Lecture 2 Glutamate & GABA Flashcards

(15 cards)

1
Q

What are the primary excitatory and inhibitory neurotransmitters in the brain?

A

Glutamate (primary excitatory)
GABA (primary inhibitory).

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2
Q

Why are glutamate and GABA considered “true” neurotransmitters?

A

“They directly affect the likelihood of the post-synaptic neuron firing (glutamate increases firing, GABA decreases it).”

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3
Q

How is glutamate synthesized in the brain?

A
  • Synthesized from glutamine (released by neighboring glial cells)
  • Cannot cross the blood-brain barrier (BBB), so must be produced locally
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4
Q

Name the 4 major types of glutamate receptors.

A

3 are Ionotropic: NMDA, AMPA, Kainate.
1 is G-protein-coupled / Metabotropic: mGluR

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5
Q

What makes the NMDA receptor unique?

A

particularly complex!
* It has at least 6 different binding sites
o For example, it only works if
o there is also a glycine (甘氨酸) molecule (another amino acid) attached
o if magnesium ion is NOT bound to inside

  • The other binding cites modulate receptor function.
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6
Q

How do alcohol, ketamine, and PCP affect NMDA receptors?

A

All are NMDA antagonists (reduce excitatory function).
Alcohol: Sedation & memory impairment
Ketamine/PCP: Dissociative hallucinations

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7
Q

Why is ketamine used to treat depression?

A
  • Effective for weeks, but relaps after
  • relatively Safe
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8
Q

How might glutamate dysfunction contribute to psychosis?

A
  • NMDA antagonists can cause positvie and negative synptoms of psychosis
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9
Q

What is GABA’s role in the brain?

A

Primary inhibitory neurotransmitter.
Decrease post-synaptic neuronal firing (e.g., seizures)

  • Most short local neurons are inhibitory, so they form a dense web around and between the excitatory neurons (~20% of cerebral cortex interneurons) –> Inhibitory networks reduce the likelihood neurons fire for their non-preferred stimulus
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10
Q

How is GABA synthesized?

A

“Produced from glutamate via enzymatic conversion (GAD enzyme).”

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11
Q

Name the two GABA receptor types and their mechanisms.

A
  1. GABA_A: Ion channel (target of alcohol, benzodiazepines).
  2. GABA_B: G-protein-coupled.
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12
Q

What happens when GABA function is impaired?

A

“Seizures (uncontrolled neuronal firing due to lack of inhibition).”

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13
Q

What are generalized vs. partial seizures?

A

Generalized: Whole brain (e.g., tonic-clonic)
Partial: small part of brain, often due to injury or abnomal development(simple = no consciousness loss; complex = loss of consciousness).”

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14
Q

Why are benzodiazepines (e.g., Valium) used in alcohol withdrawal?

A

They enhance GABA activity, counteracting excessive glutamate excitation that causes seizures.

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15
Q

Key clinical point about glutamate/GABA balance?

A

Disruption (e.g., excess glutamate or low GABA) leads to seizures, psychosis, or neurotoxicity.

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