Pontine reticular neurons provide tonic excitation to neurons in rostral ventrolateral medulla in rats

1994 ◽  
Vol 266 (1) ◽  
pp. R237-R244 ◽  
Author(s):  
K. Hayes ◽  
F. R. Calaresu ◽  
L. C. Weaver

To determine whether the pontine reticular formation (PRF) is a source of tonic activity for cardiovascular neurons in the rostral ventrolateral medulla (RVLM), the discharge of PRF neurons was inhibited by unilateral microinjections of glycine (1.0 M; 60 nl) while recording the discharge of single neurons in the RVLM in 14 Saffan-anesthetized rats. RVLM units were characterized as cardiovascular if their spontaneous activity was changed by baroreceptor activation and was synchronized to the cardiac cycle. Glycine injection into the ipsilateral PRF eliminated the ongoing activity of six cardiovascular units and reduced the activity of four (mean decrease -91 +/- 4%). Inhibition of these units lasted 20-115 s (mean 59 +/- 9 s). Glycine injection into the PRF had no effect on the discharge of five cardiovascular units. Activity of six noncardiovascular units did not respond to PRF blockade. Glycine injection into the PRF caused decreases in arterial pressure (-28 +/- 5 mmHg), heart rate (-23 +/- 3 beats/min), and renal nerve activity (-42 +/- 7%) that also returned to control values between 25 and 120 s (mean 55 +/- 5 s). These results indicate that PRF neurons provide tonic excitatory drive to some cardiovascular neurons located 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.


1989 ◽  
Vol 257 (2) ◽  
pp. R265-R270 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu

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.


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.


1993 ◽  
Vol 61 ◽  
pp. 134
Author(s):  
Kyoji Taguchi ◽  
Shuji Ozaki ◽  
Motoaki Ainano ◽  
Takanobu Tshizuka ◽  
Takao Kubo

1994 ◽  
Vol 266 (3) ◽  
pp. H1075-H1086 ◽  
Author(s):  
C. G. Wilson ◽  
A. C. Bonham

This study investigated the effects of area postrema stimulation on the activity of cardiovascular-related neurons in the rostral ventrolateral medulla and determined whether the effects were mediated by cell bodies. Results are based on recordings of extracellular spikes from 113 neurons in 37 alpha-chloralose- or pentobarbital sodium-anesthetized rabbits. Single sequential stimuli evoked an excitation (onset, 22 +/- 8 ms; duration, 20 +/- 14 ms) followed by an inhibition (onset, 53 +/- 21 ms; duration, 127 +/- 82 ms) in 1) 58 neurons with discharge patterns that were correlated with sympathetic nerve activity (determined by spike-triggered averaging) and with the cardiac cycle (determined by post-R wave-triggered histograms) and that were inhibited by increasing arterial pressure and 2) 27 neurons that exhibited a cardiac rhythm but not a sympathetic rhythm. Area postrema-evoked excitation and inhibition were markedly attenuated by kainic acid injections in area postrema, suggesting that both inputs were derived from cell bodies. The results suggest that area postrema neurons may modulate the activity of medullary neurons in the baroreflex-sympathetic arc as well as neurons in other networks that share baroreceptor input but may not be related to sympathetic nerve activity.


2001 ◽  
Vol 281 (1) ◽  
pp. R98-R107 ◽  
Author(s):  
Rubia Grecco Menegaz ◽  
Daniel R. Kapusta ◽  
Helder Mauad ◽  
Antonio de Melo Cabral

The contribution of α2-receptor mechanisms in the rostral ventrolateral medulla (RVLM) in mediating the enhanced renal excretory responses evoked by the intravenous infusion of the α2-receptor agonist xylazine was examined in ketamine-anesthetized rats. In ketamine-anesthetized rats, the bilateral microinjection of the α2-receptor antagonist yohimbine into the RVLM significantly reduced the enhanced levels of urine flow rate (V) and urinary sodium excretion (UNaV) produced by xylazine. In contrast, microinjection of yohimbine into the RVLM of chronically bilaterally renal-denervated rats significantly reduced the xylazine-evoked diuretic, but not natriuretic, response. In separate ketamine-anesthetized rats, intravenous xylazine infusion produced a near complete inhibition of renal sympathetic nerve activity (RSNA). The subsequent microinjection of yohimbine into the RVLM reversed this neural response and concurrently decreased V and UNaV. Together, these results indicate that during intravenous infusion, xylazine activates α2-receptor mechanisms in the RVLM to selectively promote urinary sodium excretion by a renal nerve-dependent pathway. In contrast, activation of α2-receptor in the RVLM affects the renal handling of water by a pathway independent of the renal nerves. This latter pathway may involve an interaction with other brain regions involved in antidiuretic hormone release (e.g., paraventricular nucleus of the hypothalamus).


1999 ◽  
Vol 815 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Weifang Rong ◽  
Weizhong Wang ◽  
Wenjun Yuan ◽  
Yizhang Chen

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