Opposing influences on behavior mediated by muscarinic and nicotinic receptors in the rat posterior hypothalamic nucleus.

Microinjection of carbachol into the posterior hypothalamic nucleus (PHN) of freely moving rats evoked marked behavioral changes characterized by an escape reaction. This response was quantitated by measuring locomotor activity. In contrast, cholinergic stimulation of the PHN with neostigmine produced sedation and inactivity. Local pretreatment with the nicotinic receptor blocking agent mecamylamine blocked the excitatory effects of carbachol while the muscarinic antagonist atropine abolished the inhibitory effect of neostigmine on motor activity. It is concluded that behavioral changes evoked through cholinergic stimulation of the PHN may be mediated by a muscarinic system which controls sedation and a nicotinic pathway which mediates arousal.