Influence of a deletion of protein kinase C gamma isoform in the G-protein activation mediated through opioid receptor-like-1 and mu-opioid receptors in the mouse pons/medulla.

Abstract:

:The aim of the present study was to investigate whether mice with a deletion of the gene that encodes the protein kinase C gamma (PKC gamma) isoform could affect the G-protein activation mediated through the opioid receptor-like (ORL-1) receptor and mu-opioid receptor in the mouse pons/medulla and spinal cord, monitoring the guanosine-5'-o-(3-[(35)S]thio) triphosphate ([(35)S]GTP gamma S) binding assay. The increases in [(35)S]GTP gamma S bindings to pons/medulla membranes of the wild-type mice induced by either an endogenous ligand for the ORL-1 receptor, nociceptin or a selective mu-opioid receptor agonist [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin were significantly enhanced in PKC gamma knockout mice. In contrast, the levels of [(35)S]GTP gamma S binding stimulated by nociceptin in spinal cord membranes obtained from PKC gamma knockout mice were similar to those from wild-type mice. These findings suggest that the loss of the PKC gamma gene may protect the functional ORL-1 and mu-opioid receptors from degradation by phosphorylation in the mouse pons/medulla. Furthermore, the present data provide first evidence for the differential mechanism of the ORL-1 receptor-mediated signaling between the supraspinal and spinal sites.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Narita M,Mizoguchi H,Khotib J,Suzuki M,Ozaki S,Yajima Y,Narita M,Tseng LF,Suzuki T

doi

10.1016/s0304-3940(02)00753-x

keywords:

subject

Has Abstract

pub_date

2002-10-04 00:00:00

pages

5-8

issue

1

eissn

0304-3940

issn

1872-7972

pii

S030439400200753X

journal_volume

331

pub_type

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