Abstract
The hyper-reactivity of the septal syndrome was produced in adult male Long-Evans rats by electrolytic lesions in the septal region. Various groups of the rats with septal lesions were handled postoperatively for either 5 or 18 days or left unhandled for 18 days. The operated control group was also not handled. Following these handling periods, the septal syndrome was found to have declined in both handled groups, and the animals were at normal reactivity levels. The unhandled group with septal lesions still displayed the syndrome. Neocortical ablations did not reinstate the syndrome in either handled group, nor did they change the reactivity level of the unhandled groups. The septal syndrome in another group of rats was reduced to normal levels by handling for 21 postoperative days. Spreading depression, induced by application of 25% KCl to the neocortex, did not reinstate the septal syndrome. These results differ from and restrict the generality of previous findings.
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