Fig. 5.

Hypothetical model showing how various manipulations of SCN function might affect learning. (Left) In entrained nocturnal animals, both sleep and SCN neuronal firing rate are high during the day. Presumably, GABA release from the SCN is highest at this time as well. The SCN would thus provide cyclic inhibitory input to structures such as the septum, which would permit normal daily oscillations in the balance of excitatory (+) and inhibitory (−) tone in the hippocampus. (Center) In SCN-lesioned animals, the absence of GABA input to the septum (dashed line) would permit chronic cholinergic excitation of the hippocampus and might explain why learning deficits are not observed in SCN-lesioned animals. (Right) In our arrhythmic (AR) hamsters, the SCN might provide a steady release of GABA to inhibit (−−) the septum because of continuous neuronal activity in the SCN. This, in turn, would reduce septal cholinergic input to the hippocampus, thereby attenuating memory formation there. Black and white rectangles indicate relative times of dark and light, respectively, in the animal facility.