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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Trichloroethanol impairs NMDA receptor function in rat mesencephalic and cortical neurones.

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 Ca2+ concentration ([Ca2+]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 (IC50 = 2.76 mM) and mesencephalic neurones (IC50 = 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.[1]

References

  1. Trichloroethanol impairs NMDA receptor function in rat mesencephalic and cortical neurones. Scheibler, P., Kronfeld, A., Illes, P., Allgaier, C. Eur. J. Pharmacol. (1999) [Pubmed]
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