Ethanol and opiate decrease the axonal transport of substance-P like immunoreactive material in rat vagus-nerves.

Abstract

Since an enhanced retrograde axonal transport of receptor-bound opiate was observed in the ligated vagus nerves of rats treated chronically with alcohol, we decided to look at the anterograde axonal transport of substance P in the same experimental conditions and, after opiate administration. From 1 day up to 24 days' treatment with alcohol, we observed a decrease in the accumulation of substance P like immunoreactive material (SPLM) in rat ligated vagus nerves. Acute administration of lofentanil, an mu opiate agonist, caused the same reduction of anterograde axonal transport of SPLM and this effect could be prevented by naloxone. When naloxone or bezitramide, an opiate agonist, was given during the alcoholization period, the preference for alcohol in a choice test was reduced or prevented suggesting that opioid peptides are probably involved in chronic alcoholism. The present results support the idea that a common denominator could exist in drug addition and in chronic alcoholism and that substance P may be directly or indirectly involved.