Open AccessEffects of chlorpromazine in the nucleus reticularis lateralis on the cat cerebellar potentials.
Author(s) -
Yukihiko Hagiwara,
Yukiko Suzuki
Publication year - 1989
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.51.1
Subject(s) - phenylephrine , prazosin , yohimbine , agonist , chemistry , clonidine , locus coeruleus , cerebellum , stimulation , medicine , microinjection , endocrinology , autoreceptor , adrenergic receptor , antagonist , receptor , central nervous system , blood pressure
In the experiments reported here, we investigated chlorpromazine (CPZ)-induced (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 alpha 2-antagonist, yohimbine, these enhancements were not recognized by pretreatment with an alpha 1-antagonist, prazosin. Microinjection of norepinephrine (NE: 10 micrograms) into LRN decreased cerebellar potentials, and conversely, 30 micrograms of NE significantly increased them. Although microinjection of an alpha 2-adrenoceptor agonist, clonidine, into the LRN depressed cerebellar potentials, clonidine-induced decrease was obviously antagonized by pretreatment with CPZ. Furthermore, an alpha 1-adrenoceptor agonist, phenylephrine, into the LRN increased cerebellar potentials. Pretreatment with CPZ hardly changed phenylephrine-induced enhancement. We though that CPZ blocked alpha 2-autoreceptors in adrenergic terminals from the LC rather than alpha 1-adrenoceptors within the LRN. As a result, NE released from the LC terminals may act on alpha 1-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 alpha 2-autoreceptors.