lecture 8 Flashcards

(49 cards)

1
Q

2 classes of neurotransmitters

A
- small molecules
can synthesize with precursors 
- peptides
streams of amino acids
require Golgi and ER to make
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2
Q

classes of small molecule NTs

A
acetylcholine 
amino acids
purines
catecholamines - dopamine, nor/epinephrine
indoleamine- serotonin
imidazoleamine- histamine
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3
Q

small molecules that aren’t in vesicles

A

endocannabinoids - lipid soluble
nitric oxide and carbon monoxide - gas
adenosine - made from ATP

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4
Q

peptide NT com position

A

around 3-30 amino acids long

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5
Q

how can you find a neutron releasing a specific NT

A

look for the enzyme that is used to make that transmitter because the neuron will only spend energy making that enzyme if it needs it

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6
Q

acetylcholineaseteras

A

Ach esterase - converts acetylcholine to acetate + choline

gets rid of Ach in synapse so receptor doesn’t keep responding which prevents desensitization

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7
Q

choline acetyl-transferase

A

ChAT - makes acetylcholine from acetyl CoA + choline

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8
Q

transport system to load vesicles

A

requires ATP to form a proton gradient by driving protons into vesicle

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9
Q

toxins that bind postsynaptic receptors

A

bungarotoxin- cobra - nACh antagonist
epibatidine- frog- n and m AChR
conotoxin- snail - block Glu and ACh receptors (N type)
arecoline - betel nut- m AChR agonist

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10
Q

key to normal N.S

A

balance between inhibition and excitation

many toxins take advantage of this

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11
Q

general structure of ligand gated receptor

A

5 subunits

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12
Q

why do each receptors require 2 Act molecules

A

increases the steepness of the relationship between concentration of ACh and release
larger difference between ACh increasing or decreasing in concentration

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13
Q

3 glutamate receptors

A

AMPA
NMDA
kainate

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14
Q

AMPA

A

Glu R1
Glu R2- calcium impermeable
Glu R3
Glu R3

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15
Q

all classes of ligand gated receptors (ionotropic)

A
AMPA, NDMA Kainate
GABA Glycine
nACh 
serotonin
purines
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16
Q

myasthenia gravis

A

autoimmune disease that attacks nACh receptors in neuromuscular junctions which causes disorganization and weakness
treatment- ACh esterase inhibitor that keeps ACh around in synapse longer alleviation of symptoms

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17
Q

structure of metabotropic receptors

A

doesn’t have a pore- no ion movement

activates a G protein that goes on to produce cellular affects

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18
Q

classes of metabotropic receptors

A
glutamate, GABA
dopamine
NE, Epi
histamine
serotonin
purines 
muscarinic
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19
Q

glutaminase

A

converts glutamine to glutamate

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20
Q

how is glutamate recycled

A

transferred from neuron to glia through excitatory amino acid transporters
enzyme - glutamine synthetase

21
Q

NDMA receptors

A

both voltage and ligand gated receptor

22
Q

NDMA receptor requirements

A
glycine - required modulator (co-ligand)
2 glutamates- to bind
Mg- voltage dependant blocker 
during depolarization magnesium comes away and receptor becomes activated
Ca- contribute to current
23
Q

why does NMDA receptor current get smaller around -60mV

A

once the membrane potential passes -60 and starts to approach 0 the electrochemical gradient gets smaller (approaches reversal potential) and therefor so does the current

24
Q

what happens to NDMA current when theres no magnesium

A

without magnesium the receptor doesn’t behave like a voltage dependant and there will be a linear relationship

25
compare NMDA to AMPA
NMDA is longer lasting | NMDA has Ca permeability (and AMPA Glu R2)
26
AMPA receptor structure
dimer of dimers | 4 subunits
27
glutamic acid decarboxylase
GAD - converts glutamate to GABA
28
serine hydroxy-methyltransferase
converts serine to glycine
29
ionotropic gaba receptor permeability
lets chloride pass but not Na or K many sites for ligands to bind and potentiate or block barbiturates and steroids GABA binds and chloride enters
30
how does valium (and benzodiazepines) affect GABA receptors
it increases the efficacy- receptor more sensitive to GABA and more chloride can flow in inhibitory to firing because it pulls potential below threshold - reduce excitability and produce tranquility
31
what are the 2 places for potentiation of GABA
1. benzodiazepines (valium) | 2. barbiturates - bind inside the receptor
32
why isn't GABA inhibitory during early development
because the developing neutrons have different Cl transporters which concentrate chloride inside the cells at higher levels and GABA is excitatory
33
epinephrine pathway
tyrosine --> DOPA --> dopamine --> nor epinephrine --> epinephrine
34
tyrosine hydroxyls
tyrosine --> DOPA | RATE LIMITING ENZYME
35
DOPA decarboxylase
DOPA--> dopamine | used in therapy for Parkinson's patients
36
dopamine B hydroxylase
dopamine --> norepinepherine
37
phenyl ethanol amine methyl-transferase | PAM
norepinephrine --> epinephrine
38
substantia nigra
responsible for dopamine
39
locus coerulus
responsible for norepinephrine
40
medullary epinepherine neurons
responsible for epinephrine
41
tuberomammilary nucleus of hypothalamus
responsible for histamine
42
raphe nuclei
responsible for serotonin
43
synthesis of histamine
histidine --> histamine | histidine decarboxylase
44
synthesis of serotonin
tryptophan --> 5-hydroxytryptophan --> serotonin (5HT) | 2 enzymes
45
processing of pre-propeptides
have to be made in cell body metabotropic- slow pe-propetide --> propeptide
46
brain gut peptides
VIP, CCK-8, substance P
47
opiod peptides
leucine enkephalin, a endorphin, dynorphin A
48
endocannabinoid signal
synthesized in dendrites - not stored in vesicles calcium is required to activate enzymes part of motivation system and short term memory exogenous ligand shift excitation and disrupt
49
nitric acid
produced from arginine - NO | regulate vascular tone