Butt AE, Corley S, Cabrera S, Chavez C, Kitto M, Ochetti D, Renovato A, Salley T, Sarpong A (2003) 192 IgG-saporin lesions of the nucleus basalis magnocellularis in rats fail to disrupt acquisition or retention of differential reinforcement of low rate responding. Neuroscience 2003 Abstracts 425.5. Society for Neuroscience, New Orleans, LA.
Summary: The frontal cortex has been implicated in supporting timing behavior in tests of differential reinforcement of low rate responding (DRL) in rats. DRL performance is similarly influenced by anticholinergic drugs; scopolamine interferes with DRL performance by increasing the number of nonreinforced responses and thus decreasing DRL efficiency. Because the frontal cortex receives significant cholinergic input from the nucleus basalis magnocellularis (NBM) in rats, we hypothesized that NBM lesions would disrupt DRL performance in the current experiment. Male Long-Evans rats were placed first in a DRL 10 s schedule of reinforcement before advancing to a DRL 20 s schedule. Rats received 50 trials per day for 20 consecutive days on both DRL schedules. When rats reached stable performance, they received either bilateral 192 IgG-saporin lesions of the NBM or sham lesions. Upon recovery, rats were reintroduced to the DRL 20 s task for 10 days of post-operative testing. Finally, rats were tested using a novel delay interval in a DRL 30 s task. Testing continued for 10 additional days. Results showed that the NBM lesion group showed no significant change in either the total number of responses or in DRL efficiency (reinforced responses / total responses) between pre- and post-operative DRL 20 s testing. Subsequent acquisition in the DRL 30 s task was similarly not disrupted by NBM lesions. The effectiveness of the lesions was verified by acetylcholinesterase (AChE) staining, which showed pronounced depletion of cortical AChE with normal AChE-positive staining in the hippocampus and medial septal area. These data suggest that the NBM is not critically involved in either the acquisition or retention of DRL performance.
Related Products: 192-IgG-SAP (Cat. #IT-01)