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Amobarbital (formerly known as amylobarbitone or sodium amytal) is a drug that is a barbiturate derivative. It has sedative-hypnotic properties. It is a white crystalline powder with no odor and a slightly bitter taste. It was first synthesized in Germany in 1923. If amobarbital is taken for extended periods of time, physical and psychological dependence can develop. Amobarbital withdrawal mimics delirium tremens and may be life-threatening. ==Pharmacology== In an ''in vitro'' study in rat thalamic slices amobarbital worked by activating GABAA receptors, which decreased input resistance, depressed burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increased both the amplitude and decay time of inhibitory postsynaptic currents. Amobarbital has been used in a study to inhibit mitochondrial electron transport in the rat heart. A 1988 study found that amobarbital increases benzodiazepine receptor binding ''in vivo'' with less potency than secobarbital and pentobarbital (in descending order), but greater than phenobarbital and barbital (in descending order). It has an in mice of 212mg/kg s.c. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Amobarbital」の詳細全文を読む スポンサード リンク
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