5.4 Flashcards

(37 cards)

1
Q

What is the major excitatory neurotransmitter in the nervous system?

A

Glutamate.

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2
Q

What does glutamate receptor activation cause?

A

Neuronal excitation and membrane depolarisation.

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3
Q

How is glutamate synthesised?

A

From glucose (via the Krebs cycle) or from glutamine (from glial cells).

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4
Q

How is glutamate recycled?

A

Astrocytes convert it to glutamine, which is resupplied to neurons.

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5
Q

What are the two major classes of glutamate receptors?

A

Ionotropic (iGluRs) and metabotropic (mGluRs).

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6
Q

What type of receptor is NMDA?

A

Ionotropic.

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7
Q

What type of receptor is AMPA?

A

Ionotropic.

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8
Q

What type of receptor is Kainate?

A

Ionotropic.

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9
Q

What type of receptor is mGluR?

A

Metabotropic (GPCR).

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10
Q

What happens when glutamate binds to iGluRs?

A

Pore opens and cations (Na⁺, K⁺, Ca²⁺) flow into the neuron.

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11
Q

How are iGluRs structured?

A

Composed of 4 subunits with ligand-binding domains and transmembrane domains.

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12
Q

What subunits form AMPA receptors?

A

GluA1–GluA4 (or GluR1–GluR4).

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13
Q

What determines AMPA Ca²⁺ permeability?

A

Lack of GluA2 subunit → high Ca²⁺ permeability.

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14
Q

What is the function of AMPA receptors?

A

Mediate fast excitatory synaptic transmission.

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15
Q

Where are AMPA receptors located?

A

Throughout dendrites during development; concentrated at post-synaptic sites.

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16
Q

What subunits make up NMDA receptors?

A

GluN subunits.

17
Q

What ions are NMDA receptors permeable to?

A

Ca²⁺ and other cations.

18
Q

What is the magnesium block?

A

A voltage-dependent Mg²⁺ ion that blocks the channel until depolarisation removes it.

19
Q

What removes the magnesium block?

A

Depolarisation from AMPA receptor activation.

20
Q

What is required for NMDA receptor activation?

A

Binding of both glutamate and glycine.

21
Q

What are silent synapses?

A

Synapses with NMDA receptors but no AMPA receptors.

22
Q

When do NMDA receptors open in relation to AMPA?

A

After AMPA receptors depolarise the membrane enough to remove Mg²⁺.

23
Q

How many mGluRs exist?

A

8 (mGluR1–mGluR8), divided into 3 groups.

24
Q

How do mGluRs work?

A

Activate G-protein pathways → second messenger signalling and/or indirect ion channel opening.

25
Do mGluRs directly open ion channels?
No, they influence them indirectly through signalling cascades.
26
What role do GluRs play in synaptic plasticity?
Mediate long-term changes in synaptic strength.
27
How is a synapse strengthened?
By adding or increasing AMPA receptor density.
28
How is a synapse weakened?
By removing or decreasing AMPA receptor density.
29
What happens when GluRs are blocked?
Synaptic plasticity is disrupted.
30
What recruits AMPA receptors to the synapse?
Activation of mGluRs and NMDA receptors.
31
What does ketamine do?
Blocks NMDA receptors.
32
What are the effects of ketamine?
* Blocks NMDA receptors * Wide effects ○ Hypnotic/psychomimetic ○ Analgesia ○ Increase sympathetic activity ○ Maintain airway tone and respiration * Slow off rate: when glutamate dissociates from NMDA receptor, ketamine is trapped inside receptor and blocks it (increase off rate)
33
Why is ketamine's effect prolonged?
It has a slow off-rate and remains trapped inside the receptor after glutamate dissociates.
34
What is perampanel?
A negative allosteric modulator (antagonist) of AMPA receptors.
35
What is perampanel used to treat?
Epilepsy.
36
Does perampanel affect NMDA or kainate receptors?
No, it is selective for AMPA receptors.
37
What are some side effects of perampanel?
Dose-dependent dizziness and other CNS effects.