If rodents do not display the behavioral complexity that is subserved in primates by prefrontal cortex, then evolution of prefrontal cortex in the rat should be doubted. Primate prefrontal cortex has been shown to mediate shifts in attention between perceptual dimensions of complex stimuli. This study examined the possibility that medial frontal cortex of the rat is involved in the shifting of perceptual attentional set. We trained rats to perform an attentional set-shifting task that is formally the same as a task used in monkeys and humans. Rats were trained to dig in bowls for a food reward. The bowls were presented in pairs, only one of which was baited. The rat had to select the bowl in which to dig by its odor, the medium that filled the bowl, or the texture that covered its surface. In a single session, rats performed a series of discriminations, including reversals, an intradimensional shift, and an extradimensional shift. Bilateral lesions by injection of ibotenic acid in medial frontal cortex resulted in impairment in neither initial acquisition nor reversal learning. We report here the same selective impairment in shifting of attentional set in the rat as seen in primates with lesions of prefrontal cortex. We conclude that medial frontal cortex of the rat has functional similarity to primate lateral prefrontal cortex.

Within the last few years, research into the cause and progression of Alzheimer's disease has made significant advances. Although there is still no preventative treatment or cure for this neurodegenerative illness, the development of drugs that may alleviate some of the cognitive symptoms associated with it is advancing. Cholinesterase inhibitors are at present the most effective form of treatment and have shown significant overall response rates in clinical trials. However, although some patients show substantial improvement when treated with this class of drugs, there is considerable variability in the amount of benefit gained in different individuals in terms of their cognitive and behavioural functioning. Furthermore, unfortunately some patients gain little or no benefit from these drugs. It would therefore be of great advantage to explore alternative therapeutic possibilities. This article reviews the potential involvement of the nicotinic cholinergic system in Alzheimer's disease and discusses the possibility of nicotinic pharmacotherapy. Substantial evidence indicates the involvement of the nicotinic cholinergic system in the pathology of Alzheimer's disease. Drugs targeting these sites may not only have a positive effect on cognitive function, but also have additional therapeutic benefits in terms of restoring the hypoactivity in the excitatory amino acid pyramidal system and even slowing the emergence of Alzheimer's disease pathology. The conclusion of this review is that nicotinic treatments are an important potential source of new therapeutic interventions in Alzheimer's disease.