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Re: Glutamatergic neurotransmission and mood disor

Posted by SLS on September 13, 2006, at 23:35:30

In reply to Re: Glutamatergic neurotransmission and mood disor, posted by linkadge on September 13, 2006, at 19:00:31

> One aspect of the monoamine theory which I never understood was the following:
>
> Evidence for a serotonin deficiancy was based on the idea that serotonin metabolite levels 5-htaa were low in the brains of suicide victoms.

Review for the audience:

serotonin = 5-HT = neurotransmitter

MAO = monoamine oxidase = catabolic (breakdown) enzyme

5-HT <MAO> -> 5-HIAA

5-HT is broken down by MAO into 5-HIAA.

I know the amount of 5-HIAA found in urine and CSF is thought to reflect the rate of 5-HT turnover in the brain. I imagine the same is true of the amount that is found in the post-mortem brain. Turnover is usually interpreted as being indicative of neurotransmitter amounts or brain activity. The higher the level of 5-HIAA, the greater the activity of serotonergic neurons.

> Though, I was under the impression that reuptake inhibitors and MAOI's actually *decrease* the level of these metabolites?

When physiological conditions are changed by medication, the consequence is a reduced 5-HT catabolism as either the MAO enzyme is directly inhibited (MAOI) or 5-HT is prevented from reaching it due to its sequestration in the synaptic cleft (reuptake inhibitor). The result of reduced catabolism of 5-HT is reduced 5-HIAA.


- Scott

 

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