Posted by desolationrower on March 9, 2009, at 4:51:07
the initial nardil extra-social period
increased alanine aminotransferase -> i think this woudl reduce synthesis of excitatory amino acids, alhtough i'm not sure yet. it depends on which way the equasion is running. one author also suggested lowered lactate formation is antipanic effect of PLZ. but one study found increased alanine, so that means less glutamate.
and look, i found this study then, which confirms
Effects of the MAO inhibitor phenelzine on glutamine and GABA concentrations in rat brain.
Paslawski TM, Sloley BD, Baker GB.Department of Psychiatry, University of Alberta, Edmonton, Canada.
Phenelzine (PLZ), a frequently prescribed monoamine oxidase (MAO) inhibitor, is used as an antidepressant/antipanic drug and has been shown to cause marked increases in rat brain levels of the amino acids gamma-aminobutyric acid (GABA) and alanine. In an extension of previous studies related to GABA metabolism, we investigated the effects of PLZ on rat brain levels of glutamine (GLN). At 1, 3 or 6 h after injection of PLZ (15 mg kg-1 i.p.), rats were killed and the brains removed. Analyses (using HPLC with fluorescence detection of OPT derivatives) of whole brain or hypothalamus revealed a decrease in brain levels of GLN and an increase in GABA levels at 3 and 6 h after PLZ injection. The effects of PLZ on GLN and GABA were blocked by prior treatment of the rats with tranylcypromine, a MAO inhibitor that had been shown previously to have no direct effect itself on GABA levels in rat brain. Since PLZ is known to be a substrate (as well as an inhibitor) of MAO, the studies with tranylcypromine pretreatment suggest that the effects on GLN and GABA are caused, at least in part, by a metabolite of PLZ.
most studies found higher glutamate in depressed. also alanine is a weak agonist at glycine-nmda site.
GABA-elevating effects of the antidepressant/antipanic drug phenelzine in brain: effects of pretreatment with tranylcypromine, (-)-deprenyl and clorgyline.
Todd KG, Baker GB.Department of Psychiatry, University of Alberta, Mackenzie Health Sciences Centre, Edmonton, Canada.
The antidepressant/antipanic drug phenelzine (PLZ) is both an inhibitor of, and a substrate for, monoamine oxidase (MAO). PLZ also causes an elevation of brain levels of the amino acid neurotransmitter gamma-aminobutyric acid (GABA); this action can be reversed by pretreatment with the MAO inhibitor tranylcypromine (TCP), suggesting that the GABA-elevating effect is largely the result of a metabolite of PLZ formed by MAO. In the present report, rats were pretreated with the nonselective MAO inhibitor TCP, the MAO-A inhibitor clorgyline and the MAO-B inhibitor (-)-deprenyl: at the doses used, clorgyline and (-)-deprenyl caused selective inhibition of MAO-A and MAO-B, respectively. Both TCP and (-)-deprenyl caused a greater reduction in the GABA-elevating action of PLZ than did clorgyline, suggesting that MAO-B is more important than MAO-A in the formation of the active metabolite of PLZ. The results also suggest that an effect other than, or in addition to, inhibition of GABA transaminase by the metabolite may be important in the GABA-elevating action.
given the slow recovery of MAOb, TCP->PLZ switch probably results in a slow effecttiveness for PLZ
poster:desolationrower
thread:884555
URL: http://www.dr-bob.org/babble/20090304/msgs/884555.html