Overview
- Higgins, G.M. and Gardier, R.W. (1990) Toxicol. Appl. Pharmacol. 105, 103.
- Rossi, J. et al. (2001) Prog. Neuropsychopharmacol. Biol. Psychiatry 25, 1323.
Alomone Labs Etbicyphat inhibits GABA(A) receptors expressed in Xenopus oocytes.Representative time course of GABA(A) α1/β2 current, activated by a continuous application (top dotted line) of 0.1 µM γ-aminobutyric acid (#G-110), and inhibited by 2 µM and 10 µM Etbicyphat (#E-175), as indicated (bar), at a holding potential of -60 mV.
- Rijal, S.O. and Gross, G.W. (2008) J. Neurosci. Methods 173, 183.
- Rossi, J. et al. (2001) Prog. Neuropsychopharmacol. Biol. Psychiatry 25, 1323.
- Rossi, J. et al. (1998) Drug Metab Dispos. 26,1058.
- Lindsey, J.W. et al. (1998) Neurotoxicology 19, 215.
- Pomara, N. et al. (2015) Prog. Neuropsychopharmacol Biol. Psychiatry 56, 35.
Etbicyphat, also called trimethylopropane phosphate, is a synthetic convulsing compound that acts as a potent antagonist of GABA(A) receptors. TMPP acts through binding to the picrotoxinin and benzodiazepine receptor sites of the GABA(A) ionophore complex. TMPP is eliminated through the urine with no evidence of phase I or phase II metabolism and shows rapid clearance from the blood system1,2.
Several studies showed that infusion of TMPP into the nucleus accumbens of adult rats induces subclinical seizures and hyperlocomotor activity3.
GABA(A) receptors are members of the Cys-loop superfamily of ligand-gated ion channels. They mediate GABA action, a major inhibitory neurotransmitter, through the central nervous system and play an important role in inhibiting cell excitation in the central nervous system. The GABA(A) receptor is a major target of antiseizure drugs4.
Etbicyphat (#E-175) is a highly pure, synthetic, and biologically active compound.
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