Posted by JohnX2 on October 29, 2001, at 0:58:31
In reply to Re: Post Traumatic Stress Disorder and etc., posted by JGalt on October 28, 2001, at 15:01:23
I think I need to understand GHB's workings a bit
better to answer your questions.
From what little I remember about it is was easy to make using supplements
for weight lifting, and people starting taking it recreationally
and the government decided that people should have
this recreational fun, end of story....Usually mania is less thought to be related to dopamine
overproduction/overflow (which is more like a shizophrenic psychosis), and
more related to hyperactive electrical impulses.
Most of the anti-manic agents are indeed epilepsy
meds. They work by inhibiting Na+ and K+
and/or enhancing cl- release. The effect is
to impact the membrane voltage potential so that the
nerve cells fire in a more orderly fashion.
Some of the newer treatments for bipolar do
target dopamine postsynaptic receptors themselves
instead of the electrolytes, zyprexa being a good
example."I'll be back"
-John
> Interesting about the hypodopaminergic state also causing teeth grinding. Obviously while on GHB you go to a much lower than normal dopamine release rate, but I've never noticed the bruxism. Probably because at any dosage in which you feel the effects, the drug is also serving as a mild muscle relaxer, inhibits obsessive-compulsive behavior, and recurring thoughts/movements, all postulated to be through the GABA system. Thus it makes sense that teeth grinding would occur.
>
> Interesting on the 5ht-xx drugs. I've never read deeply on the specific receptors, but from your brief explanation, I agree that an experiment wtih memantidine seems in order. Oh, and I'll warn anyone I know going on Serzone to increase car insurance.
>
> By the way, what did you think about what I said with using GHB for mania? Obviously well under pass out doses, just enough to curtail dopamine release sufficiently for the patient to live normally. From what I understand, mania is almost completely dopamine driven, but I do not know for sure if the body is 1. also producing more dopamine or just releasing what it has and producing at a normal rate or 2. if the body has a definite reachable capacity for dopamine storage which isn't sky high beyond what a normal person is storing. If the body is producing and releasing an incredible amount more of dopamine during mania and if it has a very high amount of storage capacity, and the storage capacity does not greatly lower when they go back to normal or depressive, then my idea wouldn't work very well. Otherwise it would seem like it would, at worst the person might have to go through a simple dopamine reduction program, wherein they take an extra hour or two between doses of GHB, to let those high levels come back to normal, which shouldn't take too long. Of course, finding the right dosage here would be tricky, and the person would have to know how long their eposides generally last and/or allow themselves to come down competely once in a while, so that they aren't taking ghb during the depressive state, which might have the potential to produce another manic state (too much dopamine in storage, can that do it?). It'd just seem like it'd be nicer to the patient to exchange their wild euphoria for something better than having dead emotions as many of the antipsychotics seem to do, provided that not both of the aforementioned conditions were true.
>
> By the way, found this interesting, maybe you've already read it:
>
>
> Adaptation of N-methyl-D-aspartate (NMDA) receptors following antidepressant treatment: implications for the pharmacotherapy of depression
> by
> Skolnick P; Layer RT; Popik P; Nowak G; Paul IA; Trullas R
> Laboratory of Neuroscience, NIDDK,
> National Institutes of Health, Bethesda, USA.
> Pharmacopsychiatry, 1996 Jan, 29:1, 23-6
>
> ABSTRACT
>
> NMDA antagonists mimic the effects of clinically effective antidepressants in both preclinical tests predictive of antidepressant action and procedures designed to model aspects of depressive symptomatology. These findings led to experiments demonstrating that chronic administration of NMDA antagonists to rodents results in a downregulation of cortical beta-adrenoceptors, a phenomenon also observed following chronic treatment with many antidepressants. These neurochemical and behavioral similarities between antidepressants and NMDA antagonists prompted us to examine the impact of chronic antidepressant treatment on NMDA receptors. Chronic (14 days) but not acute (1 day) administration of seventeen different antidepressants to mice produced adaptive changes in radioligand binding to NMDA receptors. Detailed studies with three antidepressants (imipramine, citalopram, and electroconvulsive shock) show that these changes develop slowly, persist for some time after cessation of treatment, and (for imipramine and citalopram) are dose dependent. Moreover, following chronic treatment with imipramine, these changes in radioligand binding to NMDA receptors appear restricted to the cerebral cortex. Based on the consistency of these effects across antidepressant treatments, we propose that adaptive changes in NMDA receptors may be the final common pathway for antidepressant action. The recent demonstration (Nowak et al., 1995) that radioligand binding to NMDA receptors is altered in frontal cortex of suicide victims (compared to age and post-mortem interval matched controls) is consistent with the hypothesis (Trullas and Skolnick, 1990) that this family of ligand gated ion channels is involved in the pathophysiology of depression.
> ---------
>
> Of course, they find a lot of things low in suicide victims, but the interesting part is the other antidepressants role on NMDA receptor.
>
> Anyway, I found the cpc viewer page, I'll download it later. I'll make up an email later today so that you can send them over.
>
> Best Regards,
> JGalt
poster:JohnX2
thread:81980
URL: http://www.dr-bob.org/babble/20011025/msgs/82532.html