Posted by linkadge on May 14, 2009, at 17:53:23
In reply to Re: Little more, posted by SLS on May 14, 2009, at 10:25:40
There are a lot of new studies which are challenging old theories.
Originally they though that 5-ht2a receptors were upregulated in depression. Some new research is suggesting that they are downregulated or at least less responsive in depression than normal controls.
There is some evidence of an insensitivity to serotonin in mood disorders, especially those with comorbid diabetes. Agents like chromimum actually increase insulin sensitivity as well as serotonin sensitivity.
There is a decrease in temporal lobe 5-ht1a binding in depression in temporal lobe epilepsy. This is interesting because post synaptic 5-ht1a receptors exert anticonvulsant effects in animal models of epilepsy. ECT apparently increases the sensitivty of limbic 5-ht1a receptors (which may play a role in its anticonvulsant effect).
The problem with SSRI's is that by agonizing all the serotionin receptors they don't really exert a single clean effect. I think some of the work with monoaminergic or neuropeptide agonists/antagonists is going to slowly give us a better pictue of what is relavent in mood disorders.
Theraputic serotonergic targets (that I know of) include 5-ht1a,b,d 5-ht2a,c 5-ht3 5-ht7.
I'd personally like to see some more work on the development of selective serotoniergic modulators without the dopamine effect. We need drugs like rianserin and gepirone.
Linkadge
poster:linkadge
thread:895287
URL: http://www.dr-bob.org/babble/20090505/msgs/895809.html