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Intracellular recordings in vivo from noradrenergic neurons in the rat locus coeruleus showed that membrane potential was hyperpolarized by the administration of clonidine (an alpha 2-adrenoceptor agonist) or after a burst of spikes evoked by intracellular pulses; both types of hyperpolarization were associated with a decrease in membrane input resistance, and both could be blocked by the alpha 2-adrenoceptor antagonist piperoxane. These results suggest that a hyperpolarization of membrane potential mediated by an alpha 2-adrenoceptor underlies both clonidine- and activation-induced inhibition of locus coeruleus cell firing.
Aghajanian et al. (Fri,) studied this question.
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