Supramedullary inputs to cardiovascular neurons of rostral ventrolateral medulla in rats

1993 ◽  
Vol 265 (1) ◽  
pp. R111-R116 ◽  
Author(s):  
S. K. Agarwal ◽  
F. R. Calaresu

Experiments were done to test the hypothesis that selective activation of cell bodies in different nuclei known to be involved in central cardiovascular control could excite or inhibit the discharge of neurons in the rostral ventrolateral medulla (RVLM). It is known that chemical stimulation of the lateral parabrachial nucleus (LPBN), locus ceruleus (LC), and lateral hypothalamic area (LHA) in anesthetized animals elicits increases (LPBN) or decreases (LC and LHA) in arterial pressure. We therefore recorded extracellularly spontaneous activity from RVLM units in urethan-anesthetized rats and monitored the changes in firing frequency of these neurons during chemical stimulation of one of LPBN, LC, and LHA. Thirty-two units were classified as cardiovascular neurons because their activity was inhibited by baroreceptor activation (1-3 micrograms phenylephrine iv) and displayed a cardiac cycle-related rhythmicity. Chemical stimulation with sodium glutamate of arterial pressor sites in the ipsilateral LPBN increased the firing frequency (40.3 +/- 1.3%) of 11 cardiovascular neurons. Activation of cell bodies in arterial depressor sites in the ipsilateral LC inhibited the firing rate (59.1 +/- 7.1%) of 10 cardiovascular neurons and excited 1 unit. Activation of cell bodies in arterial depressor sites in the ipsilateral LHA inhibited the discharge rate (25.4 +/- 4.7%) of six cardiovascular neurons, excited one unit, and did not alter the rate of the remaining three units. These results provide direct evidence for the existence of excitatory and inhibitory pathways from neurons located in the LPBN, LC, and LHA to cardiovascular neurons in the RVLM.

1990 ◽  
Vol 258 (5) ◽  
pp. R1271-R1278 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu

Experiments were done to test the hypothesis that inhibition of neurons in the rostral ventrolateral medulla (RVLM) elicited by stimulation of the nucleus tractus solitarii (NTS) is relayed through the caudal ventrolateral medulla (CVLM). We recorded activity from 56 spontaneously firing units in the right RVLM of urethan-anesthetized and artificially ventilated rats. Eleven of these units were classified as cardiovascular neurons, because they were silenced by baroreceptor activation (1-3 micrograms phenylephrine iv) and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Single pulses (0.1 ms, 30-75 microA) delivered 1/s to depressor sites in the ipsilateral NTS inhibited the activity of all these cardiovascular neurons. Microinjection of the glutamate antagonist kynurenic acid (0.15 M, 50 nl) into the ipsilateral CVLM blocked the inhibitory response of RVLM units to the administration of phenylephrine and increased the firing frequency of cardiovascular neurons in the RVLM by 43%. Moreover, kynurenic acid administration attenuated the inhibitory response of cardiovascular neurons in the RVLM to NTS stimulation. Finally, stimulation of the NTS that elicited depressor responses under control conditions produced a pressor response after kynurenic acid administration. The remaining 45 RVLM neurons were barosensitive but lacked cardiac cycle-related rhythmicity. These results provide direct evidence for the existence of a tonic inhibitory pathway from NTS to RVLM that is relayed through the CVLM probably by a glutamatergic projection from NTS to CVLM.


1993 ◽  
Vol 265 (1) ◽  
pp. R35-R40 ◽  
Author(s):  
R. Ermirio ◽  
P. Ruggeri ◽  
C. Molinari ◽  
L. C. Weaver

Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play an essential role in the generation of basal sympathetic tone and in the reflex regulation of blood pressure. In this study responses of RVLM "cardiovascular" neurons to somatic and visceral afferent stimulation were investigated. The activity of 34 RVLM neurons was recorded in urethan-anesthetized paralyzed and artificially ventilated rats. These neurons were identified as cardiovascular based on their baroreceptor sensitivity and their pulse-synchronous discharge. Electrical stimulation of the sciatic nerve excited 31 of the 34 RVLM units (91%). Renal nerve stimulation inhibited firing of 14 of 22 RVLM neurons tested (64%), not affecting the remaining 8 units. Stimulation of splenic nerves inhibited the discharge of 7 of 12 RVLM neurons tested (58%), whereas the remaining 5 units were not affected. All RVLM units responsive to visceral afferent stimulation were also responsive to sciatic nerve stimulation. These results indicate that RVLM cardiovascular neurons receive somatic and visceral inputs, suggesting an involvement of these units in the integration of homeostatic responses to changes in the internal and external environment.


2000 ◽  
Vol 279 (5) ◽  
pp. H2549-H2557 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.


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