Abstract

The intrahypothalamic injection of 0·003 and 0·006 μmol of carbamylcholine chloride (CCh) was found to elicit a dose-dependent increase in rectal temperature in unanaesthetized, normothermic golden hamsters. In agreement with a proposed depolarization block in heat gain pathways, the similar administration of 0·01 μmol of this cholinergic agonist produced a significant hypothermic response. In the case of hyperthermia, thermogenesis appeared to be initiated mainly by shivering with a possible lesser contribution from an increase in cardiac rate. Heat conservation in this instance was indicated by the occurrence of peripheral vasoconstriction. Heat loss and the resultant hypothermia elicited by the highest CCh dose was primarily achieved by peripheral vasodilation. In addition, a possible decrease in thermogenesis was indicated by a reduction in cardiac rate. However, this dose of agonist also produced marked behavioural agitation and struggling which led to a substantial increase in electromyographic activity. The effects of both 0·006 and 0·01 μmol of CCh were abolished by the prior central administration of atropine, whereas similar pretreatment with phentolamine and methysergide failed to alter either CCh response.

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