Chronic ethanol exposure inhibits ATP-stimulated but not KCl-stimulated dopamine release in PC 12 cells

W. K. Kim, R. G. Johnson, Leighton T Izu, R. A. Rabin

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The functional significance of the ethanol-induced alterations in intracellular concentration of free calcium ([Ca++]i) was determined in PC 12 cells by measuring agonist-stimulated dopamine (DA) release after ethanol exposure. ATP and KCl produced a concentration-dependent release of DA, which was linearly related to the net increase in [Ca++]i, but different relationships were observed with ATP and KCl. Acute addition of 150 mM ethanol inhibited KCl-stimulated release of DA, but did not alter the response to ATP. In contrast, a 4-day exposure to 150 mM ethanol led to a reduction in ATP-evoked DA release without altering the response to KCl. Furthermore, a 7-day treatment with 25 mM ethanol also decreased the response to ATP. Acute and chronic ethanol exposures, however, did not alter the relationships between DA release and the increase in [Ca++]i observed with ATP and KCl. The data indicate that acute and chronic ethanol treatments have differential effects on the responses to extracellular ATP and KCl and alter DA release primarily by altering the calcium influx stimulated by agonists.

Original languageEnglish (US)
Pages (from-to)336-341
Number of pages6
JournalJournal of Pharmacology and Experimental Therapeutics
Volume270
Issue number1
StatePublished - 1994
Externally publishedYes

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Dopamine
Ethanol
Adenosine Triphosphate
Calcium
Dopamine Agonists

ASJC Scopus subject areas

  • Pharmacology

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Chronic ethanol exposure inhibits ATP-stimulated but not KCl-stimulated dopamine release in PC 12 cells. / Kim, W. K.; Johnson, R. G.; Izu, Leighton T; Rabin, R. A.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 270, No. 1, 1994, p. 336-341.

Research output: Contribution to journalArticle

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