Vagal bradycardia elicited by stimulation of the external cuneate nucleus in the cat.

The role of the external cuneate nucleus (ECN) in the control of heart rate was systematically investigated in 26 chloralosed and 2 decerebrated, paralyzed, and artifically ventilated cats. Electrical stimulation of histologically verified sites in the ventral ECN and dorsal spinal trigeminal tract elicited a marked decrease in heart rate, with threshold currents of 5-25 muA and an optimal frequency of 20 Hz when using a 0.2 ms pulse; this response was shown to be due to vagal excitation. In seven experiments intravenous pentobarbital sodium decreased the magnitude of the bradycardia elicited by stimulation of the ECN, of the nucleus ambiguus (AMB), and of the cervical vagus significantly less than the response from the nucleus of the tractus solitarius. In eight additional experiments in cats with lesions of the AMB made 11-27 days earlier stimulation of the ECN elicited a bradycardia of the same magnitude as that observed in intact animals, although the bradycardia elicited by stimulation of the ipsilateral cervical vagus was significantly reduced by the lesion. Similarly, lesions of the ECN in four cats significantly attenuated the bradycardia elicited by stimulation of the ipsilateral cervical vagus. These results suggest that the ECN is a site of origin of cardioinhibitory axons in the cat.