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 Lettjournal_title
Neuroscience lettersauthors
Narita M,Mizoguchi H,Khotib J,Suzuki M,Ozaki S,Yajima Y,Narita M,Tseng LF,Suzuki Tdoi
10.1016/s0304-3940(02)00753-xkeywords:
subject
Has Abstractpub_date
2002-10-04 00:00:00pages
5-8issue
1eissn
0304-3940issn
1872-7972pii
S030439400200753Xjournal_volume
331pub_type
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