Posted by tessellated on November 11, 2006, at 16:49:38
In reply to well, there are a few other studies:, posted by halcyondaze on November 8, 2006, at 19:12:49
> [Many researchers are also naming glutamate as the true culprit for both amphetamine psychosis and schizophrenia - I work in psych. research and the dopamine theory is scoffed by anyone who involved in psych. research.]
uhmmm, so help me out. i know in the UK, there's been a call to replace schizophrenia with the term dopamine dysregulation syndrome.
my BA/research pointed to the altered dopamine receptor sensitivity in the mesocortical DA system via chronic administration of DA agonist like amph. which makes sense in regard to that area's routing of internal and externally generated output to other parts of the brain i.e. metacortical processing.
IMHO, i can see how an enhanced receptor sensitivity in/around the hypothalamus could trigger various sorts of hallucinations etc, by creating false positive nueral activation/input that is misrecognized as coming from the occipital or temporal lobes.parkinsons occurs due to a deficit of DA receptor activity in the basal ganglia, a seperate structure that creates output to the medulla, less so (as far as i understand) to the cerebral cortex in general. so the DA antagonist would inhibit DA receptor sensitivity therefore potentially causing parkinson like symptoms. as well the SSRI's seem to create parkinson like symptoms due to their indirect affect on DA. parkinsonism can be alleviated via the implantation of stem cells around the basal ganglia, pointing to some form of nueral degeneration aside from mere DA receptor down regulation. If you don't use it you loose it-dendritically.
simply put, the particular structures that are involved with dopamine activity are critically important, as dopamine and the catecholamines are used throughout the body. so i would imagine that dopamine does have a role in psychosis, but only in relation to specific neural curcuitry.
however, i wonder with the MAIO's since they can increase catecholaminergic activity throughout the body, wouldn't they increase dopamine activity accross all neural structures? whereas things like buproprion might be more selective?
or am i just treading on older studies?
l8
poster:tessellated
thread:701609
URL: http://www.dr-bob.org/babble/20061110/msgs/702644.html