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
poster:SLS
thread:685302
URL: http://www.dr-bob.org/babble/20060909/msgs/685762.html