Abstract
Heart rate was telemetrically recorded from rats self-stimulating in a two-day shuttle-box. Blood pressure changes to intracranial stimulation (ICS) were determined in acute studies with the same subjects. Stimulus-bound heart rate decreases were found only at sites in the anterodorsal aspect of the lateral hypothalamus, whereas no changes in heart rate were observed at ventral or posterior sites. In the acute experiments, stimulation of the anterodorsal sites produced either decreases or no change in blood pressure. Stimulus-bound blood pressure increases were observed only in the ventrolateral hypothalamus. The differential topographical distribution of the electrode sites producing the heart rate and blood pressure changes suggests that these two aspects of cardiovascular function are subserved by separate neural systems in the hypothalamus and that the bradycardia during self-stimulation is a primary response to ICS and is not a reflex elicited by blood pressure increases. Blockade of the bradycardia with the peripheral cholinergic blocker methyl-hyoscine HBr had no effect on the initiation of or escape from ICS indicating that peripheral parasympathetic activity is not causally related to either the rewarding or aversive components of hypothalamic ICS.
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