Reversible colchicine-induced disruption of amygdaloid function in sodium appetite.

Bilateral injections of the antimitotic drug colchicine into the medial amygdaloid nuclei resulted in a dissociation of the normally concurrent sodium appetite and water thirst in rats following formalin-induced hypovolemia and hyponatremia. While control rats drank the normally aversive sodium solution as well as water after formalin injection, colchicine-treated animals failed to ingest the sodium solution but did consume the expected amount of water in order to compensate for hypovolemia. Sodium consumption, but not water consumption, remained significantly depressed in the colchicine-treated rats when they were challenged again with formalin 11 days but not 20 days after amygdaloid injections. The latter result suggested complete recovery from the colchicine-induced amygdaloid dysfunction. This study indicates that colchicine may serve as a potentially useful technique for producing reversible lesions of known duration for the assessment of brain-behavior relationships.