Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Effects of chlorpromazine in the nucleus reticularis lateralis on the cat cerebellar potentials. 255 41

1) In the experiments reported here, we investigated effects of CPZ on the amplitude of cerebellar potentials using decerebrated or spinal cat; furthermore, we also examined the effects of microinjecting CPZ, DA or NE into the precerebellar nuclei on the amplitude of the cerebellar potentials. 2) Purkinje cell spontaneous discharge was either hardly changed or was depressed by CPZ. 3) CPZ did not change the potentials evoked by peripheral stimulation on the dorsal surface of the spinal cord. 4) CPZ depressed significantly the cerebellar potentials evoked by stimulation of the nucleus reticularis lateralis (LRN) or nucleus olivaris inferior (ION) in intact, decerebrated and spinal cats. 5) The cerebellar potentials evoked by the peripheral nerve stimulation were increased by microinjection of CPZ into the bilateral LRN but not into the bilateral ION. Microinjection of NE or CPZ into the contralateral LRN hardly influenced the cerebellar evoked potentials. 6) Although electrical stimulation at high frequencies of the ipsilateral LRN depressed significantly the cerebellar evoked potentials; similar stimulation after i.v. pretreatment of CPZ failed to affect them. Microinjection of CPZ into the ipsilateral LRN enhanced the cerebellar evoked potentials, and microinjection of NE or DA depressed them significantly. Furthermore, after pretreatment with CPZ, microinjection of DA failed to depress the potentials. 7) We suggest that intravenous CPZ-induced enhancement of the cerebellar potentials may be due to depression of the descending inhibitory mechanism, resulting from CPZ-induced blockage of the catecholamine receptors of the ipsilateral LRN and of the spinal level.
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PMID:Studies of chlorpromazine-induced enhancement of the potentials evoked by peripheral stimulation of the cat cerebellum. 365 85