Alcohol modulation of single GABAA receptor-channel kinetics

Abstract

Alcohol modulation of single-channel kinetics of GABA(A) receptor currents was studied with rat dorsal root ganglion neurons using the excised outside-out patch clamp technique. GABA (1 microM) alone or GABA (1 microM) plus ethanol (30-300 mM) or n-Octanol (30-300 microM) were applied by pressure ejection to evoke single-channel currents. The main single-channel conductance was not changed by either ethanol or n-Octanol at 25 pS. Both alcohols exerted the same effects on the single-channel kinetics, although n-Octanol was more potent than ethanol. The frequency of openings, the mean open time, the percentage of open time, the frequency of bursts, and the mean burst duration were all increased, but the mean closed time was decreased. These changes in channel kinetics account for the increase in whole-cell current amplitude caused by ethanol and n-Octanol.

Clinical signs and organ pathology in rats exposed to graded doses of pyrethroids- containing mosquito coil smoke and aerosolized insecticidal sprays

“…They are also potent inhibitors of the mitochondria complex I (Gassner et al, 1997), oxygen consumption (Gosh 1989, Reddy andPhilip, 1992), hence they inhibit the production of adenine triphosphate (ATP) in the mitochondria of cells. This leads to the alteration of the Na + /K + pump kinetics, a principal molecular mode of action of synthetic pyrethroids (Vijverberg et al, 1982;Vijverberg and van den Bercken, 1990;Tatebayashi and Narahashi, 1994). There is sodium and water transport into the cell cytosol, cellular water overload, deranged protein synthesis and mechanical function (Guyton and Hall, 2000).…”

Suppression of Voltage-Gated Sodium Currents by the Dihydropyrazole Insecticide, DPX-JW062 in Rat Dorsal Root Ganglion Neurons

“…Such responses lie within the linear portion of the DRG sodium channel currentvoltage curve. 9) This study was supported in part by a Grant-in-Aid for Developmental Scientific Research (No. 07406003 and 07556014) from the Ministry of Education, Science, Sports and Culture of Japan, and by the University of Tsukuba Research Projects.…”

Effects of Ethanol on GABAA Receptors in GABAergic and Glutamatergic Presynaptic Nerve Terminals

“…In cultured cell or isolated nerve cells, EtOH acts on extrasynaptic GABA A receptors to potentiate GABA-induced Cl Ϫ currents (Reynolds and Prasad, 1991;Weight et al, 1992;Aguayo et al, 1994), by increasing their open probability caused by an increase in the open time of single GABA A receptor channels (Tatebayashi et al, 1998). EtOH also acts on excitatory glutamate receptors where it has been shown to inhibit glutamate-induced currents in rat cultured hippocampal and cerebral cortex neurons (Lovinger et al, 1989;Weight at al., 1992;Fischer et al, 2003) and in rat ventral tegmental area neurons (Zhu et al, 2002).…”