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Block 5 Week 1 Meg > Kenyon: Neurotransmission > Flashcards

Kenyon: Neurotransmission Flashcards

1
Q

What’s this?

A single transmembrane, multimeric protein binds the neurotransmitter and is the channel.

A

ligand-gated ion channels aka ionotropic receptors

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2
Q

T/F: By mixing and matching subunits, there is an enormous number of potential ionotropic receptors

A

True!

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3
Q

What’s this?
Binding of the neurotransmitter activates trimeric G-proteins that directly and indirectly influence the opening and closing of ion channels

A

GPCRs or metabotropic receptors

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4
Q

What’s this?
Hundreds of potential receptor types for a given neurotransmitter made by mixing and matching subunits.
Binding of the neurotransmitter opens a channel.
The response is limited to a change in membrane potential unless the channel allows Ca2+ through.

A

ionotropic receptors

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5
Q 
What's this?
A couple (
A

metabotropic receptors

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6
Q

What’s this?
Binding of the ligand (neurotransmitter?) activates a tyrosine kinase that indirectly influence the opening and closing of ion channels

A

enzyme-linked receptors

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7
Q

T/F: Unconventional neurotransmitters have receptors, too.

A

True

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8
Q 
ACh
Postsynaptic effect?
Precursor?
Removal mechanism?
Type of vesicle?
A

excitatory
choline + acetyl CoA
AChE
small, clear

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9
Q

Glutamate
Postsynaptic effect?
Removal mechanism?
Type of vesicle?

A

excitatory
transporters
small, clear

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10
Q

GABA
Postsynaptic effect?
Removal mechanism?
Type of vesicle?

A

inhibitory
transporters
small, clear

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11
Q

Glycine
Postsynaptic effect?
Removal mechanism?
Type of vesicle?

A

inhibitory
transporters
small, clear

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12
Q 
Catecholamines
Postsynaptic effect?
Precursor?
Removal mechanism?
Type of vesicle?
A

excitatory
tyrosine
transporters, MAO
small, dense-core

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13
Q 
Serotonin
Postsynaptic effect?
Precursor?
Rate-limiting step in synthesis?
Removal mechanism?
Type of vesicle?
A

excitatory
tryptophan
tryptophan hydroxylase
transporters, MAO

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14
Q

Histamine
Postsynaptic effect?
Removal mechanism?

A

excitatory

transporters

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15
Q

ATP
Postsynaptic effect?
Precursors?
Removal mechanism?

A

excitatory
ADP
hydrolysis to AMP and adenosine

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16
Q 
Neuropeptides
Postsynaptic effect?
Precursors?
Removal mechanism?
Type of vesicle?
A

excitatory/inhibitory
amino acids
proteases
large, dense-core

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17
Q

Endocannabinoids
Precursors?
Rate-limiting step in synthesis?
Type of vesicle?

A

membrane lipids
enzymatic modification of lipids
none

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18
Q 
Nitric oxide
Precursors?
Rate-limiting step in synthesis?
Removal mechanism?
Type of vesicle?
A

arginine
NO synthase
spontaneous oxidation
none

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19
Q

Where is ACh found?
What synthesizes it?
How is it inactivated?
How is choline recovered?

A

neuromuscular junction, preganglionic autonomic ganglia, post-ganglionic parasympathetic neurons, many CNS neurons;
choline acetyltransferase;
extracellular acetylcholineterase;
Na+/choline transporter

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20
Q

Nicotinic AChR are (blank) receptors.
How many different muscle nACh receptors are there?
How many different neuronal nACh receptors are there?

A

ionotropic;
two kinds;
a zillion kinds

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21
Q

Two kinds of nicotinic AChR in muscle?

A

Pentamers in fetal mammals (and Torpedo)

Pentamers in adult mammals

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22
Q

Where are ACh, nicotine, curare, and bungarotoxin binding sites located?

A

on the alpha1 subunits

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23
Q

Muscarinic AChR are (blank) receptors.

A

metabotropic

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24
Q

Where are mACh receptors found?

A

neurons
smooth muscle
cardiac muscle

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25
Q

The principle fast excitatory neurotransmitter in the nervous system. Half of the synapses in the brain have receptors for this neurotransmitter.

A

glutamate

26
Q

What collects glutamate after its release into the synaptic junction? What cells are involved in its removal and inactivation?

A

EAATs; glial cells

27
Q

3 ionotropic glutamate receptors?

A

AMPA
NMPA
kainate receptors

28
Q

All ionotropic glutamate receptors pass (blank). Some specialize in passing (blank). All mediate (blank).

A

cations; Ca++; EPSPs

29
Q

Neurons receiving glutamatergic input commonly have a mix of (blank) receptors that mediate kinetically distinct responses

A

ionotropic

30
Q

What ions can pass through an NMDA receptor? What is the implication of this?

A

Na+, K+, Ca++

there is potential for both depolarization and activation of Ca+ dependent processes

31
Q

What is a complication with NMDA receptors?

A

Mg++ blocks the channel if the membrane portential is negative
**NDMA receptors alone may not do anything at the resting potential

32
Q

How can you relieve the block of Mg++ on the NMDA ion channel?

A

depolarize the neuron **Mg++ will pop out of the channel

activate neighboring AMPA receptors & depolarize the neuron **synaptic plasticity

33
Q

Upon (blank), no Mg++ blocks the channel pore of the NMDA receptor

A

depolarization

34
Q

With postsynaptic depolarization caused by activation of AMPA receptors there is Ca2+ entry through NMDA receptors that can activate many things including (blank)

A

long-term potentiation

35
Q

What enables NMDA receptors to pass Ca++ and triggers biochemical events that don’t happen in NMDA alone?

A

AMPA depolarization

36
Q

The power of a glutamate synapse is adjustable. After high frequency stimulation, stimulation of the pathway results in a larger EPSP. This effect lasts a long time (hours). What is this referred to as?

A

long-term potentiation

37
Q

The combination of activation of both AMPA and NMDA receptors is required for (blank) entry. Once you have (blank) in the picture, anything is possible.

A

Ca++; Ca++

38
Q

What is this?
Reduced blood flow –> high levels of extracellular glutamate –> elevates Ca++ –>kills neurons with glutamate receptors

A

excitotoxicity

39
Q

coupled to various types of G-proteins regulating multiple cellular processes including the opening and closing of ion channels

A

metabotropic glutamate receptors

40
Q

A major inhibitory neurotransmitter.

A

GABA

41
Q

How is GABA inactivated?
What are the ionotropic receptors that commonly mediate IPSPs?
What activates GABA(a)?
What is the metabotropic receptor?

A

inactivated by uptake;
GABA(a) and GABA(c)
Benzodiazepines
GABA(b)

42
Q

(blank) (Valium® and Librium®) activate ionotropic GABA receptors reducing anxiety.
(blank) (phenobarbital, pentobarbital) activate some ionotropic GABA receptors in anesthesia.
Some effects of (blank) are mediated by ionotropic GABA receptors

A

Benzodiazepines
Barbiturates
alcohol

43
Q

The other inhibitory neurotransmitter that also activates ionotropic Cl- channels.
Particularly important in the spinal cord where they are blocked by strychnine

A

Glycine

44
Q

List some biogenic amines.

A

catecholamines (dopamine, norepi, epi)
histamine
serotonin

45
Q

What’s the rate limiting enzyme in the formation of the catecholamines?

A

tyrosine hydroxylase

tyrosine –> DOPA –> dopamine –> norepi –> epi

46
Q

How is dopamine inactivated? What inhibits its inactivation?

A

Na+ dependent uptake; cocaine

47
Q

Dopaminergic neurons projecting from (blank) to corpus striatum (caudate and putamen) are important in coordinating movements (Parkinson’s Disease)

A

substantia nigra

48
Q

Dopaminergic neurons projecting from substantia nigra to (blank) (caudate and putamen) are important in coordinating movements (Parkinson’s Disease)

A

corpus striatum

49
Q

The neurotransmitter released by sympathetic post-ganglionic neurons. Also important in the CNS

A

Norepi

50
Q

How is norepi inactivated?

A

NET

  • *also transports dopamine
  • *inhibited by amphetamines
51
Q

A transmitter in the CNS.
Inactivation mechanism is uptake but the transporter is not identified (yet).
a- and b-adrenergic receptors (metabotropic).
Adrenergic neurons are located in lower brainstem (medulla). They project to hypothalamus and thalamus. The function is not clear.

A

epinephrine

52
Q 
A neurotransmitter in the CNS.
Very important PERIPHERALLY as well
allergic responses
pain
itch
Metabotropic receptors
Inactivation mechanism is uptake
A

histamine

53
Q

Disregulation of (blank) pathways in the CNS is linked to psychiatric disorders. (blank) is also important in pain and in the GI tract.

A

serotonergic; serotonin

54
Q

What is serotonin synthesized from? What enzyme is involved?

A

tryptophan; tryptophan-5-hydroxylase

55
Q

How is serotonin inactivated?

A

by a specific transporter (SERT)

**inhibited by Prozac and other anti-depressants

56
Q

(blank) receptors 5-HT1, 5-HT2, 5-HT4 – 5HT7 do the usual things.
(blank) receptors 5-HT3 are nonselective cation channels.

A

metabotropic

ionotropic

57
Q

What are the purines?

A

ATP
ADP
AMP
adenosine

58
Q

(blank) transmission is important in the periphery (smooth muscle) and in the central nervous system (mechanosensation and pain).
(blank) is released along with all the other neurotransmitters (co-transmission). There are important purinergic receptors with different sensitivities to each of the purines.
Extracellular ecto-5’ nucleotidases convert the ATP to a soup of purines. Thus, one has a mix of purines (ATP, ADP, AMP, adenosine) hitting a mix of receptors.

A

purinergic;

ATP

59
Q 
Genes encoding (blank) have a signal sequence that targets the pre-propeptides to the ER and Golgi.
**processed to produce more than one
A

neuropeptides

60
Q

List some neuropeptides

A

brain/gut peptides *substance P
opioid peptides *endorphins, enkephalins, dynorphins
pituitary peptides
hypothalamic peptides

61
Q

Virtually all receptors of neuropeptides are (blank) receptors that do the usual G-protein coupled things.

A

metabotropic

62
Q

(blank) can travel to affect distant neurons.

The effects of (blank) are slow and long lasting.

A

neuropeptides

Block 5 Week 1 Meg (8 decks)

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