Trichloroethanol impairs NMDA receptor function in rat mesencephalic and cortical neurones
1999
Abstract The effects of 2,2,2-trichloroethanol, the active compound of the sedative–hypnotic chloral hydrate, were investigated on N -methyl- d -aspartate (NMDA)-induced increases in intracellular Ca 2+ concentration ([Ca 2+ ] i ) in cultured mesencephalic and cortical neurones by means of the fura-2 method. Trichloroethanol inhibited the NMDA response in a concentration-dependent manner in cortical (IC 50 =2.76 mM) and mesencephalic neurones (IC 50 =1.12 mM), with a maximum effect of approximately 85 and 94%, respectively. Ethanol was considerably less potent than trichloroethanol. In conclusion, the trichloroethanol-induced impairment of NMDA receptor function may contribute to the sedative–hypnotic properties of chloral hydrate.
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