Pathways through cingulate, neo- and entorhinal cortices mediate atropine-resistant hippocampal rhythmical slow activity.

Rats prepared with a lesion separating the entorhinal cortex from the neocortex and cingulate cortex displayed apparently normal hippocampal rhythmical slow activity (RSA) with a frequency of 6-12 Hz in both CA1 and dentate gyrus during Type 1 behavior (locomotion, head movements, changes in posture). Variations in the commissural average evoked potential (AEP) and increased power in the 30-100 Hz range (fast waves) also correlated with Type 1 behavior. Urethane did not abolish the RSA. However, systemic administration of atropinic drugs eliminated all RSA and eliminated or attenuated the Type 1 behavior-related variations in the AEP and fast waves. Thus, the normally present atropine-resistant RSA was eliminated by the cortical lesion while atropine-sensitive RSA remained intact. Removal of cingulate cortex alone was partially effective in suppressing atropine-resistant RSA but a lesion of the neocortex only, sparing cingulate cortex, had a minimal effect on it. Lesions of the amygdala, the anterior or medial thalamus or the cerebellum had little or no effect on atropine-resistant RSA. Previous work has shown that lesions of the entorhinal cortex or lateral hypothalamus eliminate atropine-resistant RSA. We suggest that atropine-resistant RSA is mediated by a somewhat diffuse pathway which traverses the hypothalamus, cingulate cortex, and neocortex before reaching the hippocampus via the entorhinal cortex.