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Neurobiology I > Neurotransmitters and Receptors > Flashcards

Neurotransmitters and Receptors Flashcards

1
Q

A classical neurotransmitter is released from the _____ side and binds to the _____ side.

A

Pre-synaptic

Post-synaptic

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2
Q

A classical neurotransmitter is regulated when pre-synaptic ____ binds to _____, causing the release of ____.

A

Ca+2
Synaptotagmin
Vesicles

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3
Q

A classical neurotransmitter functions by binding the _____ side and causing a _____.

A

Post-synaptic

Change

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4
Q

A small molecule neurotransmitter is made and put into synaptic vesicles near where?

A

Synapse

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5
Q

The vesicles used to contain small molecule neurotransmitters are what size and opaqueness?

A

Small, clear

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6
Q

Are small molecules released at the active zone?

A

Yes

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7
Q

Peptide neurotransmitters are made where from what?

A

Cell body

Proteins

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8
Q

After being packaged into vesicles, what happens to the proteins used to make peptide neurotransmitters?

A

They are processed into peptides

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9
Q

Where are peptide neurotransmitters released relative to the active zone?

A

Near, but not at active zone

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10
Q

The vesicles that contain peptide neurotransmitters are called ___ ___ because they appear ____ and are ____ than the vesicles of small molecules.

A

Dense core
Dark
Bigger

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11
Q

During low frequency stimulation, are small molecule, peptide, or both neurotransmitters released by the pre-synaptic neuron?

A

Small molecule

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12
Q

During high frequency stimulation, are small molecule, peptide, or both neurotransmitters released by the pre-synaptic neuron? Why is this the case?

A

Both

Ca+2 accumulated on pre-synaptic side diffuses to cause peptide neurotransmitter release

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13
Q

2 reasons why releasing both small molecule and peptide neurotransmitters would be useful (signals sent, distance from synapse)

A

Differences in signal sent between low and high frequency

Release from farther away from synapse

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14
Q

Small molecule neurotransmitters include what 4 categories?

A

Acetylcholine
Amino acids
Biogenic amines
Purines

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15
Q

What are 3 small molecule amino acid neurotransmitters?

A

Glutamate
GABA
Glycine

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16
Q

What are 3 classes of small molecule biogenic amine neurotransmitters?

A

Catecholamines (dopamine, norepinephrine, epinephrine)
Indoleamine (serotonin)
Imidazoleamine (histamine)

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17
Q

What type of purine is a small molecule neurotransmitter?

A

ATP

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18
Q

Neuropeptide neurotransmitters include what subcategory?

A

Opioids

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19
Q

3 types of unconventional neurotransmitters

A

Adenosine
Endocannabinoids
NO

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20
Q

2 types of neurotransmitter receptors

A

Ionotropic

Metabotropic

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21
Q

Ionotropic neurotransmitter receptors are also called what? What happens when a neurotransmitter binds to it?

A

Ligand-gated receptor

Ion channel opens

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22
Q

Metabotropic neurotransmitter receptors are also called what? What happens when a neurotransmitter binds to it?

A

G protein-coupled receptors
Binding of neurotransmitter triggers interaction with G-protein, which triggers intracellular signaling, which may affect ion channels

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23
Q

8 types of ligand-gated receptors

A 
nACh (nicotinic acetylcholine)
AMPA
NMDA
Kainate
GABA
Glycine
Serotonin (5-HT 3 type)
Purines (P2X type)
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24
Q

About how many subunits required to make a functional ligand-gated receptor? Is the functional channel made up of the same or different type of subunits?

A

4-5

Different (heterotetramer or pentamer)

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25
Q

How are AMPA receptor subunits designated?

A

GluA#

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26
Q

How are NMDA receptor subunits designated?

A

GluN#

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27
Q

How are kainate receptor subunits designated?

A

GluK#

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28
Q

What 4 neurotransmitters have no ion channel receptors?

A

Dopamine
Epinephrine
Norepinephrine
Histamine

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29
Q

A ligand-gated receptor must have at least some domains that are in what 3 places relative to the plasma membrane of the cell?

A

Transmembrane
Extracellular
Intracellular

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30
Q

In a ligand-gated receptor, what type of secondary structure would comprise a transmembrane domain?

A

Alpha helices

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31
Q

In a ligand-gated receptor, what type of structure might comprise an extracellular domain?

A

Pore loop

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32
Q

On a ligand-gated receptor, where do most ligands bind relative to the cell?

A

Extracellular side (can’t cross plasma membrane)

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33
Q

In a ligand-gated receptor, what is different between closed vs open (ligand binding causes what to happen to receptor)?

A

Conformation of receptor

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34
Q

An antagonist binding a ligand-gated receptor has what effect on its conformation?

A

Closes it

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35
Q

8 different types of metabotropic receptors

A 
Muscarinic
Glutamate
GABA B
Dopamine
Adrenergic
Histamine
Serotonin
Purines (Adenosine and P2Y)
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36
Q

All G protein-coupled receptors can function with ____ subunit(s). Some act as ______ (same or different subunit type, number of subunits together).

A

1 (monomer)

Heterodimers

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37
Q

Type of neurotransmitter for which there is no G protein-coupled receptor

A

Glycine

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38
Q

Does a G protein-coupled receptor have a pore? Why or why not?

A

No- it isn’t an ion channel

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39
Q

How many transmembrane helices per G protein-coupled receptor?

A

7

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40
Q

What side of the G protein-coupled receptor (extra- or intra-cellular) interacts with the G protein? On which side does the ligand bind?

A

Intracellular

Extracellular

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41
Q

What happens to the G protein-coupled receptor when the ligand binds to it? What does it then bind to? What happens to the G protein?

A

G protein-coupled receptor undergoes conformational change
G protein
Gets activated

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42
Q

How many subunits does a G protein have?

A

3 (trimeric G protein)

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43
Q

The ___ subunit of the G protein binds ____ in order to become activated. What happens to the subunit after the protein is activated?

A

Alpha
GTP
Alpha subunit dissociates and interacts with effector

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44
Q

In terms of number of subunits necessary to make a functional receptor, how does a ligand-gated receptor differ from a G protein-coupled receptor?

A

Ligand-gated receptor needs multiple subunits to be functional, whereas a G protein-coupled receptor needs only 1

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45
Q

What are the 3 types of trimeric G proteins?

A

Gs
Gi
Gq

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46
Q

Each type of G protein-coupled receptor binds to how many types of trimeric G protein?

A

1

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47
Q

For a given ligand, can there be multiple types of G protein-coupled receptors (each one binding 1 type of trimeric G protein)?

A

Yes

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48
Q

What 2 types of trimeric G proteins work on adenylyl cyclase? Adenylyl cyclase turns ___ into ____, a secondary messenger which activates _____.

A 
Gs
Gi
ATP
cAMP
Protein kinase A
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49
Q

Gs _____ adenylyl cyclase, while Gi ______ it.

A

Stimulates

Inhibits

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50
Q

What type of trimeric G protein works on phospholipase C, and in what manner? Phospholipase C turns ____ into ____ and ____.

A

Gq
PIP2
DAG
IP3

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51
Q

After phospholipase C turns PIP2 into DAG and IP3, DAG activates ______, while IP3 uses the ion _____ to activate ______ and ____.

A

Protein kinase C
Ca+2
Protein kinase C
Calcium calmodulin kinase (CaMK)

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52
Q

In a designer receptor exclusively activated by designer drugs (DREADD), the G protein-coupled receptor is ____ so that it no longer binds the ____ ligand. It only binds the artificial ligand ____. Adding the artificial ligand enables ____ of the G protein-coupled receptor.

A

Mutated
Endogenous
Clozapine-N-oxide (CNO)
Activation

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53
Q

4 mechanisms used to stop neurotransmitter signaling

A

Diffusion
Enzymatic degradation
Presynaptic reuptake
Glial uptake

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54
Q

Acetylcholine is synthesized where by what? What 2 molecules are used to synthesize it?

A

Axon terminal
Choline acetyltransferase
Acetyl CoA, choline

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55
Q

The 2 receptors for acetylcholine are the _____ acetylcholine receptor and the ____ acetylcholine receptor. Which is a ligand gated ion channel and which is a G protein-coupled receptor?

A

Nicotinic
Muscarinic
nAchR is ligand-gated ion channel and mAchR is GPCR

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56
Q

What is the name of the acetylcholine vesicular transporter that puts acetylcholine into vesicles? How is acetylcholine removed from the receptor? Can it be taken back up through reuptake?

A

VAChT (vesicular acetylcholine transporter)
Degradation by acetylcholinesterase
No

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57
Q

What part of the acetylcholine molecule can undergo reuptake/recycling?

A

Choline

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58
Q

Organophosphates in insecticides and nerve gas inhibit what enzyme associated with what neurotransmitter?

A

Acetylcholinesterase

Acetylcholine

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59
Q

Is the nicotinic acetylcholine receptor (nAchR) ion selective? What ions does it pass?

A

No

Na+ and K+

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60
Q

Is the nAchR a heterotetramer or heteropentamer?

A

Heteropentamer

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61
Q

What are the 2 agonists for the nAchR? Which is endogenous?

A

Acetylcholine (endogenous)

Nicotine

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62
Q

What is the antagonist for the nAchR?

A

Mecamylamine

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63
Q

Do endogenous and non-endogenous agonists bind in the same place on a receptor?

A

Not necessarily

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64
Q

Myasthenia gravis is what type of condition that does what to the number of nAchRs? How is it treated?

A

Autoimmune
Reduces
Treated with acetylcholinesterase inhibitors

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65
Q

What are the 2 agonists for the mAchR? Which one is endogneous?

A

Acetylcholine (endogenous)

Muscarine (mushroom toxin)

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66
Q

What are the 2 antagonists for the mAchR?

A

Atropine

Scopolamine

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67
Q

Acetylcholine released by the vagus nerve binds to what subunit of the mAchR on the heart to cause slowing down of contraction? What trimeric G protein does that subunit act upon to cause this effect?

A

M2

Gi (inhibitory effects)

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68
Q

The most abundant excitatory neurotransmitter is _____.

A

Glutamate

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69
Q

What does glutamatergic mean in respect to a neuron?

A

It synthesizes glutamate

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70
Q

Can glutamate cross the blood brain barrier? What are its 2 sources of synthesis?

A

No
Glutamine from glia
2-oxoglutarate from TCA cycle

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71
Q

Is glutamate degraded, or taken back up?

A

Taken back up

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72
Q

What molecule loads glutamate into vesicles?

A

VGLUT

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73
Q

In the glutamate-glutamine cycle, (glutamate/glutamine) is made in the glia, transported out by _____, taken into the neuron by _____, made into (glutamate/glutamine) by ____, pumped into vesicles by ____, released into the synaptic cleft, then taken back into glia by _____, where it is turned into glutamine and the cycle starts over.

A 
Glutamine
SN1
SAT2
Glutamate
Glutaminase
VGLUT
EAATs
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74
Q

What are the 3 ligand-gated glutamate receptors?

A

AMPA
NMDA
Kainate

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75
Q

Are the ligand-gated glutamate receptors ion-specific? What ions do they always pass, and which do they sometimes pass?

A

No

K+, Na+, maybe Ca+2

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76
Q

Are the ligand-gated glutamate receptors heterotetramers or heteropentamers?

A

Heterotetramers

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77
Q

What 2 ligand-gated glutamate receptors can also pass Ca+2? For which one is the permeability dependent on its subunits?

A

AMPA and NMDA

AMPA

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78
Q

The NMDA receptor binds what ion at (depolarized/hyperpolarized) potentials?

A

Mg+2

Hyperpolarized

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79
Q

Mg+2 does what to the NMDA receptor pore? When is this reversed?

A

Blocks it

Depolarization

80
Q

NMDA requires what 2 possible co-agonists for efficient gating?

A

Glycine

D-serine

81
Q

Of the 3 ligand-gated glutamate receptors, which has the longest and slowest currents? Which one has the fastest and most current passed during that period of time? Which one also opens quickly, but doesn’t pass as much current during that time?

A

NMDA
AMPA
Kainate

82
Q

What subunit of the AMPA receptor is subject to RNA editing? What subunit is modified into what different subunit, and what is the result?

A 
GluA2
GluA2 (Q)- calcium permeable is modified into GluA2(R)- calcium impermeable
83
Q

Which domain of an ion channel determines its ion specificity?

A

Pore loop

84
Q

Agonists cause a ____ conformational change to the endogenous ligand, whereas antagonists ____ the receptor in an _____ state.

A

Similar
Lock
Inactive

85
Q

Opening of an NMDA receptor requires both ____ (endogenous ligand) and ____ or ____ (co-agonists).

A

Glutamate

Glycine or D-serine

86
Q

When looking at Vm vs current for an NMDA receptor, when there are glycine/D-serine and glutamate only, current is directly proportional to _____ _____, so the plot appears ____.

A

Driving force

Linear

87
Q

When looking at Vm vs current for an NMDA receptor, when glycine/D-serine, glutamate, and Mg+2 are present, the current is ____ at a low/hyperpolarized voltage and becomes directly proportional to ____ ____ and in the ____ direction after a mildly depolarized voltage is reached. Why is this?

A

0
Driving force
Inward
Mg+2 blocks pore at low/hyperpolarized voltage, but is forced out after depolarization

88
Q

The mAchR can bind to what 2 types of trimeric G proteins?

A

Gq and Gi

89
Q

In a glutamate system, at Vrest on the post-synaptic cell, the ____ receptor is activated first and passes what ion? This ion causes _____ of the membrane, which removes the ____ blockage.

A

AMPA
Na+
Depolarization
Mg+2

90
Q

Why is it said that the NMDA receptor acts as a “dual sensor” (what 2 things does it require to function)?

A

Neurotransmitter

Voltage

91
Q

NMDA receptors undergo post-translational modification that has what 2 possible effects on current? How are the modifications that create one effect different from the other?

A

Increase/extend or reduce

They are opposites

92
Q

Serine/threonine and tyrosine _____ increases NMDA current, whereas serine/threonine and tyrosine _____ decreases NMDA current.

A

Phosphorylation

Dephosphorylation

93
Q

Cysteine ______ increases NMDA current, whereas cysteine _____ decreases NMDA current.

A

Oxidation

Reduction

94
Q

During development, NMDA receptors are (more/less) inhibited by Mg+2, so they are (more/less) dependent on AMPA receptors for activity.

A

Less

Less

95
Q

Glutamate excitotoxicity is caused by _____ of the ____ receptors. This condition leads to high intracellular levels of _____ and eventually _____.

A

Overexcitement of the NMDA receptors
Ca+2
Apoptosis/cell death

96
Q

Glutamate excitotoxicity occurs with what 2 conditions?

A

Ischemia (oxygen deprivation)

Brain trauma

97
Q

Harm caused by glutamate excitotoxicity can be reduced by blocking ______ ______ and activating (pre-synaptic/post-synaptic) voltage-gated ____ channels, leading to ____ of the cell.

A

NMDA receptors
Post-synaptic
K+
Hyperpolarization

98
Q

Would knocking out K+ channels increase or decrease damage caused by glutamate excitotoxicity?

A

Increase

99
Q

Glutamate excitotoxicity can be decreased by decreasing _____ and _____ receptor activation, lessening the amount of _____ (ion) passage, and increasing the activity of ____ channels.

A

NMDA
AMPA
Ca+2
K+

100
Q

What are the 3 types of metabotropic glutamate receptors?

A

Class I
Class II
Class III

101
Q

Class I glutamate bind what type of trimeric G protein for (activation/inhibition) of ____? Classes II and III bind what different type of trimeric G protein for (activation/inhibition) of ____?

A

Gq
Activation of phospholipase C
Gi
Inhibition of adenylate cyclase

102
Q

GABA is an (excitatory/inhibitory) neurotransmitter that is made from ____ that is made into _____.

A

Inhibitory
Glucose
Glutamate

103
Q

What is the name of the vesicular transporter for GABA?

A

VIAAT (vesicular inhibitory amino acid transporter)

104
Q

How is GABA removed from synapses? What is the name of the protein that accomplishes this?

A

Re-uptake

GAT transporter

105
Q

What is the name of the ionotropic GABA receptor? Is it inhibitory or excitatory? What ion(s) does it pass? Is it a heterotetramer or heteropentamer?

A

GABA-A
Inhibitory
Cl- only
Heteropentamer

106
Q

What is the name of the metabotropic GABA receptor? It decreases action potential length and ability of neurons to fire action potentials by activating ____ channels and inhibiting ____ channels, respectively.

A

GABA-B
K+
Ca+2

107
Q

What are 3 drug agonists for the GABA-A receptor?

A

Benzodiazepines
Barbiturates
Steroids

108
Q

What are 2 toxin antagonists for the GABA-A receptor and what are their sources?

A

Strychnine (plant toxin)

Picrotoxin (snail toxin)

109
Q

Immature GABA-A receptors are (excitatory/inhibitory), whereas mature GABA-A receptors are (excitatory/inhibitory). This is because the immature neurons use a __/__/__ co-transporter that sets up a (low/high) intracellular Cl- concentration, whereas the mature neurons use a ___/___ co-transporter that sets up a (low/high) intracellular Cl- concentration.

A 
Excitatory
Inhibitory
Na+/K+/Cl-
High
K+/Cl-
Low
110
Q

A high intracellular concentration of Cl- means that the Ex of Cl- (increases/decreases) and becomes (more/less) than threshold, meaning that activation of the immature neuron is (excitatory/inhibitory). A low intracellular concentration of Cl- means the the Ex of Cl- (increases/decreases) and becomes (more/less) than threshold, meaning that the activation of the mature neuron is (excitatory/inhibitory).

A 
Increases
More
Excitatory
Decreases
Less
Inhibitory
111
Q

In the mature neuron, when the channel opens at Vrest, the driving force on Cl- is (inward/outward) because the intracellular concentration of Cl- is low. This results in a (depolarization/hyperpolarization) of the cell because Cl- is a negative ion. In the immature neuron, when the channel opens at Vrest, the driving force on Cl- is (inward/outward) because the intracellular concentration of Cl- is high. This results in a (depolarization/hyperpolarization) of the cell.

A

Inward
Hyperpolarization
Outward
Depolarization

112
Q

Because GABA-A channels only pass Cl-, the reversal potential for the channel is equal to ____ _____ of _____.

A

Equilibrium potential of Cl-

113
Q

In order to cause an action potential, the Ex of Cl- in GABA-A receptors must be greater than what 2 values?

A

Vrest and threshold

114
Q

If Erev is greater than threshold, then the effect of stimulation is (excitatory/inhibitory), whereas an Erev that is less than threshold causes stimulation to have an (excitatory/inhibitory) effect.

A

Excitatory

Inhibitory

115
Q

Glycine is more commonly released in the (brain/spinal cord). Is it inhibitory or excitatory?

A

Spinal cord

Inhibitory

116
Q

Glycine is synthesized from _____.

A

Serine

117
Q

What is the vesicular transporter for glycine? What other neurotransmitter uses this vesicular transporter?

A

VIAAT

GABA

118
Q

How is glycine removed from synapses and by what?

A

Re-uptake

Glycine transporters

119
Q

Glycine has only (ionotropic/metabotropic) receptors.

A

Ionotropic

120
Q

The ionotropic glycine receptor passes what ion(s) and is similar to what other type of ionotropic receptor? Is it a heterotetramer or heteropentamer?

A

Only Cl-
GABA-A
Heteropentamer

121
Q

What 3 neurotransmitters are catecholamines?

A

Dopamine
Norepinephrine
Epinephrine

122
Q

All the catecholamines are synthesized from _____ by ____ _____ in neurons that have their cell bodies in the ____ ____.

A

Tyrosine
Tyrosine hydroxylase
Brain stem

123
Q

Dopamine is made by neurons with cell bodies in what 2 parts of the midbrain?

A

Substantia nigra pars compacta

Ventral tegmental area

124
Q

What is the vesicular transporter for dopamine?

A

VMAT (vesicular monoamine transporter)

125
Q

Dopamine has only (ionotropic/metabotropic) receptors.

A

Metabotropic

126
Q

Dopamine binds G protein-coupled receptors _____ and ____. Which is Gs coupled and which is Gi coupled?

A

D1R (Gs coupled)

D2R (Gi coupled)

127
Q

Is dopamine removed by reuptake, degradation, or both? What molecule mediates reuptake? What 2 molecules mediate degradation?

A

Both
Na+ dependent transporter (DAT)
Monoamine oxidase (MAO) and catechol O-methyl-transferase (COMT)

128
Q

How do amphetamine and cocaine modify the effects of dopamine?

A

Block its reuptake

129
Q

How do monoamine oxidase inhibitors modify the effects of dopamine?

A

Block its degradation

130
Q

In the synthesis of catecholamines, tyrosine is converted to _____ by ____. The molecule that tyrosine is converted into is used to synthesize ______ (catecholamine). From there, _____ (another catecholamine) is synthesized. The 2nd catecholamine is used to make ______, the final catecholamine.

A 
DOPA
Tyrosine hydroxylase
Dopamine
Norepinephrine
Epinephrine
131
Q

Though dopamine is made by neurons with cell bodies in the substantia nigra and ventral tegmental area, these neurons are ____ _____ because their axons project to other areas. The synthesis of dopamine occurs near the _____.

A

Projection neurons

Synapse

132
Q

The neurons that make norepinephrine, like dopamine, are _____ _____ because their cell bodies are located in the _____ ____ in the ____ but can be synthesized in other parts of the brain in which the axons project.

A

Projection neurons
Locus coeruleus (“ceruleus”)
Pons

133
Q

The vesicular transporter for norepinephrine, ____, is the same as the one for dopamine.

A

VMAT (vesicular monoamine transporter)

134
Q

Like dopamine, norepinephrine is removed by (reuptake/degradation/both). What molecule(s) that regulate this/these process(es) in dopamine do the same in norepinephrine?

A

Both
Reuptake- Na+ dependent transporter (NET)
Degradation- Monoamine oxidase (MAO), catechol O-methyl transferase (COMT)

135
Q

How does phenelzine, an MAOI, modify the effects of norepinephrine?

A

Prevents its degradation

136
Q

Like dopamine, norepinephrine has only (ionotropic/metabotropic) receptors.

A

Metabotropic

137
Q

Norepinephrine binds ____ G protein-coupled receptors. The subgroups of these types of receptors are called ____ and ____.

A

Adrenergic
Alpha
Beta

138
Q

The Alpha1 norepinephrine metabotropic receptors are ____ coupled, whereas the Alpha2 norepinephrine metabotropic receptors are ___ coupled. The beta norepinephrine receptors are only ____ coupled.

A

Gq
Gs
Gs

139
Q

The beta norepinephrine receptors are inhibited by what?

A

Beta blockers

140
Q

Epinephrine is also known as _____.

A

Adrenaline

141
Q

Epinephrine is made by neurons in the _____ and is secreted in the ______, which contains the thalamus and hypothalamus.

A

Medulla

Diencephalon

142
Q

In the kidneys, epinephrine is made in the ____ ____. In the body (not the brain), epinephrine acts as a ____ rather than a neurotransmitter.

A

Adrenal cortex

Hormone

143
Q

The regulation and receptors of epinephrine are similar to those of _____. It binds the ____ metabotropic receptors with subgroups _____ and ____.

A

Norepinephrine
Adrenergic
Alpha
Beta

144
Q

Is the function of epinephrine in the brain well understood?

A

No

145
Q

Serotonin is made by neurons with cell bodies in the ____ ____, which extends from the _____ to the _____.

A

Raphe nucleus
Midbrain
Pons

146
Q

Serotonin is synthesized from ____.

A

Tryptophan

147
Q

The vesicular transporter for serotonin is ____, the same as for the catecholamines.

A

VMAT

148
Q

Serotonin undergoes (reuptake/degradation), which is mediated by the ______.

A

Reuptake

SERT (serotonin reuptake transporter)

149
Q

The SERT (serotonin reuptake transporter) is the target of _____ (antidepressants) and _____ (illegal drug), which both extend the amount of serotonin in the synapse.

A

SSRIs

MDMA

150
Q

Serotonin has (ionotropic/metabotropic/both) receptors. What do they start with?

A

Both

5-HT

151
Q

The catecholamines can all be synthesized in the _____, though their cell bodies are located elsewhere.

A

Cortex

152
Q

Serotonin regulates ____, ____ of ____, ____, and ____ ____.

A

Emotions
State of arousal
Movement
Circadian rhythms

153
Q

Histamine is synthesized from ____ from cells that have their cell bodies in the _____.

A

Histidine

Hypothalamus

154
Q

In addition to neurons, histamine is secreted by what immune cells?

A

Mast cells

155
Q

Histamine mediates _____ and ____ as well as modifies ___ ____ (balance).

A

Arousal
Attention
Vestibular function

156
Q

Like the other biogenic amines, the vesicular transporter for histamine is ____.

A

VMAT (vesicular monoamine transporter)

157
Q

Histamine is removed from the synapse by (reuptake/degradation/both), which is moderated by ____ and ______ ______.

A

Degradation
Histamine methyltransferase
Monoamine oxidase (MAO)

158
Q

Histamine has (ionotropic/metabotropic/both) receptors.

A

Metabotropic only

159
Q

ATP is co-packaged into vesicles with most _____ ____ neurotransmitters.

A

Small molecule

160
Q

2 ways that ATP is synthesized

A

Glycolysis

Oxidative phosphorylation in mitochondria

161
Q

The vesicular transporter for ATP is thought to be ____, though it is uncertain.

A

VNUT

162
Q

ATP is degraded to ____ in the synaptic cleft.

A

Adenosine

163
Q

Why is adenosine not considered to be a conventional neurotransmitter?

A

It isn’t released in synaptic vesicles

164
Q

ATP has ionotropic and metabotropic receptors that are called _____. The ionotropic receptors are designated ____, where the metabotropic receptors are designated ____ or ____.

A

Purinergic
P2X
Adenosine
P2Y

165
Q

The metabotropic ATP receptors differ in binding affinities because the A2A receptors prefer to bind ____, whereas the P2Y receptors bind ____ and ____ equally.

A

Adenosine

Adenosine and ATP

166
Q

The P2X ion receptors are _____ because they are made up of ____ subunits.

A

Trimers

3

167
Q

Peptide neurotransmitters can also act as ____.

A

Hormones

168
Q

Peptide neurotransmitters modulate ____.

A

Emotion

169
Q

2 types of peptide neurotransmitters are ____ ____ and _____, which modulate what?

A

Substance P
Opioids
Pain perception

170
Q

In the synthesis of peptide neurotransmitters, the ___-____ are made in the ____ ____ ____ and processed into _____ in the _____. They are loaded into ____ and converted into active neuropeptides there.

A 
Pre-propeptides
Rough endoplasmic reticulum
Propeptides
Golgi
Vesicles
171
Q

Is a vesicular transporter necessary for peptide neurotransmitters?

A

No

172
Q

Peptide neurotransmitters activate G protein-coupled receptors at ____ concentrations, so they are considered to be very powerful.

A

Low

173
Q

Peptide neurotransmitters regulate the ____ ____, especially the ___.

A

Internal organs

Gut

174
Q

The difference between the pre-propeptide and the propeptide is the ____ ____, which is required for secretion into the ____ ____ and is removed in the propeptide.

A

Signal sequence

Endoplasmic reticulum

175
Q

A single gene can be used to make (one/multiple) peptide neurotransmitter(s).

A

Multiple

176
Q

What are the 3 classes of endogenous opioids?

A

Dynorphins
Enkaphalins
Endorphins

177
Q

The endogenous opioids bind to which 3 G protein-coupled receptors?

A

Mu
Delta
Kappa

178
Q

The drugs that bind opioid receptors are much ____ in size than the endogenous opioids.

A

Smaller

179
Q

The endocannabinoids are synthesized from ______.

A

Phospholipids

180
Q

2 types of endocannabinoids

A

Arachidonylglycerol (2-AG)

Anandamide (AEA)

181
Q

A plant-derived cannabinoid is ____. Because it is more stable than endocannabinoids, it has a ____ lasting effect.

A

THC

Longer

182
Q

Why is it that the endocannabinoids can’t be put into synaptic vesicles? What does this mean for their synthesis?

A

They are lipid soluble and would diffuse out of the vesicles

They must be synthesized on demand

183
Q

Where are endocannabinoids synthesized (pre- or post-synaptic cell)? This synthesis is dependent on ___-_____.

A

Post-synaptic cell

Second messangers

184
Q

The endocannabinoids bind what type of metabotropic receptors? What are the 2 designations for this type of receptor?

A

Cannabinoid

CB1 and CB2

185
Q

The endocannabinoids are degraded by what?

A

Fatty acid amide hydroxylase

186
Q

Stimulation of the ____-synaptic neuron (excitatory or inhibitory) causes production of endocannabinoids. The endocannabinoids stimulate the ____ receptor on the ___-synaptic neuron. Activation of the trimeric G protein causes a reduction in ____, which causes fewer ____ or ___ vesicles to be released on the ____-synaptic side. Fewer vesicles released means decreased ____-synaptic current.

A 
Post
CB1
Pre
Ca+2
GABA
Glutamate
Pre
Post
187
Q

Nitric oxide is a gas, so it is highly ____.

A

Diffusible

188
Q

Nitric oxide is synthesized from _____ by ____ ____.

A

Arginine

NO synthase

189
Q

Nitric oxide acts on ____ _____, which produces ____ which activates ____ ____ ____.

A

Guanalyl cyclase
cGMP
Protein kinase G

190
Q

Because of its ability to diffuse, nitric oxide regulates cells not necessarily connected by _____.

A

Synapses

191
Q

SSRIs (selective serotonin reuptake inhibitors) block what reuptake modulator?

A

SERT (serotonin reuptake transporter)

192
Q

Monoamineoxigenase inhibitors (MAOIs) block which degradation enzyme that is used with what 4 neurotransmitters?

A

Monoamine oxidase

Serotonin, epinephrine, norepinephrine, dopamine

193
Q

Norepinephrine and dopamine reuptake inhibitors (NRDIs) block what 2 reuptake modulators, affecting what 3 neurotransmitters?

A

DAT, NERT

Epinephrine, dopamine, norepinephrine

194
Q

The norepinephrine and dopamine reuptake inhibitors (NRDIs) include what 2 antidepressants?

A

Wellbutrin, Bupropion

195
Q

Dextromethorphan affects (one/multiple) neurotransmitter signaling pathway(s). It can cause what syndrome if taken with SSRIs or MAOIs?

A 
Multiple
Serotonin syndrome (excess serotonin)

Neurobiology I (18 decks)

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