The significance of cholinergic modulation for associative memory performance in the piriform cortex was examined in a study combining cellular neurophysiology in brain slices with realistic biophysical network simulations. Three different physiological effects of acetylcholine were identified at the single-cell level: suppression of neuronal adaptation, suppression of synaptic transmission in the intrinsic fibers layer, and activity-dependent increase in synaptic strength. Biophysical simulations show how these three effects are joined together to enhance learning and recall performance of the cortical network. Furthermore, our data suggest that activity-dependent synaptic decay during learning is a crucial factor in determining learning capability of the cortical network. Accordingly, it is predicted that acetylcholine should also enhance long-term depression in the piriform cortex.

Previously we have shown that Gluck and Myers's (1993) corticohippocampal model could be extended to incorporate Hasselmo and Schnell's (1994) hypothesis that septohippocampal cholinergic processes regulate the amount of information storage in hippocampus. The generalized model could account for the effect of the anticholinergic drug scopolamine in delaying onset of eyeblink conditioning . Here, we show that the model also accounts for additional eyeblink results, including quick recovery after scopolamine is removed, preserved latent inhibition, learned irrelevance and extinction under scopolamine, and no effect of systemic scopolamine after hippocampal lesion. Additionally, the model is consistent with data concerning localized scopolamine iI\iections to the medial septum, the lateral septum, and the hippocampus and their effect on eyeblink conditioning.

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