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Neuropharmacology > GluRs > Flashcards

GluRs Flashcards

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1
Q

Where does glutamate act as a fast transmitter

A

majority of excitatory synapses in mammalian CNS, squid giant synapse, insect NMJ, molluscan CNS, and some peripheral neurons

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2
Q

What types of cells also express glutamate receptors

A

other neurons, bacteria, and plant cells

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3
Q

What determines glutamate’s diverse postsynaptic responses

A

receptor subunit composition and auxiliary subunits

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4
Q

What are auxiliary subunits

A

proteins that modify AMPA receptor properties and trafficking

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5
Q

Which receptors are present at most excitatory synapses

A

AMPA and NMDA

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6
Q

Which synapses contain only NMDA receptors

A

some early developmental synapses

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7
Q

Which synapses contain only AMPA receptors

A

some in mature tissues

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8
Q

What is the main function of AMPA receptors

A

mediate fast component of synaptic current

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9
Q

What are the kinetics of AMPA receptors

A

rise time less than 1ms and decay time around 1-3ms

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10
Q

What ions are AMPA receptors permeable to

A

Na+, K+ and sometimes Ca2+

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11
Q

What are calcium-permeable AMPA receptors blocked by

A

intracellular polyamines at depolarised potentials

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12
Q

What determines calcium permeability in AMPA receptors

A

presence or absence of GluA2 subunit

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13
Q

What is the structure of AMPA receptors

A

tetramer of GluA1, GluA2, GluA3, GluA4

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14
Q

What is the difference between flip and flop isoforms of AMPARs

A

flip desensitizes slower and is dominant in immature tissue

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15
Q

Where is the Q/R site located

A

within GluA2 subunit at pore lining

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16
Q

What does RNA editing of GluA2 result in

A

arginine at Q/R site making AMPAR calcium impermeable

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17
Q

Which AMPARs are calcium permeable

A

those lacking GluA2

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18
Q

What blocks CP-AMPARs

A

intracellular polyamines like spermine

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19
Q

What is the function of polyamine block

A

neuroprotective mechanism reducing Ca2+ entry

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20
Q

What diseases are linked to CP-AMPARs

A

ALS, stroke, hypoxia and cerebral palsy, glioma, pain plasticity

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21
Q

What is the main function of NMDA receptors

A

mediate slow component of synaptic current

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22
Q

What are the kinetics of NMDA receptors

A

rise time under 10ms and decay time over 100ms

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23
Q

What ions are NMDA receptors permeable to

A

Na+, K+ and Ca2+

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24
Q

What blocks NMDA receptors at rest

Study These Flashcards
A

extracellular Mg2+ in a voltage dependent manner

25
What co-agonist is required for NMDA activation
glycine
26
What additional modulator blocks NMDA receptors
protons
27
What triggers Mg2+ unblock in NMDA receptors
AMPAR-mediated depolarisation
28
What is the NMDA receptor structure
heteromeric complex of GluN1 and GluN2 or GluN3
29
What subunits are involved in NMDARs
GluN1 GluN2A-D GluN3A-B
30
What contributes to cognitive decline in aging
reduced expression of GluN2B-containing NMDARs
31
What happens to NMDARs during stroke or acidosis
inhibited by proton block
32
What are the four types of iGluRs
AMPA, NMDA, Kainate, and delta receptors
33
What are common issues with iGluRs
channelopathies and pathophysiological mechanisms
34
What causes excitotoxicity
excessive activation of glutamate receptors
35
What diseases is excitotoxicity linked to
ALS, multiple sclerosis, Parkinson’s disease
36
What leads to Ca2+ overload in excitotoxicity
sustained Glu release activates NMDA AMPA and mGluRs
37
What organelles buffer intracellular Ca2+
mitochondria and ER
38
What does excessive Ca2+ do to mitochondria
disrupts ATP synthesis and increases ROS
39
What are consequences of excitotoxic Ca2+ entry
oxidative stress, NO production, apoptosis, and lipid damage
40
What common toxins cause excitotoxicity
MSG, domoic acid, and BMAA
41
What does domoic acid activate
kainate and AMPA receptors
42
What symptoms does BMAA cause
Parkinsonism and cognitive dysfunction
43
What causes cerebral ischemia
restricted blood flow from clots or cardiac arrest
44
What is the role of glutamate in ischemia
increased release causes NMDA-mediated Ca2+ influx
45
Why are NMDA blockers not effective treatments
they have widespread effects and side effects
46
Why is CP-AMPAR a better target
more localized expression and calcium permeability
47
What is ALS
progressive degeneration of motor neurons
48
Why are motor neurons susceptible to excitotoxicity
low Ca2+ buffering and CP-AMPAR expression
49
What gene mutation is linked to ALS
SOD1
50
What role do glutamate transporters play in ALS
impaired uptake increases synaptic Glu
51
What does low GluA2 mRNA indicate
high expression of CP-AMPARs and neuron vulnerability
52
What drug is prescribed for ALS
Riluzole
53
What is the NMDA hypothesis of SCZ
NMDA hypofunction especially on cortical interneurons
54
What symptoms are linked to mesolimbic hyperactivity
positive symptoms
55
What symptoms are linked to mesocortical hypoactivity
negative symptoms
56
What supports glutamate dysfunction in SCZ
reduced NMDAR expression and transporter activity
57
How do PCP and ketamine affect SCZ symptoms
mimic and exacerbate all symptoms
58
What are possible glutamatergic treatments for SCZ
glycine site modulators, mGluR agonists, and ampakines

Neuropharmacology (6 decks)

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