Effects of cations on binding, in membrane suspensions, of various opioids at μ‐sites of rabbit cerebellum and κ‐sites of guinea‐pig cerebellum

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Abstract
1 At the μ-sites of rabbit cerebellum, NaC1, LiC1, KCl, choline chloride and MnCl2 were tested for potentiation and inhibition of the binding of several opioids. Naloxone, (–)-bremazocine and diprenorphine are μ-antagonists in pharmacological assays and their binding is potentiated by the lower concentrations and inhibited by the higher concentrations of NaCl. The binding of the agonists [3H]-[d-Ala2, MePhe4, Gly-ol5]enkephalin and [3H]-dihydromorphine is inhibited. MnCl2/potentiates the binding of the agonist [3H]-[d-Ala2, MePhe4, Gly-ol5]enkephalin but not the binding of the antagonists. The thresholds of inhibition and slopes of the dose-response curves for inhibition by MnCl2 and LiCl vary. This finding may indicate that potentiating effects of MnCl2 and LiCl are masked by simultaneous inhibition. 2 At the κ-sites of guinea-pig cerebellum, NaCl, KCl and MnCl2 inhibit the binding of [3H]-dynorphin A (1–8), [3H]-dynorphin A (1–9), [3H]-(–)-bremazocine, [3H]-tifluadom, and [3H]-diprenorphine. NaCl also causes a small potentiation of the binding of [3H]-diprenorphine, which is a κ-agonist in the guinea-pig myenteric plexus but a κ-antagonist in the rabbit vas deferens. The slopes of the inhibitory dose-response curves and the thresholds of inhibition vary with the different ligands. Therefore some potentiating effects may have been masked. 3 The results support the view that NaCl, and perhaps LiCl, but not KCl and choline chloride, potentiate the binding of μ-antagonists but not the binding of μ-agonists. It is not yet possible to decide whether, at the κ-site, there is a similar differentiation of the binding of agonists and antagonists.