrine, amphetamine on reputake inhibitor of norepinephrine

36
Q

glutamate - receptors and effect

A

NMDA, AMPA, excitatory

37
Q

NO effects

A

smooth muscle relaxation and blood vessel dilation (due to relaxation)

Physiology (25 decks)

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