Cardiovascular responses and changes in neural activity in the rostral ventrolateral medulla elicited by electrical stimulation of the amygdala of the rat

Abstract

Electrical stimulation of the central nucleus of the amygdala (ACe) in anesthetized animals produces a decrease in arterial pressure (AP) as a result of an overall decrease in peripheral resistance. As the cardiovascular neurons that presumably mediate these changes are located in the rostral ventrolateral medulla (RVLM) [11], we recorded spontaneous activity from 89 histologically verified units in the RVLM of urethan-anesthetized rats. Twenty-two of these units were classified as cardiovascular neurons because their spontaneous activity was inhibited by baroreceptor stimulation (2–4 μg phenylephrine i.v.) and displayed a cardiac cycle-related rhythmicity. Single or twin pulses (0.5 ms, 180 ± 55 μA) delivered once per second to arterial depressor sites in the ipsilateral ACe inhibited the activity of 18 of these neurons and excited 4. In 27 additional barosensitive neurons that lacked cardiac cycle rythmicity, a similar distribution of effects was obtained by electrical stimulation of the ACe: 13 inhibited, 5 excited, 9 not affected. Finally, 40 non-barosensitive units were found; stimulation of the ACe inhibited the activity of 16, excited 12 and had not effect in 12. These results are interpreted to indicate that the differential effects of ACe stimulation on different vascular beds are mediated probably by differential influences on cardiovascular neurons in the RVLM, and that functions other than respiratory and cardiovascular control are represented in the RVLM.