Basal forebrain lesions and memory: alterations in neurotensin, not acetylcholine, may cause amnesia.

Behavioral impairments produced by lesions of the nucleus basalis magnocellularis (NBM) are usually attributed to the loss of cholinergic cells. A comparison between the effects of 2 different neurotoxins, ibotenic (IBO) and quisqualic (QUIS) acid, reveals that this interpretation is inconsistent with the data. Rats were given injections of either IBO or QUIS into the NBM and tested on an alternation task in a T-maze. At the start of behavioral testing, both IBO and QUIS rats had impaired choice accuracy. At the end of behavioral testing, however, IBO rats, but not QUIS rats, were more impaired than controls, and IBO rats were more impaired than QUIS rats. IBO decreased choline acetyltransferase (ChAT) activity and [3H] neurotensin binding in the neocortex. QUIS decreased ChAT activity but did not change [3H] neurotensin binding. The cholinergic system may not be the critical component responsible for behavioral impairments following NBM lesions.