Abstract

Many studies have demonstrated that stressors can modify the physiological action of drugs, mainly morphine. The present study investigated the effects of a mild stressor on chloral hydrate (Chl)-induced sedation in mice. For 4 consecutive days, NaCl and Chl-treated mice (300 mg kg −1) were stressed (S) either by a 5 min exposure to a brightly lit inescapable open field, or i.p. injected with corticosterone (Cor) (15 mg kg −1). Then, their spontaneous motor activity was recorded on an actisystem during 20 min and compared with that of the unstressed (US) NaCl and Chl-treated mice. On day 1 and 4, neither stressor nor i.p. administered Cor had any influence on the spontaneous motor activity of NaCl-treated mice. In Chl-treated mice, the spontaneous motor activity was very low. On day 1, it was similar in S mice, Cor-injected mice, and US mice. On the contrary, on day 4, both stress and Cor enhanced the anesthetic-induced hypoactivity, showing that the magnitude of sedation increased. It can then be stated that stressor, provided it was repeatedly administered, potentiated the sedative action of chloral hydrate and that such a potentiation was probably, but not only, Cor-dependent. Given that stress and Chl both produce dopamine overflow, it can be hypothesized that S, potentiates the sedative action of Chl through a dopaminergic link.

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