The potentiation of the non-behavioural effects of amphetamine by carbon disulphide.
In agreement with the inhibition of dopamine-beta-hydroxylase by exposure to CS2, the extension of exposure time from 4 to 16 h increased dopamine concentrations in the hypothalmus and adrenals, and decreased noradrenaline concentration in the hypothalmus. The extension of exposure time also increased the toxicity of amphetamine. In conscious animals the stereotypic activity produced by 6.0 mg/kg and even that of 3.0 mg/kg amphetamine sulphate was suppressed by severe hyperthermia resulting in exhaustion, prostration and eventually death. A 16 h exposure to CS2 did not increase the lethal or hyperthermic effects of amphetamine in rats anaesthetized with 60 mg/kg sodium pentobarbitone. In fact the CS2 exposed rats became more hypothermic than non-exposed rats.
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism; D000661:Amphetamine / Q000633:toxicity*; D000818:Animals; D001831:Body Temperature / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002246:Carbon Disulfide / Q000633:toxicity*; D002395:Catecholamines / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism; D004357:Drug Synergism; D007031:Hypothalamus / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013239:Stereotyped Behavior / Q000187:drug effects*
D002395:Catecholamines; D000661:Amphetamine; D002246:Carbon Disulfide