Central pharmacological control of corticosterone secretion in the intact rat. demonstration of cholinergic and serotoninergic facilitatory and ?-adrenergic inhibitory mechanisms

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Abstract
A method is described for demonstrating the hypothalamic control of corticosterone in the intact rat. Oxotremorine 0.01–0.05 mg/kg IP and 5-hydroxy-l-tryptophan 1–50 mg/kg IP raise plasma corticosterone levels in dose-related fashion. The oxotremorine response is blocked by atropine 1 mg/kg SC and the 5-hydroxy-l-tryptophan response by mianserin 10 mg/kg IP. α-Methylparatyrosine methyl ester 400 mg/kg IP raises plasma corticosterone levels 14–16 h later. This rise can be suppressed by clonidine 0.01–0.05 mg/kg IP and this suppression is antogonized by piperoxane 5–50 mg/kg IP. Apomorphine 5 mg/kg IP does not lower plasma corticosterone levels in rats pre-treated with α-methylparatyrosine. The response to oxotremorine cannot be blocked by atropine methylbromide or by mianserin. The response to 5-hydroxy-l-tryptophan is unaffected by benserazide or atropine sulphate. These data suggest separate cholinergic and serotoninergic facilitation of corticosterone release in the intact rat. The stimulating drugs used appear to be acting centrally. The data also support the presence of a noradrenergic inhibitory system mediated by α-adrenoceptors. Dopaminergic receptors appear to play no part in the central control of corticosterone secretion after pre-treatment with α-methylparatyrosine.

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