Abstract
Effects of lead acetate exposure (0.05% and 0.1% in drinking water for 7, 14, 21, or 28 days) on m orphine withdrawal syndrome has been studied in m ice. Animals were rendered dependent on m orphine by subcutaneous injections of morphine sulfate, 3 times a day for 3 days. Jumping behavior was induced by intraperitoneal administration of naloxone (5 mg/kg) 2 hours after the tenth morphine injection on day 4. Jumping behavior was tested in two groups of dependent and nondependent animals that were exposed tolead for 7, 14, 21, and 28 days. Lead acetate but not sodium acetate tends to significantly decrease the jumping behavior in nondependent animals on days 7 (0.1%), 14, and 21 (0.05%). However, in dependent anim als, jumping behavior was decreased significantly by both lead acetate and sodium acetate exposure. These results demonstrate that lead acetate and sodium acetate suppress naloxone-induced jum ping in morphine-dependent mice and support earlier observations that implicate these cations, particularly lead, in pathophysiological opioid agonist and antagonist functions.