Posted by Cam W. on December 14, 2001, at 16:00:21
In reply to Re: Journal of Clinical Psychiatry » Cam W., posted by jazzdog on December 13, 2001, at 17:54:27
Jane - Sorry, I forget people don't always follow this stuff. Hell, the EAA stuff is my type of bathroom reading material (god!...I am a geek!).
Essentially, what the articles says is that, because of their relative toxicity (ie narrow therapeutic window), and their involvement in many, many bodily processes (intracellular energy regulation, calcium homeostasis, cognitive functioning, etc.), it is difficult to use EAAs directly, to treat specific disorders (they use glutamate as the example, but others excitatory amino acids can also stimulate the myriad of excitatory receptors. Some of these other EAAs are: S-sulfo-L-cysteine, L-homocysteate, L-aspartate,
homoquinolinate, L-homo-cysteinesulfinate, L-cysteinesulfinate, L-serine-O-sulfate,
L-cysteate, and quinolinate. This is in order - greatest to least - of their potencies, with glutamate being the most potent.Therefore, to treat disorders caused by a malfuncrion of EAAs, researchers have been forced to look at other steps in the specific pathways where the breaks have occurred. Some of these therapeutic targets could be EAA-related G-proteins, the phosphoinositol (PI) pathway (where lithium may act), or at one of the various sub-receptors of EAAs. The do stress that the several receptor subtypes that of EAAs have very diverse actions and are controlled in a myriad of ways.
Before any medication can be made to work on defiencies or breakdowns of these excitatory systems, most selective agonists and antagonists are needed to tease out the subtle, but complex functioning, and neural correlates of excitatory neuronal functioning.
The article then goes on to show what is being tried by researchers, to modify single connections, in this highly interconnected system. The medications are still a few years away. - Cam
poster:Cam W.
thread:86151
URL: http://www.dr-bob.org/babble/20011213/msgs/86920.html