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PSYC3030 > Glutamate and GABA > Flashcards

Glutamate and GABA Flashcards

1
Q

Glutamate differs from other neurotransmitters such as acetylcholine (ACh), dopamine (DA), and serotonin (5HT) in that

a. glutamate also plays a role in protein synthesis and cell metabolism
b. glutamate can only be synthesized by a single chemical reaction
c. only specialized neurons in the brain synthesize and release glutamate
d. glutamate is the only neurotransmitter that causes EPSPs

A

a. glutamate also plays a role in protein synthesis and cell metabolism

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2
Q

Which statement about astrocytes is false?

a. They contain glutamine synthetase
b. They prevent excessive neuronal excitation and degeneration
c. They remove glutamate from the extracellular fluid
d. They use the transporter EAAT3

A

d. They use the transporter EAAT3

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3
Q

Which event does not have to occur for NMDA receptor channel opening?

a. The membrane must be depolarized by some other receptor
b. An excitatory amino acid like glutamate must bind to the receptor
c. The PCP block must be removed
d. A co-agonist must bind at the glycine site

A

c. The PCP block must be removed

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4
Q

Which statement about GABA is false?

a. It is found in many local interneurons
b. It is found in projection neurons carrying inhibitory information
c. It is found in Purkinje cells of the cerebellar cortex
d. It is found only in subcortical locations

A

d. It is found only in subcortical locations

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5
Q

GABA-B receptors

a. are better studied than GABA-A receptors
b. cause potassium channel opening when stimulated
c. are ionotropic
d. exert excitatory effects on cyclic AMP

A

b. cause potassium channel opening when stimulated

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6
Q

A decrease in ___ activity can lead to toxicity, including flushing, nausea, and vomiting.

a. acetaldehyde dehydrogenase
b. formaldehyde
c. acetaldehyde
d. alcohol dehydrogenase

A

a. acetaldehyde dehydrogenase

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7
Q

In ___ tolerance, the effects of alcohol ___ when blood alcohol levels are falling compared to when they are rising.

a. acute; increase
b. acute; decrease
c. acute; remain the same
d. pharmacodynamic; increase

A

b. acute; decrease

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8
Q

Alcohol and benzodiazepines most likely show cross-tolerance and cross-dependence because they both ___ the effects of ___ at ___ receptors.

a. enhance; GABA; GABA-A
b. decrease; glutamate; NMDA
c. enhance; glutamate; NMDA
d. decrease; GABA; GABA-A

A

a. enhance; GABA; GABA-A

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9
Q

Describe the synthesis of glutamate.

A

Glutamine -glutaminase + ATP-> Glutamate

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10
Q

What are some good markers for glutamatergic neurons, and what is their role?

A

VGLUT1, VGLUT2, VGLUT3.

They are involved in the storage of glutamate into vesicles

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11
Q

Which transporter (mainly) is found in neurons which co-express glutamate with other neurotransmitters?

A

VGLUT3

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12
Q

What is gliotransmission?

A

Astrocytes also release glutamate. It is uncertain whether it is released from vesicles or membrane channels.

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13
Q

Does the glutamate system have autoreceptors?

A

Some metabotropic receptors on nerve terminals act as presynaptic autoreceptors to inhibit glutamate release.

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14
Q

What proteins are responsible for the reuptake of glutamate?

A

Excitatory Amino Acid Transporters 1-5.

Also, astrocyte transporters

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15
Q

What happens after astrocytes take up glutamate?

A

Glutamate -glutamine synthetase-> glutamine. Then, glutamine is transported out of astrocytes back to neurons.

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16
Q

Which enzyme is responsible for the breakdown of glutamate?

A

Glutamine synthetase

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17
Q

What type of receptors utilize glutamate?

A

Ionotropic and metabotropic. AMPA, kainate, and NDMA.

mGluR1-mGluR8.

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18
Q

Are glutamate receptors used exclusively by glutamate?

A

No, they are also used by aspartate and other excitatory amino acid transmitters.

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19
Q

Describe the mechanism and composition of AMPA and kainate receptors.

A

Ionotropic, and allow for flow of Na+.

4 subunits.

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20
Q

Which receptors are necessary for LTP expression?

A

AMPA receptors

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21
Q

What type of receptor are NMDA receptors?

A

Ionotropic receptors which allow Na+ and Ca2+ to pass

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22
Q

What must happen for NMDA receptors to open?

A

The membrane must depolarize. Glutamate and a co-agonist (glycine or D-serine) must bind NMDA receptors. Mg ions must be dissipated due to depolarization.

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23
Q

How many subunits do NMDA receptors have?

A

4 subunits

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24
Q

Which phase of E-LTP are NMDA receptors critical for?

A

Induction

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25
Q

What happens as a result of NMDA activation?

A

Ca2+ ions flow through and activate several protein kinases, including CaMKII, and more AMPARs are inserted into the postsynaptic membrane

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26
Q

Describe the mechanism of mGluRs.

A

They are coupled to G proteins. Some inhibit cAMP formation and others activate phosphoinositide second-messenger system.

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27
Q

How does glutamate activation of receptors differ with single stimulus or tetanic stimulation?

A

With single stimulus, only AMPA has flow.

With tetanic stimulation, Mg block is released in NMDA receptors due to greater depolarization.

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28
Q

What are three pathways utilized by glutamate?

A

Cerebral cortex -> pyramidal cells.
Cerebellar cortex -> parallel fibers.
Hippocampus -> several pathways.

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29
Q

What functions do mGluRs play a role in?

A

Locomotor activity, motor coordination, cognition, mood, pain perception.

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30
Q

What functions is glutamate implicated in?

A

Synaptic plasticity, learning, memory, cell death, drug addiction, schizophrenia

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31
Q

Describe the process of long-term potentiation.

A

Release of glutamate from the terminal plus NMDA activation in postsynaptic cell can lead to strengthening of synapse.
Involves coincidence detection as postsynaptic membrane must be depolarized simultaneously with glutamate binding. Rate of AMPA receptor insertion is increased, enhancing sensitivity to glutamate.

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32
Q

How long early vs. late LTP last?

A

Early LTP lasts a few hours, and late LTP lasts a few days or months.

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33
Q

Other than neurotransmission, what other roles does glutamate play?

A

Metabolic roles

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34
Q

What are the two phases of E-LTP?

A

Induction - during and immediately after tetanic stimulation.
Expression - enhanced synaptic strength.

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35
Q

What is excitotoxicity? When can it occur?

A

Prolonged depolarization of receptive neurons leads to eventual damage or death.
Can occur with brain ischemia as a result of prolonged activation of NMDARs and also possibly in ALS.

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36
Q

What decides whether necrosis or apoptosis occurs?

A

Amount of glutamate, length of exposure, and types of receptors activated

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37
Q

Where does glycine act as a neurotransmitter?

A

Mainly in brainstem and spinal cord

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38
Q

Describe the synthesis of GABA.

A

Glutamate -glutamic acid decarboxylase-> GABA

39
Q

What protein stores GABA in vesicles?

A

VGAT (or VIAAT)

40
Q

GABA is sometimes coreleased with which neurotransmitters?

A

Glycine, ACh, glutamate, and DA

41
Q

What is the advantage of neurons coreleasing GABA and glutamate?

A

Fine-tuning of postsynaptic response

42
Q

Does GABA have autoreceptors, and if so, what are they?

A

Yes, GABA-B receptors are postsynaptic autoreceptors.

43
Q

Which proteins are responsible for reuptake of GABA?

A

GAT-1, GAT-2, GAT-3

44
Q

Describe the metabolism of GABA. Where does it occur?

A

GABA -GABA aminotransferase-> glutamate and succinate. Then, glutamate is converted to glutamine.
Occurs in GABAergic neurons and astrocytes

45
Q

What are the receptors which are bound by GABA?

A

GABA-A and GABA-B

46
Q

Describe the mechanism and composition of GABA-A receptors.

A 
Ionotropic Cl- channel.
5 subunits (combination of alpha, beta, gamma, delta)
47
Q

What other molecules bind GABA-A receptors?

A

Benzodiazepines, barbiturates, neurosteroids

48
Q

Describe the mechanism and composition of GABA-B receptors.

A

Metabotropic receptor that works by inhibiting cAMP and opening K+ channels.
2 subunits.

49
Q

Where are GABA-B receptors found?

A

As presynaptic autoreceptors and postsynaptically.

50
Q

10-40% of nerve terminals in what 3 locations use GABA as the neurotransmitter?

A

Cerebral cortex, hippocampus, and substantia nigra

51
Q

In what type of neurons is GABA found?

A

Local interneurons and longer distance neurons

52
Q

Describe 2 pathways utilized by GABA.

A

Striatum -> globus pallidus and substantia nigra.

Purkinje cells of cerebellar cortex -> deep cerebellar nuclei and brainstem

53
Q

What are Purkinje cells important for?

A

Fine muscle control and coordination

54
Q

What behaviours do GABA-B receptors have a role in?

A

Learning and memory, anxiety and depression-like behaviours, and responses to drugs of abuse

55
Q

What 2 disorders might GABA play a role in?

A

Epilepsy and anxiety

56
Q

What happens to VGLUT2 knckout mice?

A

Die immediately after birth

57
Q

What happens to VGLUT1 knockout mice?

A

They survive birth but begin to die during 3rd week

58
Q

What happens to VGLUT3 knockout mice? Why?

A

They are viable but completely deaf. The inner hair cells of cochlea use glutamate as their neurotransmitter.

59
Q

What happens to EAAT2 knockout mice? Why?

A

They are more susceptible to brain injury, have seizures and a shortened lifespan due to hyperactivity.

60
Q

What is epilepsy?

A

A class of neurological disorders characterized by recurrent convulsive and nonconvulsive seizures

61
Q

What happens to some neurons during interictal periods?

A

Some neurons exhibit periodic episodes of prolonged depolarization, called a paroxysmal depolarization shift (PDS) followed by a hyperpolarization phase

62
Q

What phase of the action potential may be affected in epilepsy?

A

Seizure may be caused by a decrease in hyperpolarizing phase, and a failure of inhibition

63
Q

Which receptors mediate electrical activity of neurons?

A

Electrical activity of neurons is mediated by ionotropic glutamate receptors and GABA-A receptors.

64
Q

What happens when ionotropic glutamate receptors and GABA-A receptors are blocked?

A

Blocking either eliminates spontaneous discharge

65
Q

How does the function of GABA-A receptors shift over time?

A

During development, opening of Cl channels leads to depolarization (as higher Cl inside).
Once mature, Cl channel opening leads to hyperpolarization (as Cl is higher outside).

66
Q

How might GABA-A receptors differ in those with epilepsy?

A

In epilepsy, some GABA-A receptors may return to an earlier developmental state

67
Q

What drugs can be used to treat epilepsy?

A

GABA-A agonists

68
Q

What is active due to anxiety?

A

Sympathetic nervous system

69
Q

Which chemical modulate anxiety?

A

CRF, NE, EPI, 5-HT, GABA

70
Q

What is ketamine?

A

A NMDA antagonist

71
Q

What does NBQX do? What are its side effects?

A

Blocks AMPA and kainate receptors.

Sedation, reduced locomotor activity and ataxia, and protection against seizures.

72
Q

What are PCP and ketamine?

A

NMDAR channel binding site blockers and dissociative anesthetics.
Ketamine can also be used as an atypical antidepressant.

73
Q

What are the side effects of PCP and ketamine?

A

Sensory distortions, altered body image, cognitive disorganizations, various affective changes.
Chronic exposure leads to adverse effects.

74
Q

Are PCP and ketamine reinforcing? What can they be used to model?

A

Yes.

Schizophrenia.

75
Q

What is Mk-801 (dizocilpine)?

A

NMDAR channel binding site blocker used for research

76
Q

What is memantine (Namenda) and its use?

A

NMDAR channel binding site blocker for Alzheimer’s Disease treatment

77
Q

What do ampakines do?

A

Enhance AMPA action by reducing the rate of deactivation/desensitization.
Enhance cognitive function.

78
Q

What is CX717 and what can it do?

A

An ampakine that can improve performance of monkeys in delayed match-to-sample task

79
Q

What is L-AP4?

A

A glutamate autoreceptor agonist that suppresses glutamatergic synaptic transmission.

80
Q

What are allylglycine, thiosemicarbazide, and 3-mercaptopropionic acid used for? What can be a side effect?

A

Block GABA synthesis in in vitro studies. Convulsions.

81
Q

What is the mechanism of action for tiagabine/Gabitril? What can it be used for?

A

Selectively inhibits GAT-1. Elevates extracellular GABA levels and enhances GABAergic transmission in several brain areas.
Reduces seizure onset

82
Q

What is the mechanism of vigabatrin/Sabril, and what can it be used for?

A

Irreversible inhibitor of GABA-T to prevent GABA metabolism.

Can be used for epilepsy, but it affects vision through the GABAergic interneurons in the retina.

83
Q

What is muscimol used for? What is a side effect?

A

Stimulatory/hallucinogenic effects.

Macroscopia (perception of objects being larger than they are)

84
Q

What do benzodiazepines do?

A

Act on sites distinct from GABA binding site. When it binds, it increases potency of GABA to open receptor channel. They can only modulate GABA-A receptors and have no effect in absence of GABA.

85
Q

What do barbiturates do differently than benzodiazepines?

A

They increase the affinity of the GABA-A receptor for GABA, and have the ability of opening the Cl channel without GABA (so can be toxic).

86
Q

What does benzodiazepine sensitivity require?

A

Gamma subunit

87
Q

Which GABA subunit is responsible for sedating action? anxiolytic action?

A

Alpha 1

Alpha 2

88
Q

What do anesthetics do?

A

Induce a state of unconsciousness and block sensory awareness by positively modulating GABA.

89
Q

Where are neurosteroids synthesized and what do they do?

A

Synthesized in brain and act as local signaling molecules.

Enhance GABA receptor function.

90
Q

Who tends to have low levels of neurosteroids?

A

People with generalized anxiety disorder and social phobia

91
Q

What is bicuculline and what does it do?

A

A competitive GABA-A antagonist.

When taken systemically, can have a potent convulsant effect

92
Q

What are pentylenetetrazol (Metrazol) and picrotoxin?

A

Convulsant drugs; GABA-A antagonists.

93
Q

What is baclofen (Lioresal) and what is it used for?

A

GABA-B agonist.

Muscle relaxant and antispastic agent.

94
Q

What are saclofen and 2-hydroxysaclofen?

A

Competitive GABA-B antagonists.

PSYC3030 (12 decks)

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