Effects of stimulation of the mediodorsal nucleus and its projection cortex on heart rate in the rabbit.

Electrical stimulation of prefrontal cortex in anesthetized rabbits evoked small (less than 10%) changes in heart rate. In contrast, stimulation of the thalamic mediodorsal nucleus (MD) elicited decreases in heart rate proportional to the stimulating current. The maximal peak reductions in heart rate evoked by higher current intensities were 85% from prestimulus levels. The bradycardiac response had a short latency after stimulus onset (less than 1 s, peak within 5 s), and the heart rate usually returned to baseline within 30 s after stimulation. Vagal cholinergic innervation of the heart was suggested as the final effector pathway since bilateral vagotomy or administration of atropine (sulfate or methyl nitrate, 0.15-0.4 mg/kg, i.v.) virtually abolished the rapid bradycardiac responses. Administration of a beta-adrenergic receptor blocker (propranolol, 3 mg/kg, i.v.) was without effect on the heart rate response. The effective medial thalamic area for evoking a response was localized to MD, the thalamic midline nuclei between both MDs and a region continuous with, but posterior to MD (e.g. parafascicular nucleus). A descending effector pathway from the thalamus was implicated since complete bilateral ablation of prefrontal cortex did not reduce the stimulus-produced bradycardia evoked from MD. Similar large bradycardiac responses were obtained in an unanesthetized preparation to both MD stimulation and to sensory stimuli, suggesting a possible physiological correlate for these intracranially-evoked heart rate changes.