RESEARCH NOTE Lack of Recovery of Cortical Cholinergic Function following Quinolinic or lbotenic Acid Injections into the Nucleus Basalis Magnocellularis in Rats

The use of excitotoxins to produce animal models of human neurodegenerative disorders such as Huntington’s disease and temporal lobe epilepsy has been proposed (17). Neurotoxic (7, 9, 11) or electrothermic (15, 16) lesions of the nucleus basalis magnocellularis (nbM) produce marked reductions in all presynaptic cholinergic markers in the neocortex, indicating that a major component of the cholinergic innervation to the cortex originates from this site in the basal forebrain. Spontaneous recovery of two cholinergic markers (choline acetyltransferase and high-affinity choline uptake) in the neocortex following unilateral injection of the excitotoxin, ibotenic acid, into the nbM has recently been reported (20). Considerable evidence indicates that central cholinergic systems play an important role in learning and memory (12, 14). Thus, the implication of recovery of cortical cholinergic function after lesions