Sodium channel toxins veratrine and veratridine modify opioid and muscarinic but not beta-adrenergic binding sites in brain slices

Abstract

We have examined the influence of the sodium channel toxins veratrine and veratridine on mu-opioid ([3H]-DAGO), muscarinic ([3H] NMS) and beta-adrenergic ([3H] CGP) receptors in rat brain slices. These drugs reduce opioid and muscarinic binding while leaving beta-receptors unaffected. Veratrine is inhibitory at 0 degree or at 30 degrees C whereas veratridine is without effect at 0 degree C. These data suggest that some factor contained in the mixture of drugs (veratrine) can block opioid and muscarinic receptors independently of depolarization. Veratridine does not affect muscarinic receptors at ice temperature. Similar observations were made in thin sections of cat brain at 0 degree C. The concentrations of the toxins which cause 50% inhibition of binding are well within the range (5 x 10(-5) M-10(-4) M) routinely used for depolarization experiments. We suggest that caution be used in the interpretation of results obtained from veratrum alkaloid-induced depolarizations. It would not be surprising if the binding of other ligands to their receptors was also affected.