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Research ArticleArticle

Potentiation of Ethanol Effects in Cerebellum by Activation of Endogenous Noradrenergic Inputs

Yun Wang, Ronald K. Freund and Michael R. Palmer
Journal of Pharmacology and Experimental Therapeutics January 1999, 288 (1) 211-220;
Yun Wang
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Ronald K. Freund
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Michael R. Palmer
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Abstract

We previously found that beta adrenergic agonists such as norepinephrine and isoproterenol potentiate the depressant actions of ethanol (EtOH) on cerebellar Purkinje neurons. Furthermore, antagonism of the beta adrenergic effects of endogenously released catecholamines with timolol reduced EtOH-induced depressions of neuronal activity in that brain area. In the present study, we further investigated the hypothesis that activity of the endogenous noradrenergic innervation to the cerebellar cortex can potentiate this EtOH action. We investigated the interaction of synaptically released catecholamines on EtOH-induced depressions of cerebellar Purkinje neurons in three different experiments: (1) endogenous catecholamine release was facilitated by applying the catecholamine uptake inhibitor desmethylimipramine, (2) activity of the noradrenergic innervation of the cerebellar cortex from locus ceruleus was increased by causing acute withdrawal from 7 days of chronic morphine treatment with the opiate antagonist naloxone, and (3) the noradrenergic innervation of the cerebellum was activated directly by electrical stimulation of the locus ceruleus. We found that all three conditions potentiated EtOH-induced depressions in the cerebellum and that this potentiation of ethanol effects could be antagonized by the systemic administration of the beta adrenergic antagonist propranolol. Furthermore, morphine withdrawal also caused potentiation of the depressant effects of phencyclidine, which are known to be regulated by the endogenous catecholamine innervation in this brain area. Taken together with our previous data demonstrating abeta adrenergic facilitation of EtOH actions in this brain area, the present results suggest that the activity of endogenous noradrenergic synapses can regulate the depressant effects of EtOH on cerebellar Purkinje neurons.

Footnotes

  • Send reprint requests to: Dr. Ronald K. Freund, Department of Pharmacology, Box C-236, University of Colorado Health Sciences Center, Denver, CO 80262. E-mail:Ron.Freund{at}UCHSC.edu.

  • ↵1 This work was supported by U.S. Public Health Service Grants AA11465 and AA03527 and by Republic of China, Department of Health Grant DOH87-HR-612. M.R.P. was supported by ADAMHA Research Scientist Development Award AA00102.

  • Abbreviations:
    DMI
    desmethylimipramine
    LC
    locus ceruleus
    EtOH
    ethanol
    GABA
    γ-aminobutyric acid
    ANOVA
    analysis of variance
    NE
    norepinephrine
    i.p.
    intraperitoneally
    PCP
    phencyclidine
    s.c.
    subcutaneously
    • Received February 23, 1998.
    • Accepted July 31, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 1
1 Jan 1999
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Research ArticleArticle

Potentiation of Ethanol Effects in Cerebellum by Activation of Endogenous Noradrenergic Inputs

Yun Wang, Ronald K. Freund and Michael R. Palmer
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 211-220;

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Research ArticleArticle

Potentiation of Ethanol Effects in Cerebellum by Activation of Endogenous Noradrenergic Inputs

Yun Wang, Ronald K. Freund and Michael R. Palmer
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 211-220;
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