Abstract:
:In binding assays with homogenates of the myenteric plexus-longitudinal muscle of the guinea-pig, beta-funaltrexamine is more potent at displacing mu-binding than kappa-binding. Incubation of homogenates with beta-funaltrexamine (100 or 1000 nM) for 30 min at 37 degrees C followed by repeated washing with drug-free Tris buffer does not alter the binding of either the selective mu-ligand [3H]-[D-Ala2, MePhe4,Gly-ol5]enkephalin or of [3H]-(-)-bremazocine made selective for the kappa-binding site by the addition of unlabelled mu- and delta-ligands. This observation is surprising since, after treatment with beta-funaltrexamine (100 nM), the IC50 values for the inhibition of the contraction of the myenteric plexus-longitudinal muscle by the mu-ligand [D-Ala2,MePhe4, Gly-ol5]enkephalin are increased 12-fold whereas the IC50 values obtained with the selective kappa-ligand U-50, 488H remain unaltered. It is proposed that the irreversible blockade produced by beta-funaltrexamine is not due to inhibition at the mu-site per se but to an interference with the link between the binding and the effector response.
journal_name
Neuropeptidesjournal_title
Neuropeptidesauthors
McKnight AT,Paterson SJ,Corbett AD,Kosterlitz HWdoi
10.1016/0143-4179(84)90054-4subject
Has Abstractpub_date
1984-12-01 00:00:00pages
169-72issue
1-3eissn
0143-4179issn
1532-2785pii
0143-4179(84)90054-4journal_volume
5pub_type
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