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Basic Neuro Exam 2 > Biochem: GABA, glycine, glutamate > Flashcards

Biochem: GABA, glycine, glutamate Flashcards

1
Q

Name the most prevelant neurotransmitter in the brain.

A

Glutamate

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2
Q

How is glutamate recycled?

A

It is charged so it cannot cross the cell membrane and must be converted to glutamine before it can be sent back to the mitochondria for metabolism.

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3
Q

What is the main function of glutamate in the brain?

A

Excitatory NT

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4
Q

What is the main manifestation of lesions to the reticular formation?

A

Coma

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5
Q

What are the main projection sites for gluatamatergic neurons coming from the reticular formation?

A

Everywhere

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6
Q

What are the two major cortical functions does glutamate serve in the brain?

A

Memory (learning)

Alertness

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7
Q

Describe AMPA and Kainate receptors.

A

Excitatory ligand-gated sodium channel

-responds to glutamate

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8
Q

Describe the NMDA receptor.

A

Excitatory ligand-gated sodium and calcium channels

-respond to glutamate or aspartate BUT requires simultaneous glycine binding to be activated.

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9
Q

Describe the mGluR receptors.

A

Metabotropic glutamate receptors.
1&5 - excitatory IP3 DAG
the rest - inhibitory decrease cAMP

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10
Q

Describe the 3 GABA receptors.

A

All inhibitory
A and C: ligand-gated chloride channels
B: second messenger potassium channel

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11
Q

Describe the Glycine receptor

A

Mostly in spinal cord

Inhibitory: ligand gated chloride channel

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12
Q

The NMDA receptor is involved in cortex and hippocampus projections, especially involved in memory formation, name the drug that inhibits the NMDA receptor and can infleuce memory formation.

A

Phencyclidine (PCP)

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13
Q

Describe how the process of Long Term Potentiation and how it leads to memory formation.

A
  1. Stimulus that we want to convert to memory depolarizes the post-synaptic membrane and ONLY AMPA and Kainate receptors.
  2. Tetanic (or repeated) stimulation keep the post-synaptic membrane depolarized longer. (like studying the same slides over and over again)
  3. This tetanic stimulation keeps the post-synaptic cell depolarized longer so that the NMDA receptors can now open.
  4. NMDA receptors allow CALCIUM along with sodium into the cell.
  5. The calcium that enters activates proteases that break down AND remodel the post-synaptic cell mainly degrading spectrin proteins.
  6. The degrading of the spectrin proteins allows more glutamate receptors to form on the post-synaptic cell membrane.
  7. From this time on, a much smaller stimulus is required to generate the response and this is how a memory is formed.
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14
Q

What is the mechanism of short-term memory loss in Alzheimer Disease?

A

Amyloid beta plaques inhibit Long Term Potentiation (LTP).

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15
Q

Describe Excitotoxicity.

A

Occurs when tetanic stimulation occurs too long (like during seizures) and calcium channels allow too much calcium in. The calcium activated proteases start to over degrade the proteins in the cell and the cell dies.

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16
Q

Describe the induction phase of a stroke.

A

Ischemia triggers glutamate release from oxygen starved neurons. Glu binds NMDA receptors and allows sodium and calcium to enter cells.

17
Q

Describe the amplification phase of a stroke.

A

Increase of sodium in the cell activates sodium/calcium antiporters which allow more calcium into the cell.

Other calcium channels open further allowing more calcium into the cells (neurons)

The huge build up of calcium signals glutamate release which causes the same cascade to surrounding cells.

18
Q

Descrbe the expression phase of a stroke.

A

The increase in intracellular calcium activates the calcium-dependent proteases and they degrade the cellular proteins which eventually kills the cell.

19
Q

Main primary treatment of a stroke.

A

Clot busters

20
Q

Name the MOA of these drugs which inhibit the glutamate cascade.

  1. Methionine Sulphoximine
  2. Dextrophan
  3. Nimodipine
  4. Anti-oxidants
A
  1. Inhibit Glutamate Synthesis
  2. Inactivate NMDA receptors
  3. Block calcium entry
  4. Stop free radical damage
21
Q

Name two drugs that induce schizophrenia-like symptoms and how they induce these symptoms.

A

PCP and ketamine

block NMDA receptor activation

22
Q

What major anatomic structure degenerates in Huntington Chorea?

A

Striatum (mostly caudate nucleus)

23
Q

What is the most accepted mechanism for how neuronal death occurs in Huntington Chorea?

A

Altered form of huntingtin protein leads to blockage of GABA receptors and excess glutamate release which sends cells down the glutamate cascade.

24
Q

Condition associated with Fragile X syndrome.

A

Autism

25
Q

Protein that is silenced and not produced by the mutated gene in fragile X.

A

FMR-1 protein

26
Q

Malfunctioning glutamate receptor that may be a drug target in the future to combat Fragile X symptoms.

A

mGluR5

27
Q

Site where most GABA and glycine receptors are located and whether they are excitatory and inhibitory.

A

GABA - in the brain and always inhibitory
Gly - in spinal cord and always inhibitory

(glycine is excitatory in the brain but only when it binds simultaneously to the NMDA receptor with glutamate)

28
Q

What is the MOA of barbituates, benzodiazepines, picrotoxins and ethanol on the GABA receptor.

A

Binds to the GABA receptor and increases its sensitivity to binding GABA.

He made a point to state that these drugs DO NOT activate the receptor.

29
Q

How is GABA made?

A

Gamma-aminobutyric acid is made in one step from glutamate.

A decarboxylaion reaction

30
Q

How is glycine made?

A

Serine + folic acid

31
Q

Major antagonist for glycine receptors.

A

Strychnine

32
Q

What is the best accepted mechanism on how alcohol abuse causes neuron damage.

A
  1. Alcohol increases GABA receptor sensitivity to GABA.
  2. Over stimulation of the GABA receptors causes down regulation of these receptors.
  3. Once alcohol is withdrawn there is not enough GABA receptors to moderate the body’s motor functions and the patient starts to have seizures.
  4. The seizures lead to hypoxia (similar to a stroke) and neurons die.
33
Q

Describe the purigenic adenosine receptors (4).

A

A1 and A3
–>inhibitory: decrease cAMP
A2a and A2b
–>excitatory: increase cAMP, also IP3 DAG

34
Q

Describe the purigenic ATP receptor.

A

P2X (1-7)

–>excitatory: ligand-gated sodium and calcium channel

35
Q

Descrbe the general pattern of neuropeptide receptors.

A

Opiod receptors are inhibitory and the rest are excitatory.

36
Q

What type of vesicles contain peptide neurotransmitters?

A

Dense Core Vesicles.

Basic Neuro Exam 2 (6 decks)

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