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Re: Low binding = increased serotonin activation

Posted by linkadge on February 24, 2007, at 13:41:26

In reply to Low binding = increased serotonin activation, posted by hgi698 on February 23, 2007, at 16:42:57

>I think what they said in the study is that >people who had the lowest binding of the 5-ht1a >receptor were the most religious.

Yes, I belive the same is true in temporal lobe epilepsy, ie there is a very low binding of 5-ht1a. There is a link between temporal lobe epilepsy and religiosity.

>I think from a neuroscience point of view, lower >binding means a lower receptor amount. Usually a >lower serotonin receptor amount is due to >increased activation of that receptor so it is >downregulated in response.

Not necessarily. Stress for instance, decreases the activity of the gene that codes for 5-ht1a, hence decreasing the population of 5-ht1a, but I do not think that this is due to an increase of serotonin.

It is true that 5-ht receptors downregulate in response to 5-ht, but I don't think the converse is true, ie low 5-ht expression is necessarily indicative of high serotonin.

Another example would be panic disorder, which is associated with low 5-ht1a binding. SSRI's work in part by stimulating the existing 5-ht1a receptors.

>This would indicate that increased activity at >the 5-ht1a (i.e. an agonist) is associated with >increased religiosity.

Not so sure one can make that conclusion. I think that one might be able to conclude that low functional activation of 5-ht1a results in increased limbic kindling and hence increased religious awareness.

Buspar is a more potent 5-ht1a autoreceptor agonist, than it is a post-synaptic agonist. This will result in an overal decrease in hippocampal serotonin which may result in less overal post-synaptic 5-ht1a agonism.

It is the decrease in functional post-synaptic 5-ht1a agonism that I think is causing the religiosity.

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According to:

http://iangoddard.net/AD_01.htm)

buspirone reduces serotonin in the hippocampus (Sharp, McQuade, Bramwell, & Hjorth, 1993

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Post synaptic 5-ht1a agonism in limbic regions exerts anticonvusant effects which would likely quell hyper-religious feelings. Low binding of 5-ht1a in hyper religous people probably reflects an inability of 5-ht to exert its anticonvuslant effects in limbic regions. So, it is my understanding that decreasing post synaptic limbic 5-ht1a agonism would result in religiosity.

If buspar was causing religiosity through post synaptic 5-ht1a agonism, then one would expect the same thing from SSRI's which are potent functional 5-ht1a agonists. But, for many people SSRI's totally kill

Thats the way I see it at least.

Linkadge


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