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Neuro-pharmacology > Glutamate receptors > Flashcards

Glutamate receptors Flashcards

1
Q

Metabotropic glutamate receptors Group I

A
  • mGluR1, mGluR5
  • Gq → PLC, Ca2+
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2
Q

Metabotropic glutamate receptors Group II

A

mGluR2, mGluR3
* Gi → ↓ cAMP

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3
Q

Metabotropic glutamate receptors Group III

A

mGluR4, mGluR6, mGluR7, mGluR8
* Gi → ↓ cAMP

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4
Q

Group I mGluR found mostly

A

postsynaptically

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5
Q

Group II and III are often found

A

presynaptically

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6
Q

Group II and III are often found presynaptically

A

Autoreceptors
* Modulators on other NT systems

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7
Q

Metabotropic glutamate receptors Contribute to

A

plasticity of synapses

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8
Q

Metabotropic glutamate receptors Excitatory or inhibitory depending on

A

signalling, cell types

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9
Q

Knockout studies mGluR1 KO show

A

motor dysfunction

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10
Q

mGluR1 KO show motor dysfunction

A

Ataxia, intention tremor, dysmetria
* Impaired plasticity in the cerebellum

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11
Q
  • mGluR2 KO show
A

normal synaptic
transmission

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12
Q

mGluR2 KO show normal synaptic
transmission

A

Highly expressed in dentate gyrus
* KO shows reduced presynaptic inhibition

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13
Q

Receptor
distribution At postsynaptic densities mGluR
are expressed at the

A

periphery.

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14
Q

Receptor
distribution AMPAR and NMDAR are
distributed

A

throughout the PSD

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15
Q

Receptor
distribution NMDAR are

A

tightly coupled to
Ca2+
-dependent proteins such as
CaMKII

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16
Q

Plasticity Hippocampus

A
  • Important for learning and
    memory
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17
Q

Plasticity Synaptic plasticity

A

Changes in strength of
glutamatergic synapses in
response to activity

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18
Q

Plasticity LTP

A

persistent increase in synaptic
strength following tetanic
activity (100 Hz, 1 s)

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19
Q

Plasticity * Long-term depression (LTD)

A

persistent decrease in
synaptic strength following
slow repetitive activity

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20
Q

Plasticity in the HC

A

Hippocampal plasticity is widely
studied due to the role in learning
and the well defined circuits (most
glutamatergic).

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21
Q

LTP occurs through

A

coincidence detection

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22
Q

CaMKII is coupled to

A

NMDAR

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23
Q

Ca2+-calmodulin dependent
protein kinase II (CamKII) Localizes with NMDA receptors
(intracellular face)

A

Phosphorylates numerous
cellular targets and initiates
early-phase of LTP

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24
Q

LTP and glutamate

A

repeated stimulation very quickly - repeated activation of AMPA receptors causes depolarization across membrane - allows MG to be removed from NMDA receptor - calium flows in - result is LTP

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25
Q

early-phase of LTP Ca2+

A

entry through NMDAR
activates CamKII

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26
Q

Early LTP CamKII

A

phorphorylates AMPAR
– increasing their sensitivity to
glutamate

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27
Q

Early LTP CamKII phorphorylates AMPAR
–
increasing their sensitivity to
glutamate.
Signalling cascades

A

increase trafficking of AMPAR to the
postsynaptic density – increasing
the availability of receptors.

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28
Q

Early LTP
Ca2+
-entry through NMDAR
activates CamKII
.
CamKII phorphorylates AMPAR
–
increasing their sensitivity to
glutamate.
Signalling cascades increase
trafficking of AMPAR to the
postsynaptic density
– increasing
the availability of receptors. Retrograde messengers

A

signal to
the presynaptic cell initiating
presynaptic changes that increase
glutamate release.

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29
Q

Late-phase LTP Activation of CamKII and PLC converge on another signalling
kinase

A

ERK

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30
Q

Late-phase LTP ERK triggers downstream changes including phosphorylation of
transcription factors

A

Gene synthesis is induced increasing production of AMPA receptors

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31
Q

Synthesis processes are important for

A

long-term maintenance of
potentiation

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32
Q

NMDA receptors and LTP NMDAR overexpression
increases

A

learning in mice

33
Q

Mice engineered to
overexpress the NR2B subunit
* Termed Doogie mouse… * Increased

A

retention in novel
object recognition tasks

34
Q

Excitotoxicity Glutamate and excitatory analogues
can be

A

neurotoxic specifically when extracellularly

35
Q

MSG can induce

A

lesions

36
Q

lesions can be induces by other

A

agonists of the glutamate receptor

37
Q

Excitotoxicity Occurs through

A

over activation of
glutamatergic neurons

38
Q

Excitotoxicity Increased intracellular

A

Ca2+ to dangerous
levels

39
Q

Increased intracellular Ca2+ to dangerous
levels Contributes to (6)

A

pathogenesis of ischemia,
ALS, traumatic brain injury, alcoholism,
Huntington’s disease, multiple sclerosis

40
Q

Lytigo-bodig disease is a

A

neurodegenerative disease that
manifests similar to ALS and
Parkinson’s

41
Q

Lytigo-bodig disease is Localized in

A

Guam

42
Q

Local cycad seeds (Cyas circinalis)
contain

A

BMAA

43
Q

BMAA potent

A

excitotoxin at AMPA,
kainate, and NMDA receptors

44
Q
  • A mutation found in ALS patients leads to increased
A

intracellular Ca2+ in motor neurons, which
stresses mitochondria. Mitochondria produce reactive oxygen species (ROS) that are toxic and
also inhibit EAAT2 on astrocytes

45
Q

EAAT2 dysfunction leads to

A

glutamate accumulation and excitotoxicity in motor neurons.

46
Q

Ischemia

A
  • Ischemic stroke results in loss of blood flow to
    regions of the CNS
47
Q

Ischemia Lack of O2 and glucose causes

A

energy failure

48
Q

Ischemia Loss of ionic gradients causes

A

glutamatergic
synapses to dump glutamate

49
Q

Loss of ionic gradients causes glutamatergic
synapses to dump glutamate

A

ncreased intracellular Ca2+
Failure of EAAT transport (depends on ion
gradient) reverses glutamate flow

50
Q

Excitotoxic cell death Necrosis

A

Uncontrolled cell death

51
Q

Necrosis process

A
  • Na+ and Cl influx to cell causes
    hypertonicity -Osmosis causes cell swelling (edema) -Swelling leads to rupture of the cell
    membrane and cell lysis
52
Q

Excitotoxic cell death Apoptosis

A

Programmed cell death

53
Q

Apoptosis Process

A

Ca2+ influx activates intracellular
pathways
- Mitochondrial generation of ROS
• Depolarization and swelling of mitochondria
Mitochondrial damage leads to
formation of pores in mitochondrial
membrane
• Cytochrome C escapes
• Initiates apoptosis

54
Q

Two modes of cell death are initiated

A

by ischemic / glutamatergic injury

55
Q

Apoptosis is regulated cell death and
results in

A

controlled removal of cell
material by phagocytic cells.

56
Q

Necrosis results in cell lysis and

A

release
of cellular contents.

57
Q

Glutamatergic cell death In animal models, NMDA or AMPA antagonists reduce the
volume of injury in

A

n ischemic stroke

58
Q

Glutamatergic cell death - Glutamate can cause

A

over-excitation leading to cell
death by necrosis or apoptosis → Excitotoxicity

59
Q

Epileptiform activity Epilepsy

A

Heterogeneous group of neurological disorders
characterized by epileptic seizures

60
Q
  • Epilepsy Abnormal
A

excessive or synchronous neuronal activity in the brain

61
Q

Epilepsy and glutamatergic activity

A

Epileptic seizures are dependent on glutamatergic signalling

62
Q
  • Pharmacological activation of glutamatergic signalling can initiate
A

seizures in animal models

63
Q

convulsant

A

Kainate, AMPA, domoic acid are convulsants

64
Q

Early seizure activity is dependent on

A

AMPA receptor activation

65
Q

Antagonists of AMPAR can

A

prevent seizure onset (e.g. NBQX

66
Q

As seizures intensify and spread

A

NMDA receptors are involved

67
Q

Antagonists of NMDAR can reduce

A

Intensity and duration of seizures (e.g. MK801)

68
Q

Genetic causes of epilepsy * Glutamatergic changes are found in many heritable cases of
epilepsy -

A

Heterogeneous

69
Q

Genetic causes of epilepsy - Glutamate receptors

A

AMPA, kainate, and NMDA receptor subunits altered

70
Q

Genetic causes of epilepsy -Glutamate transporters

A
  • EAAT 1 and 2 show alterations in patients
71
Q

Genetic causes of epilepsy - Astrocytic glutamate recycling

A

Glutamine synthetase, glutamate dehydrogenase

72
Q

Epilepsy treatment (AEDs)

A

Anticonvulsants/antiepileptic drugs (AEDs) are one of the few drug classes that is
not tested against placebo

73
Q

AEDs typically target

A

et Na+ channel activity or increase inhibitory signalling by
affecting GABA

74
Q
  • 30% of patients are unresponsive to
A

AED therapy

75
Q

AEDs often lose

A

effectiveness over time

76
Q

Surgical resection of seizure focus remains a

A

common treatment of drug-resistant
epilepsy

77
Q

Corpus callostomy

A

Corpus callostomy is effective at
decreasing the frequency and amplitude of seizures by
disrupting bilateral synchronous discharges.

78
Q

Corpus callostomy Side effects

A

s include speech irregularities – inability to
engage in spontaneous speech, inability to follow verbal
commands using non-dominant hand, and alien hand
syndrome

Neuro-pharmacology (26 decks)

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