PMID: 7540273Mar 3, 1995Paper

Arachidonic acid may mediate the galanin-induced hyperpolarization in parasympathetic neurons from Necturus maculosus

Neuroscience Letters
J M Mulvaney, R L Parsons

Abstract

The effects of arachidonic acid (AA) and compounds that inhibit intracellular signalling pathways on membrane potential and galanin-induced hyperpolarizations were investigated in parasympathetic neurons from Necturus maculosus. Treatment for 10-90 min with 10-20 microM 4-bromophenacylbromide or 10 microM cyclosporin A caused a progressive decrease in the amplitude of galanin-induced hyperpolarizations without any change in resting membrane potential. The galanin-induced hyperpolarization was not altered following a 10-120 min treatment with the protein kinase inhibitor H-7. These results indicated that phospholipase A2 activation, but not protein kinase activation, may be required for the galanin-induced hyperpolarization. Arachidonic acid (20-100 microM) caused a concentration-dependent membrane hyperpolarization of the parasympathetic neurons and a decrease in the amplitude of the galanin-induced hyperpolarization. These data indicate that phospholipase A2-catalyzed liberation of AA may be involved in the galanin-induced membrane hyperpolarization observed in mudpuppy parasympathetic neurons.

References

Apr 1, 1993·Current Opinion in Cell Biology·D Piomelli
Jan 1, 1993·Prostaglandins, Leukotrienes, and Essential Fatty Acids·D L BooneP C Leung
Feb 1, 1993·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·R J Mayer, L A Marshall

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Citations

Dec 1, 1995·Cellular and Molecular Neurobiology·K KaskT Bartfai
Feb 26, 2000·Trends in Pharmacological Sciences·T A BranchekM W Walker
Feb 3, 1999·Annals of the New York Academy of Sciences·T BranchekM W Walker
Apr 28, 1997·The Journal of Comparative Neurology·Z ChengF J Doyle

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