Inhibition of rostral VLM by baroreceptor activation is relayed through caudal VLM

1990 ◽  
Vol 258 (5) ◽  
pp. R1271-R1278 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu
Keyword(s):  
Kynurenic Acid ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Firing Frequency ◽  
Ventrolateral Medulla ◽  
Cardiovascular Neurons ◽  
Baroreceptor Activation ◽  
Acid Administration ◽  
Stimulation Of

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.

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

1989 ◽  
Vol 257 (2) ◽  
pp. R265-R270 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu
Keyword(s):  
Direct Evidence ◽  
Cardiac Cycle ◽  
Ventrolateral Medulla ◽  
Sodium Glutamate ◽  
Inhibitory Pathway ◽  
Male Wistar Rats ◽  
Cardiovascular Neurons ◽  
Spontaneously Breathing ◽  
Baroreceptor Activation ◽  
Stimulation Of

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.

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
Keyword(s):  
Cardiac Cycle ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Cardiovascular Neurons ◽  
Reticular Neurons ◽  
Baroreceptor Activation ◽  
Tonic Excitation ◽  
Excitatory Drive

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.

Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves

1995 ◽  
Vol 268 (6) ◽  
pp. R1464-R1471 ◽  
Author(s):  
P. Ruggeri ◽  
R. Ermirio ◽  
C. Molinari ◽  
F. R. Calaresu
Keyword(s):  
Nerve Stimulation ◽  
Sural Nerve ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Electrolytic Lesions ◽  
Cardiovascular Neurons ◽  
Muscle Nerve ◽  
Stimulation Of

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVLM.

Sympathoexcitatory CVLM neurons mediate responses to caudal pressor area stimulation

2000 ◽  
Vol 279 (2) ◽  
pp. R364-R374 ◽  
Author(s):  
Madhusudan Natarajan ◽  
Shaun F. Morrison
Keyword(s):  
Arterial Pressure ◽  
Kynurenic Acid ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Homocysteic Acid ◽  
Premotor Neurons ◽  
Caudal Pressor ◽  
Excitatory Responses ◽  
Stimulation Of

Neurons in the caudal pressor area (CPA) are a source of tonic sympathoexcitation that is dependent on activation of cardiovascular sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM). In the present study, we sought to clarify the mechanism through which CPA neurons elicit increases in RVLM neuronal discharge, vasoconstrictor sympathetic tone, and arterial pressure. In urethan-chloralose-anesthetized, paralyzed, and artificially ventilated rats, bilateral disinhibition of CPA with bicuculline (Bic) after bilateral disinhibition of caudal ventrolateral medulla (CVLM) caused increases in splanchnic sympathetic nerve activity (+277% control) and arterial pressure (+54 mmHg). Inhibition of CVLM neurons with muscimol abolished the pressor response to activation of CPA neurons, suggesting that neurons within CVLM mediate the excitatory responses from CPA. Disinhibition of CVLM and CPA with Bic enhanced the sympathoexcitatory responses to stimulation of CPA with dl-homocysteic acid, which were blocked by microinjections of kynurenic acid into CVLM. We conclude that the pathway from CPA to RVLM involves an obligatory glutamatergic activation of sympathoexcitatory neurons in the vicinity of CVLM.

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
Keyword(s):  
Discharge Rate ◽  
Firing Frequency ◽  
Locus Ceruleus ◽  
Rostral Ventrolateral Medulla ◽  
Chemical Stimulation ◽  
Ventrolateral Medulla ◽  
Hypothalamic Area ◽  
Lateral Parabrachial Nucleus ◽  
Cardiovascular Neurons ◽  
Stimulation Of

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.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Pressor response from rostral dorsomedial medulla is mediated by excitatory amino acid receptors in rostral VLM

1994 ◽  
Vol 267 (1) ◽  
pp. R309-R315 ◽  
Author(s):  
Y. Hirooka ◽  
J. W. Polson ◽  
R. A. Dampney
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Amino Acid Receptors ◽  
Control Value ◽  
Afferent Fibers ◽  
Pressor Responses ◽  
Before And After ◽  
Stimulation Of

Excitatory amino acid (EAA) receptors in the rostral part of the ventrolateral medulla (VLM) have been shown to mediate pressor responses elicited by stimulation of various peripheral afferent fibers as well as other central nuclei. This study tested the hypothesis that these receptors are a critical component in the central pathway mediating the powerful pressor response that is produced by stimulation of a group of neurons within a circumscribed region in the rostral dorsomedial medulla (RDM). In anesthetized rabbits, the pressor response elicited by unilateral microinjection of glutamate into this RDM region was measured before and after injection of kynurenic acid (Kyn), a broad-spectrum EAA receptor antagonist, into the physiologically identified pressor region of either the ipsilateral or contralateral rostral VLM. The pressor response to RDM stimulation was greatly reduced (to 24 +/- 4% of control) 5-10 min after injection of Kyn (but not the vehicle solution) into the ipsilateral rostral VLM; this response returned completely to its control value within 30-60 min after Kyn injection. By contrast, after Kyn injection into the contralateral rostral VLM, the pressor response to RDM stimulation was not affected (106 +/- 15% of control). The results indicate that the descending pressor pathway from the RDM to the spinal cord is mediated by EAA receptors in the rostral VLM pressor region. Furthermore, the pathway from the RDM to the rostral VLM is predominantly, if not exclusively, ipsilateral.

Predominance of vagal bradycardia mechanism in the brain stem of turtles

1988 ◽  
Vol 140 (1) ◽  
pp. 405-420 ◽  
Author(s):  
J. H. Hsieh ◽  
C. M. Pan ◽  
J. S. Kuo ◽  
C. Y. Chai
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Cardiac Contraction ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Vagal Bradycardia ◽  
The Brain ◽  
Stimulation Of

Cardiovascular parameters of spontaneously breathing pond turtles (Cyclemys flavomarginata) anaesthetized with chloralose (4 mg 100 g-1) and urethane (40 mg 100 g-1), were examined during exploratory electrical stimulation of the brain stem. Turtles exhibited a low mean systemic arterial blood pressure (MSAP, average 25 mmHg) and slow heart rate (average 24 beats min-1). Upon stimulation, pressor (sympathetic), depressor (sympathetic inhibition), bradycardia and hypotensive (vagal) responses were elicited from regions of the brain stem extending from the hypothalamus to the medulla, principally in the medial region. The pressor response appeared after a longer latency than did the bradycardia and hypotensive responses. It developed rather slowly, and rarely attained a magnitude double its resting value. In contrast, stimulation of many points in the brain stem produced marked slowing or even cessation of the heart beat, and thus resulted in an immediate fall of the blood pressure even to zero. This cardio-inhibitory response depended on the integrity of the vagus nerves and was particularly marked upon stimulation in the caudal medulla, the areas of the ambiguus, solitary and dorsomotor nuclei of the vagus and the midline structures. When such an area was stimulated continuously the heart stopped beating throughout the stimulation. The longest period of cardiac arrest before the appearance of escape was 35 min. With continuous stimulation of the peripheral end of the cut vagus, the earliest escape beat occurred even later (65 min). Epinephrine given intravenously produced an increase of MSAP and force of cardiac contraction, although the slope of pressor rise was shallow. Reflex bradycardia, however, was not observed. These experiments show that a very prominent vagal bradycardia can be evoked from the turtle brain stem, which may contribute to its well-known capacity for tolerating anoxia.

Chemoreceptor and baroreceptor inputs to ventrolateral medullary neurons

1984 ◽  
Vol 247 (5) ◽  
pp. R872-R879 ◽  
Author(s):  
M. M. Caverson ◽  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Arterial Occlusion ◽  
Firing Frequency ◽  
Single Units ◽  
Ventrolateral Medulla ◽  
Afferent Information ◽  
Thoracic Cord ◽  
Upper Thoracic ◽  
Baroreceptor Activation ◽  
Carotid Arterial ◽  
Intermediolateral Nucleus

Recording experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated cats to identify single units in the ventrolateral medulla (VLM) projecting directly to the region of the intermediolateral nucleus of the spinal cord (T2) and responding to selective activation of peripheral chemoreceptors (sodium cyanide, 20-60 micrograms in 0.1-0.3 ml saline into medial thyroid artery) and baroreceptors (phenylephrine, 2 micrograms/kg iv). The firing frequency of 49 of the 81 antidromically identified single units was altered by activation of the peripheral cardiovascular receptors. Of these responsive units, 25 responded only to activation of chemoreceptors (17 excited and 8 inhibited), 20 responded in various combinations to activation of both chemo- and baroreceptors, and 4 responded only to activation of baroreceptors. In addition, units that altered their firing frequency during baroreceptor activation (n = 24) responded in the opposite direction to baroreceptor unloading (carotid arterial occlusion). These results suggest that neurons in the VLM are components of bulbospinal sympathoexcitatory and -inhibitory pathways that receive cardiovascular afferent information and in turn influence vasoconstrictor and cardioacceleratory neurons in the intermediolateral nucleus of the upper thoracic cord.

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