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BioPsych PSYC20006 Theme 3 > Glutamate and GABA > Flashcards

Glutamate and GABA Flashcards

1
Q

List down some properties of Glutamate and Gaba: (1) Evolution (2) Commonality (3) “True”

A

Glutamate and GABA

  • Believed to be the first to evolve and are found in very simple organisms
  • Most common neurotransmitters in the CNS
  • “True” neurotransmitters – directly affecting the likelihood of the post-synaptic neuron firing
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2
Q

What is the main excitatory NT? What does the excitation NT do in terms of firing?

A

Glutamate

Increase likelihood of post-synaptic neuron firing

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3
Q

How many of the brain synapse release glutamate?

A

Estimated over half of all brain synapses.

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4
Q

What is the acid associated with glutamate?

A

Glutamic Acid

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5
Q

Must glutamate be synthesized? Why?

A
  • Glutamate = Glutamic Acid
  • Glutamate is an amino acid that acts as a neurotransmitter in its “original” form but this amino acid does not pass the blood brain barrier so it still needs to be synthesized in the brain
  • Glutamate is synthesized from glutamine which is released by cells neighbouring the neurons

Glutamate > Glutamine >(Synthesised by neighbouring cells) > Glutamate

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6
Q

Where is glutamate found?

A

In most long projection neurons throughout cortex

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7
Q

What are the connection points like for excitatory connections”? Do they have general functions?

A

“Point-to-Point”. Direct.

No, there are many region-specific functions (e.g. vision)

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8
Q

How many types of glutamate receptors are here?

A
  • 3 Ion channels
    • NMDA Receptor
    • AMPA Receptor
    • Kainate Receptor
  • 1 G-protein coupled receptors
    • Metabotropic Glutamate Receptor
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9
Q

NMDA Receptor: How many binding sites are there? What are some conditions for glutamate to be attached?

A

6 Different Binding Sites.

  • Glycine Molecule attached
  • Magnesium ion not bound
    • Or else it won’t open

Other binding cites modulate receptor function.

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10
Q

What are some drugs discussed in Week 8 Lecture 2 that affects NMDA? What do they have in common?

A

Alcohol, PCP, Ketamine

  • NMDA antagonists (inhibit)
  • But they all have different impacts on the mind
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11
Q

How is alcohol related to NMDA receptor? What does this explain?

A
  • NMDA antagonist (inhibit)
    • Reduce glutamate
  • GABA agnoist (excite)
    • Increase GABA
  • Explains general sedative effects and brain inhibition
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12
Q

What does PCP and Ketamine cause? Are they safe?

A

PCP = “Angel Dust”

Ketamine = “Special K”

  • PCP and Ketamine are NMDA antagonists (Reduce glutamate)
    • Dissociative hallucinations
      • Feel disconnected rather than perceiving visions
    • Risk of suicidal behaviour
    • Though Ketamine is very safe
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13
Q

What is the association between glutamate and psychosis?

What is psychosis?

What changes are there in individuals with psychosis?

A
  • Some have suggested a link between glutamate and psychosis but it is controversial and likely to involve others NTs like DA.
  • Psychosis
    • Symptom cluster, not diagnosis
      • SZ = 1% (Diagnosis)
      • Psychosis = 3% (Symptom Cluster)
    • Widespread disruption & lack of coherent integration of sensory information
    • No major structural impairment in psychosis
      • Likely reflect chemical inbalances
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14
Q

Genetic studies and psychosis: What is the role of NMDA? Conclusion?

A

Genetic studies on Psychosis

  • NMDA receptor activity
    • Critical for learning, memory, perception and synaptic plasticity in general.
  • Genetic studies identify NMDA receptor genes as likely being relevant in schizophrenia, but also relevant to general function and IQ
  • Large number of genes that all may each contribute to a small amount of risk for psychosis.
  • Picture remains unclear and may simply reflect altered synaptic activity in psychosis
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15
Q

What is GABA and what does it do in to the post-synaptic neuron?

A

Main inhibitory NT - Decreasing likelihood of the post-synaptic neuron firing

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16
Q

Where is GABA found?

A

In short local neurons, forming a dense web around and between excitatory neurons

17
Q

How does GABA help in neural tuning? Are they perfect?

A
  • Delicate coordination of neurons to signal very specific information
    • “Keeping signal sharp”
  • Selective, not perfect
    • Reduce likelihood of neurons firing for non-preferred stimulus (Dosen’t stop firing for non-preferred stimulus)
    • Explains tuning curve
18
Q

What is GABA produced from? Can it convert to Glutamate?

A

Glutamic Acid (Same as glutamate)

Glutamate is converted into GABA & GABA can be converted back to Glutamate

19
Q

Are Glutamate and GABA released from the same neurons?

A

Made from same amino acid, but not released from same neurons

20
Q

How many types of GABA receptors are there?

A
  • 1 Ion
    • GABAa
  • 1 G-Protein
    • GABAb
21
Q

What is the prevalance of seizures? What are seizures? How does GABA explain epilepsy or seizures?

A
  • Relatively common (400,000) in Australia
  • Seizures
    • Sudden excessive activity of neurons
    • (Can cause muscle convulsion but not always)
  • Epilepsy (Neurological disorder characterised by seizures) are caused by abnormalities of GABA neurons and/or in GABA receptors
22
Q

What are generalized seizures?

A

Involving whole brain

23
Q

What are partial seizures? And what are simple and partial seizures?

A

Restricted to small area of brain

  • Simple
    • Can cause changes in consciousness (altered sensory, autonomic responses etc)
    • Not loss of consciousness
  • Complex
    • Loss of consciousness
24
Q

Explain the study on high fever and vaccinations?

A

High fever and Vaccinations.

  • Vaccinations cause high fevers in some children and the fevers can trigger the first epileptic event
  • Some children with epilepsy genes without vaccinations still ended up getting epilepsy
  • Some children with epilepsy gene had seizures before vaccinations
25
Q

In genetic studies, in seizures, which kind of receptors have GABA been most identified with? What is the problem?

A
  • Majority of genes so far control ion channels, BUT
  • Most seizures are not genetic and instead are due to abnormal brain tissue, requiring surgery
26
Q

Are Ion Channels more selective than G-Protein Coupled? What are some similarities and differences in relation to (1) Length and action; (2) Systems?

A

No. G Protein-coupled receptors and ion chanels are equally selective (activated by more neurotransmitters)

Length and Action

  • Both ion channels and G Protein-coupled receptors span the cell membrane
  • G Protein-coupled receptors have a relatively long action compared to ion channels

Influence

  • Only G-Protein coupled receptors can influence metabolic processes within a cell via second messenger systems

BioPsych PSYC20006 Theme 3 (6 decks)

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