Lateral tegmental field neurons of cat medulla: a source of basal activity of raphespinal sympathoinhibitory neurons.

Abstract

1. We tested the hypothesis that sympathoinhibitory (SI) neurons in the lateral tegmental field (LTF) of the cat medulla exert their actions over a pathway that includes raphe neurons whose axons innervate the thoracic intermediolateral nucleus (IML). 2. We recorded from 32 LTF neurons with sympathetic nerve-related activity [as demonstrated with spike-triggered averaging of inferior cardiac sympathetic nerve discharge (SND)] whose firing rate increased during the inhibition of SND produced by baroreceptor reflex activation. These neurons were classified as SI in function. 3. Twenty-three of these 32 LTF-SI neurons were antidromically activated by microstimulation of the raphe nuclei, 2-4 mm rostral to the obex and 3-4.5 mm below the dorsal surface of the medulla. The threshold current for eliciting the longest-latency antidromic responses [18.9 +/- 2.4 (SE) ms] was increased when the stimulating microelectrode was moved more dorsally in the midline. With one exception, these neurons could not be antidromically activated by stimulation of sites either 1.5-2.0 mm lateral to the midline, contralateral to the site of unit recording or raphe sites caudal to the obex. Threshold stimuli applied 2-4 mm rostral to the obex and 1 mm lateral to the midline, ipsilateral to the site of unit recording, elicited antidromic responses whose onset latencies were shorter than those produced by raphe stimulation. These data support the view that the axons of LTF-SI neurons terminated in the region of the raphe that contains SI neurons whose axons innervate the IML. 4. We recorded from 32 raphe neurons with sympathetic nerve-related activity whose firing rate increased during baroreceptor reflex activation. These neurons were classified as SI in function. Twenty-five of the 32 raphe-SI neurons were antidromically activated by microstimulation of the third thoracic (T3) IML. Seven (including 5 with spinal axons) of 24 raphe-SI neurons tested were synaptically activated by microstimulation of the region of the LTF containing SI neurons. The modal onset latency of synaptic activation was 22.8 +/- 8.4 ms. This value is close to the difference in spontaneous firing times (26 ms on the average) of LTF-SI and raphe-SI neurons, relative to the peak of the cardiac-related burst of SND. 5. Taken together, these data are consistent with the hypothesis that LTF-SI neurons are a source of the background discharges of raphespinal-SI neurons. 6. Thirteen raphe-SI neurons were antidromically activated by stimulation of both the medulla and T3 IML.(ABSTRACT TRUNCATED AT 400 WORDS)