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Re: Nardil and GABA

Posted by JohnB on December 8, 1999, at 21:01:58

In reply to Nardil and GABA, posted by Elizabeth on December 8, 1999, at 19:19:28

Hi, Elizabeth. I've copied and pasted an article, below, regarding Phenelzine's GABA elevating effects. There are, of course, many additional articles on MedLine, available through a no-cost PubMed search. My take on this article is that PLZ exerts its GABA elevating effects through inhibition of the anabolic enzyme glutamic acid decarboxylase (GAD) and, to a greater extent, the catabolic enzyme GABA transaminase (GABA-T)." Unfortunately, I wasn't able to find anything regarding the GABA elevating properties of Marplan, except an article suggesting complete GABA receptor blockage when Marplan is used in conjunction with Clozapine (an anti-psychotic.)

Sorry,

JohnB


-----------------
Chronic administration of the antidepressant phenelzine and its N-acetyl analogue: effects on GABAergic function.

McKenna KF, McManus DJ, Baker GB, Coutts RT
Department of Psychiatry, University of Alberta, Edmonton, Canada.

The MAO inhibitor phenelzine (2-phenylethylhydrazine; PLZ) is used widely in psychiatry for the treatment of depression and panic disorder. Its N-acetyl metabolite, N2-acetylphenelzine (N2AcPLZ) is a reasonably potent nonselective inhibitor of monoamine oxidase (MAO) that causes elevation in brain levels of the biogenic amines. In the studies reported here, PLZ (0.05 mmol/kg/day), N2AcPLZ (0.10 mmol/kg/day) or vehicle were administered to male rats for 28 days s.c. with Alzet minipumps, and their effects on GABAergic function were examined. Whole brain concentrations of gamma-aminobutyric acid (GABA) were significantly elevated in the PLZ but not in the N2AcPLZ-treated group. PLZ was found to inhibit the anabolic enzyme glutamic acid decarboxylase (GAD) and, to a greater extent, the catabolic enzyme GABA transaminase (GABA-T). The results of these investigations suggest that the free hydrazine moiety in PLZ is crucial to producing the elevated levels of GABA, probably through inhibition of GABA-T. Despite the considerable increase in whole brain GABA levels in the PLZ-treated rats, there were no significant differences in GABAA or benzodiazepine receptor binding parameters (KD or Bmax) between the groups as measured using 3H-muscimol and 3H-flunitrazepam in radioligand binding assays.

PMID: 7931216, UI: 95016587


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poster:JohnB thread:16450
URL: http://www.dr-bob.org/babble/19991123/msgs/16458.html