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Glutamate Flashcards

1
Q

Amino acid neurotransmitters

A
  1. Not required in diet
  2. Synthesized in most cells of the body
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2
Q

Two functional groups of Amino acid neurotransmitters

A

Excitatory amino acid NT
Inhibitory amino acid NT

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3
Q

Excitatory amino acid NT (4)

A

Glutamate, Aspartate, Cysteate, Homocysteate

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4
Q

Inhibitory amino acid NT (4)

A

γ-aminobutyric acid (GABA), Glycine, Taurine,
Alanine

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5
Q

Excitatory amino acid neurotransmitters Aspartate Released in a

A

Ca2+
-dependent manner

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6
Q

Aspartate May not be stored in

A

secretory vesicles

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7
Q

Aspartate May be directly released from

A

cell cytoplasm Not considered a ‘classic’ neurotransmitter

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8
Q

Aspartate Acts at

A

glutamatergic receptors

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9
Q

Aspartate Physiological functions

A

unclear

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10
Q

Excitatory amino acid neurotransmitters Glutamate

A

Most widely used excitatory neurotransmitter

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11
Q

Glutamate____of all neurons, ______of all synapses are
glutamatergic

A

90% of all neurons, 80-90% of all synapses are
glutamatergic

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12
Q

Glutamate mediates fast

A

excitatory neurotransmission

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13
Q

Glutamate Mediates fast excitatory neurotransmission

A

Sensory, motor coordination, emotion, cognition,
memory formation and retrieval

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14
Q

Glutamate Proteinogenic amino acid

A

Abundant throughout the cell
Concentrated in presynaptic compartments

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15
Q

Glutamate
synthesis from
glutamine

A

Glutamine —glutaminase —> glutamate

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16
Q

In the CNS the majority
of glutamate is
recycled from

A

glutamine by the
enzyme glutaminase

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17
Q

Glutamate
transporters

A

Vesicular glutamate transporter (VGLUT) can be
used to identify glutamatergic neurons

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18
Q

VGLUTs are structurally and functionally similar to

A

VMAT

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19
Q
  • VGLUT1 and 2 are expressed
    on
A

distinct glutamatergic
populations in the CNS.

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20
Q

VGLUT3 is expressed in (3 neurons
)

A

various neurons including
GABAergic, cholinergic, and
monoaminergic neurons
suggesting possible
modulatory functions.

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21
Q

VGLUT2 locations

A

Deep cerebellar nuclei, inferior colliculus, thalamus

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22
Q

VGLUT 1 locations

A

cerebellar cortex, hippocampus, cortex

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23
Q

Glutamate is
metabolized to

A

glutamine

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24
Q

Glutamine
synthetase is the
enzyme responsible
for

A

conversion of
glutamate to
glutamine

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25
Q

Glutamate transporters on the
cell membrane are termed

A

excitatory amino acid
transporters (EAATs)

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26
Q

Glutamate transporters on the
cell membrane are termed
excitatory amino acid
transporters (EAATs) Non-specific for both

A

glutamate and aspartate

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27
Q

how many families are in EAAT

A

5

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28
Q
  • EAAT1 and 2 are expressed on
A

astrocytes

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29
Q

EAAT3 and 4 are expressed on

A

neurons

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30
Q

EAAT5 is expressed in the

A

retina

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31
Q
  • EAAT expression
    compartmentalizes
A

glutamate
recycling

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32
Q

Neurons comprise only

A

50% of the cells in the
CNS

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33
Q

Glia in the CNS

A

Astrocytes, Oligodendrocytes
Ependymal cells
Microglia

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34
Q

Astrocytes

A

define the brain side of the BBB

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35
Q
  • Oligodendrocytes
A

myelinate axons in white
matte

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36
Q

Ependymal cells

A

generate and regulate CSF

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37
Q

Microglia

A

Immune surveillance and
development

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38
Q

Astrocyte functions * Define the

A

blood brain barrier -Regulate intake of nutrients and O2

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39
Q

Astrocyte functions -Regulate

A

blood flow in the brain

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40
Q

Astrocyte functions Form extensive

A

signalling networks -Coupled with electrical synapses – Gap junctions

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41
Q

Astrocyte functions Regulate synaptic

A

functions and
contribute to plasticity

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42
Q

Astrocytes and cognition

A
  • Proposed to contribute to cognitive
    processes - more astrocytes increased cognition
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43
Q

High levels of extracellular glutamate are

A

toxic to neurons

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44
Q

Genetic knockdown of EAAT 1 and 2
(astrocytic) result in

A

widespread increases in
glutamate levels esp. in the striatum

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45
Q

Knockdown of activity of EAAT3 (neuronal
type)

A

has much more limited effects

46
Q

Astrocyte pathway of glutamate recycling is
the

A

dominant pathway

47
Q

EAAT2 abnormalities are observed in

A

amyotrophic lateral sclerosis (ALS)

48
Q

Glutamatergic synapses are wrapped by

A

astrocyte processes expressing EAAT1/2.

49
Q

Glutamate uptake into astrocytes is

A

Is rapid,
high efficiency, and prevents spillover of
glutamate into adjacent synapses

50
Q

Astrocytes are the principal site of

A

glutamate breakdown.

51
Q

Glutamine is exported from

A

astrocytes and
taken up into neurons to be converted back
to glutamate

52
Q
  • MSG can be used experimentally
    to
A

induce glutamatergic lesions

53
Q

MSG is proposed as one of the
five basic

A

tastes (referred to as
umami)

54
Q

MSG is proposed as one of the
five basic tastes (referred to as
umami)

A

Acts on glutamate receptors on
the tongue

55
Q

MSG syndrome is a widely
reported reaction to

56
Q

Glutamatergic neurons and systems - Pyramidal neurons of the cerebral cortex (4)

A

Projections to striatum, thalamus,
limbic, brainstem

57
Q

Glutamatergic neurons and systems Corticospinal tracts

A

Voluntary motor control

58
Q

Glutamatergic neurons and systems Parallel fibers of the cerebellum

A

Excitatory inputs to Purkinje cells

59
Q

Glutamatergic neurons and systems area

A

Hippocampus

60
Q

Glutamate receptors

A

The most important receptors are
ionotropic

61
Q

Synaptic transmission elicits

A

excitatory
postsynaptic potentials (EPSP)

62
Q

Ionotropic receptors (3)

A

AMPA receptors
Kainate receptors
NMDA receptors

63
Q

Metabotropic receptors Group I

A

mGluR1, mGluR5
Gq → PLC, Ca2+

64
Q

Metabotropic receptors Group II

A

mGluR2, mGluR3
Gi → ↓ cAMP

65
Q

Metabotropic receptors Group III

A

mGluR4, mGluR6, mGluR7, mGluR8
Gi → ↓ cAMP

66
Q

AMPA Receptors
Four types of subunits and form

A

(GluR1-4)
form heterotetramers (dimers of dimers)

67
Q

AMPA Receptors Rapid kinetics Onset, offset, desensitization

A

occur within
milliseconds

68
Q

AMPA Receptors Rapid kinetics Single channel conductance on

A

n picosecond
timescale (10
-12 s)

69
Q

AMPA Receptors * Experimental antagonists (3)

A

NBQX, CNQX, DNQX

70
Q
  • Specific mutations in AMPAR
    (GRIN2A gene)
    associated with
A

58% decrease in Parkinson’s
risk if also a heavy coffee drinker

71
Q

Kainate receptors Functionally similar to

A

AMPA receptors

72
Q

Kainate receptors 5 subunits (termed

73
Q

Kainate receptors Selective agonist is

74
Q

Kainate receptors Somewhat slower than

75
Q

Kainate receptors Limited role in

A

fast, excitatory
transmission

76
Q

Kainate receptors Limited role in fast, excitatory
transmission

A

Can be expressed presynaptically at
GABAergic synapses

77
Q

AMPA and kainate receptors have very

A

similar pharmacology

78
Q

Agonists at kainate and AMPA receptors
cause

79
Q
  • Kainic acid is used as a model of
80
Q

Kainic acid is used as a model of epilepsy Repeated administration causes

A

development of spontaneous seizures

81
Q

AMPA and Kainate pharmacology Agonists (3)

A

Kainate/Kainic acid
AMPA
Domoic acid

82
Q

Kainate/Kainic acid

A

Kainate > AMPAR

83
Q

AMPA

A

AMPAR&raquo_space;
Kainate

84
Q

Domoic acid

A

Kainate > AMPAR

85
Q

Domoic acid causes

A

Causes amnesiac
shellfish poisoning
in humans

86
Q

AMPA and Kainate pharmacology Antagonists: (2)

87
Q

NBQX

A

AMPAR&raquo_space;
kainate

88
Q

NS102

A

Kainate&raquo_space;
AMPAR

89
Q

NMDA Receptors Widely distributed (5)

A

Cortex, hippocampus, basal
ganglia, septum, cerebellum

90
Q

NMDA Receptors Always co-expressed with

A

either AMPA or kainate
receptors

91
Q

NMDA Receptors Permeable to

A

Ca2+ as well as
Na+ and K+

92
Q

NMDA Receptors Highly regulated

A
  • 6 binding sites for endogenous
    ligands and modulators
93
Q

NMDA Receptors * Important in

A

learning and
memory processes by
modulating synaptic strength

94
Q

NMDAR binding sites (6)

A

Glutamate site
Glycine/D-serine site
Polyamine binding site
Mg2+ binding site
Zn2+ binding site
H+ binding

95
Q

NMDAR binding sites Glutamate site

A

obligatory agonist binding site

96
Q

NMDAR binding sites Glycine/D-serine site

A

obligatory co-agonist binding site

97
Q

NMDAR binding sites Polyamine binding site

A

Site of endogenous allosteric
modulation (positive)

98
Q

NMDAR binding sites Mg2+ binding site

A

voltage dependent block of channel
opening

99
Q

NMDAR binding sites Zn2+ binding site

A

negative allosteric modulation site

100
Q

NMDAR binding sites H+ binding

A

pH sensitive negative modulation

101
Q

NMDAR Gating resting state

A

resting state - Mg2+ occupies the
channel pore

102
Q

NMDAR Gating Agonist binding alone is

A

Is insufficient
to allow ion flux.

103
Q

NMDAR Gating The pore is ‘unblocked’ when a

A

depolarization is previously present – displacing Mg2+ in n voltage-dependent manner

104
Q

NMDAR Gating NMDA receptors are only active
after

A

an initial depolarization
(through AMPA receptors).

105
Q

NMDA is described as a
coincidence detector

A

opening
only under conditions of strong or
repeated stimulation.

106
Q

NMDAR Pharmacology Agonists:

A

Endogenous
exogenous

107
Q

Endogenous NMDAR * Agonists

A

Glutamate and glycine / D-serine (both obligatory)
Polyamines (e.g. spermine, spermidine) – allosteric modulators

108
Q

Exogenous NMDAR agonist

A

NMDA (N-methyl-D-aspartate) – synthetic amino acid

109
Q

NMDAR Pharmacology Antagonists Endogenous:

A

Zn2+ (allosteric), Mg2+

110
Q

NMDAR Pharmacology Antagonists Exogenous

A

MK801 – widely used experimental antagonist – non-competitive
PCP and ketamine – dissociative anesthetics / recreational – non-competitive

Neuro-pharmacology (26 decks)

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