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Evidence that Prostaglandin E 2 Can Block Calcium‐Activated 86 Rb Efflux from Rat Brain Synaptosomes via a Protein Kinase C‐Dependent Mechanism
Author(s) -
Ren Jun,
Benishin Christina G.
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62051840.x
Subject(s) - chemistry , mechanism (biology) , synaptosome , protein kinase a , calcium , efflux , microbiology and biotechnology , pharmacology , biophysics , biochemistry , neuroscience , kinase , biology , philosophy , organic chemistry , epistemology
Abstract: The effects of prostaglandin E 2 (PGE 2 ) on 86 Rb efflux from rat brain synaptosomes were studied to explore its role in nerve ending potassium (K + ) channel modulation. A selective dose‐dependent inhibition of the calcium‐activated charybdotoxin‐sensitive component of efflux was found upon application of PGE 2 . No significant effect was seen on basal and voltage‐dependent components over the concentration range of 10– 8 to 10– 5 M. The protein kinase C (PKC) inhibitors H‐7 (10 μ M ) and staurosporine (100 n M ), as well as prolonged preincubation (90 min) with 40‐phorbol 12, 13‐dibutyrate, which has been reported to down‐regulate PKC, abolished the PGE 2 ‐in‐ duced inhibition, whereas HA1004 (10 μ M ) and Rp ‐3′,5’cyclic phosphorothioate (100 n M ), which are relatively more selective for protein kinase A than PKC, did not. 4β‐Phorbol 12, 13‐dibutyrate (100 n M ), an activator of PKC, produced a similar inhibition of the Ca 2+ ‐dependent component of 86 Rb efflux but also had no effect on the basal and voltage‐dependent components. These data suggest that PGE 2 can inhibit rat brain nerve ending calcium‐activated 86 Rb efflux, and this inhibition may involve PKC activation.

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