Neurons in the caudal ventrolateral medulla mediate the arterial baroreceptor reflex by inhibiting barosensitive reticulospinal neurons in the rostral ventrolateral medulla in rabbits

Masuda, Norihiko; Terui, Naohito; Koshiya, Naohiro; Kumada, Mamoru

doi:10.1016/0165-1838(91)90077-g

Cited by 52 publications

(23 citation statements)

References 23 publications

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“…In contrast to the RVLM injections, administration of kynurenate into the IVLM 0-1.0 mm rostral to the obex level increased resting arterial pressure and RSNA, indicating that EAA inputs were tonically active in this portion of the ventrolateral medulla in agreement with previous studies in anesthetized rabbits (29,30). However, we also cannot exclude some leakage of kynurenate into the neighboring depressor region of the CVLM, where blockade of EAA inputs to sympathoinhibitory neurons increases arterial pressure and sympathetic activity as shown previously in anesthetized animals (27,29).…”

Section: Discussionsupporting

confidence: 78%

“…These results might seem somewhat surprising, considering that EAAs play an important role in mediating baroreceptor reflexes at the level of the CVLM, which forms afferent input to the sympathoexcitatory neurons of the RVLM (14,22,27). However, it has been shown previously that, to affect the baroreflex in the rabbit, it was necessary to treat the rostrocaudal extent of the ventrolateral medulla from 1.3 mm rostral to 3 mm caudal to the obex using three to five consecutive injections (100 nl each) of kynurenic or kainic acids (29,30). Thus, in the present study, the single injection of kynurenate was presumably not sufficient to alter the baroreflex transmission in the depressor region of the ventrolateral medulla.…”

Section: Discussionmentioning

confidence: 99%

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Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits

Mayorov

Head

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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In this study, we examined the effect of excitatory amino acid (EAA) receptor blockade in the rostral ventrolateral medulla (RVLM) on the renal sympathetic baroreflex in conscious rabbits. Rabbits were implanted with guide cannulas for bilateral microinjections into the RVLM (ϩ2 to ϩ3 mm from the obex, n ϭ 8) or into the intermediate ventrolateral medulla (IVLM; 0 to ϩ1 mm from the obex, n ϭ 5) and with an electrode for measuring renal sympathetic nerve activity (RSNA). After 7 days of recovery, microinjection of the EAA receptor antagonist kynurenate (10 nmol) into the RVLM did not affect resting RSNA or arterial pressure. Kynurenate decreased the gain of the RSNA baroreflex by 53% but did not change the reflex range. By contrast, injection of kynurenate into the IVLM increased resting arterial pressure and RSNA by 27 mmHg and 88%, respectively, but did not alter the RSNA baroreflex gain or range. Pentobarbital sodium anesthesia attenuated the gain and range of the RSNA baroreflex by 78 and 40%, respectively. Under these conditions, microinjection of kynurenate into the RVLM did not cause any further change in the gain of this reflex. These results suggest that endogenous EAA neurotransmitters in the RVLM are important in modulating the sympathetic baroreflex in conscious rabbits. Anesthesia can mask the functional significance of EAAs in the RVLM in modulating the baroreflexes, which may explain why previous studies in anesthetized animals found no effect of blocking EAA receptors in the RVLM on sympathetic baroreflexes. excitatory amino acids; kynurenate; arterial pressure; anesthesia; heart rate THE PRESSOR REGION of the rostral ventrolateral medulla (RVLM) is critical in the generation and maintenance of sympathetic activity and is also an essential part of the central baroreflex pathways (8,9,15). The GABAergic synapse is believed to be a principal relay in the RVLM in transmission of baroreceptor information, because blockade of GABA receptors in this area abolished the vasomotor component of the reflex (8,15). By contrast, the excitatory amino acids (EAAs) in the RVLM are thought to play a little role in mediating cardiovascular responses to baroreceptor stimulation. This assumption is supported by numerous findings that the blockade of ionotropic EAA receptors in the region with local administration of kynurenate did not affect sympathetic baroreflexes in rats (27, 40), rabbits (41), or cats (12). This contrasts with the essential role of EAAs in the RVLM in mediating many other cardiovascular reflexes. In particular, administration of kynurenate into the RVLM has been shown to attenuate the pressor and sympathoexcitatory reflex responses to hypothalamic stimulation (40), muscular contraction (4), noxious stimulation (34), and renal and vagal afferent stimulation (6, 41) in anesthetized animals. Furthermore, this also contrasts with the ability of glutamate, given into the RVLM, to enhance the sympathetic baroreflex, indicating that local glutamate-sensitive inputs may also play a role in modulating bar...

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits

Mayorov

Head

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The GABAergic cells of the CVLM that express Fos after PE are probably propriomedullary interneurons that provide inhibitory inputs to one or more classes of VLM neurons during activation of arterial baroreceptors and other cardiopulmonary afferents (Schreihofer and Guyenet, 2002). These GABAergic propriomedullary neurons lack projections to the spinal cord or the hypothalamus (Schreihofer and Guyenet, 2002) but they project to or through the RVLM (Jeske et al, 1993;Minson et al, 1997;Chan and Sawchenko, 1998), probably bilaterally (Li et al, 1991;Masuda et al, 1991;Minson et al, 1997). The presympathetic cells of the RVLM are among their likely targets (Jeske et al, 1993;Jeske et al, 1995;Blessing, 1997;Schreihofer and Guyenet, 2002).…”

Section: Pattern Of Fos Expression Induced By Pe In the Vlmmentioning

confidence: 97%

Fos expression by glutamatergic neurons of the solitary tract nucleus after phenylephrine‐induced hypertension in rats

Weston

Wang

Stornetta

et al. 2003

J of Comparative Neurology

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The baroreflex pathway might include a glutamatergic connection between the nucleus of the solitary tract (NTS) and a segment of the ventrolateral medulla (VLM) called the caudal ventrolateral medulla. The main goal of this study was to seek direct evidence for such a connection. Awake rats were subjected to phenylephrine- (PE-) induced hypertension (N=5) or received saline (N=5). Neuronal activation was gauged by the presence of Fos-immunoreactive (Fos-ir) nuclei. Fos-ir neurons that contained vesicular glutamate transporter 2 mRNA (glutamatergic neurons) or glutamic acid decarboxylase mRNA (GABAergic neurons) were mapped throughout the medulla oblongata. Saline-treated rats had very few Fos-ir neurons. In PE-treated rats, Fos-ir neurons were detected in both NTS and VLM. In NTS, 72% of Fos-ir neurons were glutamatergic and 26% were GABAergic. In the VLM, 41% of Fos-ir neurons were glutamatergic and 56% were GABAergic. In VLM, Fos-ir glutamatergic neurons were evenly distributed and were often catecholaminergic, whereas Fos-ir GABAergic cells were clustered around Bregma -13.0 mm. This region of the VLM was injected with Fluoro-Gold (FG) in eight rats, four of which received PE and the rest saline. Fos-ir NTS neurons retrogradely labeled with FG were detected only in PE-treated rats. These cells were exclusively glutamatergic and were concentrated within the NTS subnuclei that receive the densest inputs from arterial baroreceptors. In conclusion, PE, presumably via baroreceptor stimulation, induces Fos in glutamatergic and GABAergic neurons in both NTS and VLM. At least 29% of the Fos-ir glutamatergic neurons of NTS project to the vicinity of the VLM GABAergic interneurons that are presumed to mediate the sympathetic baroreflex.

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“…These would cause a rise in pressure and thus activate the baroreceptors and hence neurones in the nucleus tractus solitarii (NTS). The latter are known to project to the CVL [20,27]. Such a possibility is implied by the results reported by Porter and Brody [24] who have shown that a PVN pressor effect was enhanced following sino-aortic denervation.…”

Section: Discussionmentioning

confidence: 76%

“…These neurones displayed properties similar to the sympatho-inhibitory neurones in the baroreceptor reflex pathway that relay with cardiovascular premotor neurones of the RVL [1,2,10,17,20] and that have opposite characteristics to RVL neurones [8,11,26,27]. These CVL neurones were thus excited during a pressor response induced by i.v.…”

Section: Discussionmentioning

confidence: 91%

The influence of the paraventricular nucleus on baroreceptor dependent caudal ventrolateral medullary neurones of the rat

Yang

Coote

1999

Pfl�gers Archiv European Journal of Physiology

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The question of whether neurones in the paraventricular nucleus (PVN) of the hypothalamus have an influence on barosensitive vasomotor neurones of the caudal ventrolateral medulla (CVL) was addressed in this study using anaesthetised rats. Extracellular microelectrode recordings were made from 27 vasomotor neurones in the CVL, identified by their cardiac cycle-related probability of discharge, by the increase in activity in response to an increase in arterial blood pressure produced by i.v. phenylephrine and by the decrease in activity in response to a decrease in blood pressure produced by i.v. nitroprusside. Activation of neurones at different sites in the PVN with a microinjection of d,l-homocysteic acid (DLH) activated 12 CVL neurones and inhibited 6 CVL neurones. In four CVL units single-shock electrical stimulation at a PVN pressor site, first identified with DLH, elicited a synaptic action potential with a latency of 29+/-0.3 ms. It is concluded that PVN neurones can influence the CVL vasomotor neurones directly. This could be one means by which PVN-depressor and sympatho-inhibitory effects are produced.

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Neurons in the caudal ventrolateral medulla mediate the arterial baroreceptor reflex by inhibiting barosensitive reticulospinal neurons in the rostral ventrolateral medulla in rabbits

Cited by 52 publications

References 23 publications

Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits

Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits

Fos expression by glutamatergic neurons of the solitary tract nucleus after phenylephrine‐induced hypertension in rats

The influence of the paraventricular nucleus on baroreceptor dependent caudal ventrolateral medullary neurones of the rat

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