Anderson ML, Govindaraju KP, Shors TJ (2012) Acetylcholine and Learning: Are they related and does it matter for associating events across time?. Neuroscience 2012 Abstracts 600.12. Society for Neuroscience, New Orleans, LA.
Summary: Decades ago, acetylcholine was considered intrinsic to processes related to attention and/or learning and memory. Much of this was based on its presumed role in dementia associated with Alzheimer’s disease. However, in the last decade or so, this relationship has been questioned and with good reason (Parent & Baxter, 2004). That said, only a few studies have addressed the involvement of acetylcholine in tasks that require an animal to associate stimuli separated in time, such as trace eyeblink conditioning. This type of task is dependent on the hippocampus and is severely disrupted in both patients with Alzheimer’s disease and animal models of the disorder (Kishimoto, 2012; Waddell et al., 2008; Woodruff-Pak & Papka, 1996). In the present study, we hypothesized that animals with minimal Ach input to both hippocampi would not learn whereas those with input into one hippocampus could. The immunotoxin 192 IgG-Saporin was infused into the MSDB to selectively kill cholinergic neurons in Sprague-Dawley rats and then trained with either delay or trace eyeblink conditioning. Delay conditioning requires that the stimuli during training are contiguous in time and is not dependent on the hippocampus. Animals were given 200 trials for four days for 800 trials in total. A complete bilateral MSDB-cholinergic lesion was considered complete if the number of neurons that express choline acetyltransferase was reduced by 75 %. A bilateral lesion of this magnitude prevented early acquisition of the trace response (p<.05). Indeed, none of the animals so far trained reached a learning criterion of 60 % CRs during any session of training. In contrast, animals with a loss of ACh in just one hemisphere were able to learn the CR. Furthermore, preliminary data suggest delay conditioning was unaffected by the loss of ACh from the septum. Finally, animals with half the number of cholinergic neurons were still able to learn trace eyeblink conditioning regardless of whether the damage was bilateral or unilateral. Thus, it would appear that the progressive loss of ACh coincides with the loss of learning potential, especially when that learning requires associations across time. This approach and the experimental results may model the progressive nature of Alzheimer’s disease, in which the loss of neuronal function is slow but cumulative.
Related Products: 192-IgG-SAP (Cat. #IT-01)