Hippocampal slow (“arousal”) wave activation in the rostral midbrain transected cat

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The neocortical and hippocampal EEG changes of an acute rostral midbrain cat preparation (brain-stem section at the junction of the diencephalon and midbrain) are described. 1. 1. In the neocortex an alternation of very regular, large amplitude slow waves (0.5–1.5 c/sec) without prominent spindle bursts, with irregular high voltage slow waves with repetitive spindle bursts was seen. 2. 2. The hippocampal EEG showed a continuous pattern of irregular fast waves with occasional slow waves. Posterior hypothalamic stimulation elicited hippocampal “arousal” waves (1.5–3.5 c/sec) which lasted from 5 sec to 2 min after the cessation of the stimulus, while the neocortex did not show the EEG desynchronization which could be elicited before transection. Depending upon the intensity of the hypothalamic stimulus and the pattern of background activity before stimulation, the neocortex also showed some change, from slight to marked suppression of slow waves with enhancement of spindle burst. Desynchronization of the neocortex by hypothalamic stimulation was observed only briefly during extremely strong stimuli. 3. 3. Thalamic stimulation elicited phasic desynchronization in the neocortical EEG with a less marked change in the hippocampal EEG, whereas hypothalamic stimulation induced stronger regular slow wave activation in the hippocampus (hippocampal “arousal” waves) with a lesser change in the neocortex. 4. 4. In the classic cerveau isolé preparation, hypothalamic stimulation could elicit brief neocortical desynchronization as well as hippocampal “arousal”. With a more rostral transection (at the junction between diencephalon and mesencephalon), it was very difficult to produce neocortical desynchronization by posterior hypothalamic stimulation which, however, produced marked hippocampal “arousal” waves. 5. 5. It is concluded that for activation of the hippocampus, the hypothalamus is not only the primary pathway receiving impulses from the midbrain reticular formation, but it also possesses a sustained activating mechanism for the hippocampus. This tonic activating mechanism may influence the neocortex through the midbrain reticular formation. There seems to be no important direct activating pathway to the neocortex from the hypothalamus under the conditions of an acute experiment.