Abstract
In the experiments reported here, we investigated chlorpromazine (CPZ)-induced enhancement of the cat cerebellar potentials evoked by peripheral nerve stimulation, with regard to the subtypes of adrenoceptor in the nucleus reticularis lateralis (LRN). Electrical stimulus of the locus coeruleus (LC) at high frequencies enhanced cerebellar potentials evoked by peripheral nerve stimulation. Although similar stimulus increased them after pretreatment with an α2-antagonist, yohimbine, these enhancements were not recognized by pretreatment with an α1-antagonist, prazosin. Microinjection of norepinephrine (NE: 10 μg) into LRN decreased cerebellar potentials, and conversely, 30 μg of NE significantly increased them. Although microinjection of an α2-adrenoceptor agonist, clonidine, into the LRN depressed cerebellar potentials, clonidine-induced decrease was obviously antagonized by pretreatment with CPZ. Furthermore, an α1-adrenoceptor agonist, phenylephrine, into the LRN increased cerebellar potentials. Pretreatment with CPZ hardly changed phenylephrine-induced enhancement. We thought that CPZ blocked α2-autoreceptors in adrenergic terminals from the LC rather than α1-adrenoceptors within the LRN. As a result, NE released from the LC terminals may act on α1-adrenoceptors in the LRN and may attenuate activities of the LRN. Therefore, it was clear that previous CPZ-induced enhancement may be due to depression of the descending inhibitory adrenergic system via CPZ-induced blockade of α2-autoreceptors.
