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The distribution of pulvinar neurons that project to the lateral intraparietal area (LIP) and area 7a, two subregions of the inferior parietal lobule in monkeys, was determined using small injections of retrogradely transported fluorescent dyes. Both LIP and 7a received the majority of their thalamic input from contiguous but distinct zones within the medial pulvinar nucleus. Thalamocortical cell bodies that projected to LIP were arranged in a dense, horizontally oriented cluster that was sandwiched between two similar clusters of neurons that projected to 7a. There was minimal overlap of the respective clusters. LIP also received an appreciable input from the dorsal half of the lateral pulvinar nucleus, but tracer placements in 7a resulted in only occasional labeled neurons in the lateral pulvinar.

In 41 rats, bipolar electrical stimulation was administered to various regions of the frontal cortex, including the medial prefrontal cortex (MPFC), lateral prefrontal cortex (LPFC), infralimbic cortex, and convexity cortex. Resulting alterations of blood pressure and heart rate were noted. It was observed that hypotension resulted from stimulation administered to either LPFC, infralimbic cortex or ventral portion of MPFC (i.e. prelimbic cortex). Furthermore, stimulation of the LPFC typically produced bradycardia, whereas stimulation of the MPFC or infralimbic cortex had little or no effect on heart rate. Pharmacological and surgical blocks of the vagus nerves failed to attenuate the stimulus produced hypotension (SPH), as elicited from the prefrontal or infralimbic cortices, thus demonstrating that SPH in rats is not mediated by the vagus nerves. However, intraperitoneal injections of norepinephrine, which mimicked a state of increased sympathetic tone, were observed to completely block SPH. Accordingly, it is suggested that SPH may occur as the result of sympathetic inhibition. Furthermore, intravenous injections of naloxone were also observed to also completely block SPH, thus demonstrating that SPH may be mediated via opioid pathways.