Neurons in rostral VLM are inhibited by chemical stimulation of caudal VLM in rats.

Recent evidence suggests that neurons in the caudal ventrolateral medulla (CVLM) exert a tonic inhibition on the neurons in the rostral ventrolateral medulla (RVLM) that are essential for the maintenance of arterial pressure (AP). To test the hypothesis that selective activation of cell bodies in the CVLM can inhibit the discharge of neurons in the RVLM, activity from 88 neurons in the RVLM was recorded extracellularly while 2-30 nl sodium glutamate (Glu; 0.15 M) were microinjected into depressor sites of the CVLM of urethan-anesthetized male Wistar rats. Results obtained from spontaneously breathing and artificially ventilated rats were essentially similar and are presented together. Twenty-five neurons were characterized as cardiovascular because they were inhibited by baroreceptor activation and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Activation of cell bodies in the CVLM inhibited the firing rate of 23 of these cardiovascular neurons and excited 2. The remaining 63 neurons could not be considered cardiovascular because they either were not barosensitive or lacked cardiac cycle-related rhythmicity. Injection of Glu into the CVLM inhibited 26 of these neurons, excited 22, and had no effect on 15. These results provide direct evidence for the existence of an inhibitory pathway from neurons located in the CVLM to cardiovascular neurons in the RVLM.