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Neuropharmacology > Lecture 10 > Flashcards

Lecture 10 Flashcards

1
Q

What are the types of glutamate ligand-gated ion channels?

A
  • NMDA, AMPA, kainate
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2
Q

What type of transmission are the glutamate ligand-gated ion channels responsible for?

A

Fast, excitatory transmission

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3
Q

How is glutamate synthesised?

A

1) uptake of glutamate into glial cells 2) conversion of glutamate to glutamine via glutamine synthetase 3) neuron takes up glutamine 4) glutamate production - glutamine to glutamate via glutaminase - glutamate from tricarboxylic acid cycle

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4
Q

How is glutamate activity terminated?

A

Via EAAT (excitatory amino acid transporter) - 1-2 (postsynaptic neuron)- 3-4 (glial cell)

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5
Q

What is the structure of the glutamate receptors?

A

Tetrameric

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6
Q

Why is the NMDA receptor unusual?

A

Requires two agonists in order for it to be activated

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7
Q

What are the co-agonists of the NMDA receptor?

A
  • glycine, D-serine
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8
Q

What is the role of the Mg2+ ion in the NMDA receptor?

A

drawn to neuronal intracellular environment, block NMDA receptor activation under regular circumstances

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9
Q

What do we known from NMDA receptor subunit diversity?

A

Determines the properties and function of the NMDA receptor e.g. ion conductance/sensitivity, agonist potency, deactivation rate

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10
Q

How does AMPA receptor subunit diversity affect function?

A

Affects the current/voltage relationship through the receptor - rectifiers= flow of ions is favoured in one direction - linear= similar current produced at different voltages

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11
Q

How does the AMPA receptor index change with age?

A

The permeability to ions e.g. Ca2+ decreases but the flow of other ions e.g. Na+= increased transmission

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12
Q

What are the roles of glutamate?

A
  • mediates majority of fast excitatory synaptic transmission in CNS - cognition, movement, central cardiovascular, thermoregulatory and respiratory control - learning and memory - neurodevelopmental, neurological and neurodegenerative conditions - target of drugs of abuse e.g. ketamine
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13
Q

What is the electrophysiological evidence for silent synapses?

A

Lack of a response to glutamate up until a positive charge has been reached

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14
Q

What are silent synapses?

A
  • lack AMPA receptors on the post-synaptic membrane - does not transmit info at hyperpolarised membrane potential due to Mg2+ block - AMPA receptors may be stored in vesicles or at extrasynaptic sites
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15
Q

How do silent synapses become unsilent?

A
  • membrane depolarisation triggers NMDA activation - NMDA activation= Ca2+ influx - Ca2+ influx results in the movement of AMPA receptors which become inserted into the membrane
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16
Q

How do we determine that the initial activation of silent synapses is due to NMDA and not AMPA activation?

A

Use of an NMDA antagonist e.g. D-APV inhibits activity

17
Q

What is the pairing procedure?

A

Induces long-term potentiation by simultaneously stimulating glutamate fibres and activating the NMDA receptor

18
Q

What is the antibody evidence of native AMPA receptors?

A
  • green antibodies reveal AMPA receptors present before depolarisation - after depolarisation, new AMPA receptors are stained red - use of an NMDA antagonist reveals fewer new AMPA receptors
19
Q

What is long-term potentiation?

A

A persistent increase in synaptic strength following high-frequency stimulation of a synapse.

20
Q

What is long-term depression?

A

A stable and enduring decrease in the effectiveness of synapses

21
Q

Where does long-term potentiation and depression occur?

A

Hippocampus

22
Q

What happens to LTP when an NMDA antagonist e.g. AP5 is used?

A

Inhibited

23
Q

How does an NMDA antagonist affect the Morris Water Maze test?

A
  • D, L-AP5= inhibits spatial learning so animal swims around aimlessly - L-AP5 (inactive isomer)= no effect on spatial learning
24
Q

How does trafficking of AMPA receptors regulate synaptic strength?

A

Exocytosis/endocytosis of AMPA receptor subunits to the postsynaptic membrane

25
Q

What are the implications of AMPA trafficking at synapses?

A
  • brain development - learning and memory - pain - cerebral ischemia (stroke) - Alzheimer’s disease (LTD may lead to synapse loss)
26
Q

Why would an NMDA antagonist be used to treat Alzheimer’s?

A
  • overexcited receptors= excess Ca2+ - excessive Ca2+ influx can damage neurones- inhibits NMDA receptors only when they are excessively active - regular functioning is preserved

Neuropharmacology (15 decks)

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