Butt AE, Bowman TD, Novotnev JS, Rogers JL, Tanabi A (1999) Selective lesions of the nucleus basalis magnocellularis in rats do not affect simple association learning. Neuroscience 1999 Abstracts 559.4. Society for Neuroscience, Miami, FL.
Summary: We have previously argued that damage to the cholinergic nucleus basalis magnocellularis (NBM) selectively impairs complex or configural association learning while sparing simple association learning (Butt & Hodge, 1997; Butt et al., 1998, Soc. Neurosci. Abst.). However, contrary to our hypothesis, in an earlier study using the less selective neurotoxin quisqualic acid, we found that simple association learning was moderately impaired in NBM-lesioned rats (see Butt & Hodge, 1997). It remained unclear whether the observed behavioral impairment in that study was due to loss of cholinergic input to neocortex or was instead due to non-specific damage to other brain structures. In the current study, therefore, we used the highly selective immunotoxin Ig-G saporin to create bilateral lesions of the NBM in male Long-Evans rats (350 g) and then tested these rats in a simple association learning paradigm. NBM lesioned rats (n = 4) and sham-operated rats (n = 6) underwent 20 consecutive days of training in a simple operant discrimination between a food-reinforced tone (T+) and a non- reinforced light (L-). Results showed that performance in NBM-lesioned rats was normal in all respects; both groups acquired the task, committing progressively greater numbers of successful responses to T+ and progressively fewer responses to L-, as well as diminishing the number of (non-reinforced) responses committed during the inter-trial interval. The hypothesis that NBM lesions spare simple association learning was thus supported. Despite the absence of impairment in this simple association task, we maintain that the NBM is involved in complex or configural association learning as demonstrated in separate experiments (see Butt et al., 1998, Soc. Neurosci. Abst.). (Supported by a University Research Committee Grant awarded to A. E. Butt by the Indiana State University Office of Sponsored Programs).
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