Cognitive deficits associated with Alzheimer's disease are known to result from decreases in acetylcholine within the cholinergic system of the medial septal area, which projects to the hippocampus. The significance of the neurotransmitter norepinephrine within this context has not been extensively reviewed. The present study measured the effects that Guanfacine, an alpha-2 noradrenergic agonist, has on memory deficits produced by cholinergic cell lesion in the rat medial septum. Memory processing during pre-lesion, post-lesion, and post-drug administration groups was quantified using a socially transmitted food preference task. Following administration of the cholinergic neurotoxin 192 IgG-saporin, subjects exhibited a significant decrease in memory formation when compared to baseline. Furthermore, following injection of guanfacine into post-lesioned rats, subjects displayed a significant value of memory formation above chance. Memory-related effectiveness of guanfacine seems to be dependent on a baseline number of acetylcholine cells within the medial septum. Consequently, data suggests that guanfacine may carry no more therapeutic worth for patients afflicted by Alzheimer's disease than routinely prescribed acetylcholinesterase inhibitors. However, such conclusions must not be considered definitive by any means, as it is possible that future research might elaborate on possible cellular explanations for the increase in memory formation observed following guanfacine administration in the present examination.



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