Abstract

The effect of oxytocin upon the hippocampal EEG has been studied in unanesthetized cats prepared with acute lesions in the rostral brain stem or in the posterior basal diencephalon.The results are as follows.1. Following intracarotid injection of 0.1-0.3 u. of oxytocin, the alteration of the hippocampal EEG was characterized by the hippocampal hyper-arousal waves with the latency of 20-40 seconds, lasting 30-90 seconds both in the intact cat and the adrenalectomized cat. The appearance of this response is intermittent rather than continuous.2. Following intravenous injection of 0.1-0.5 u. of oxytocin, the unit discharge in the rostral midbrain reticular formation increased with the latency of 30-60 seconds and with sustained firing for 1-2 minutes. The highest rates observed, were about 20-30 cycles per second.3. Regarding lesions in the posterior midbrain tegmentum, perisqueductal grey, rostral midbrain tegmentum and posterior basal diencephalon, only the latter could block the appearance of this response elicited by the administration of oxytocin.4. Lesions in the lateral hypothalamus, the subthalamic region, or the septal region, which constitute a nodal area in the afferent pathway to the hippocampus, also block the appearance of this response.5. Intracarotid injection of 0.3-0.5 u. of vasopressin-like substance could introduce this response in 7 out of 11 cats with the acute rostral midbrain tegmental lesion.These results offer evidence in favor of the existence of an oxytocin-sensitive component within the midbrain reticular activating system, including the posterior hypothalamus and the adjacent region; also, the afferent discharge, from the oxytocin sensitive component in the midbrain activating system in response to circulating increased oxytocin, activates the hippocampus via the lateral hypothalamus and the septum.6. Authors discussed oxytocin-sensitive component in the reticular activating system from the biological viewpoint of homeostasis.These results were partly reported at the second Reproduction Symposium of the Japan Endocrine Society, in March 1962 and at the 39th General Meeting of the Physiological Society of Japan, in July 1962.

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