Localization of vagal cardioinhibitory preganglionic neurons within rat brain stem

Nosaka, Shoichiro; Yamamoto, Tetsuro; Yasunaga, K

doi:10.1002/cne.901860106

Cited by 218 publications

(87 citation statements)

References 30 publications

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“…Data demonstrating the existence ofcardiovagal neurons in the DMNV are equivocal and probably species dependent (Spyer,198 1). At least one report has demonstrated DMNV-mediated alteration ofheart rate in the rat (Nosaka et al, 1979). Although the present study was not aimed directly at this question, the observation that Glu could elicit responses (at ventral NTS sites near the level of the obex) that were totally abolished by atropine administration does suggests DMNV cardiovagal neurons in the rat.…”

Section: Discussionmentioning

confidence: 66%

Cardiovascular function is altered by picomole injections of glutamate into rat medulla

et al. 1988

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Local neural circuitry in the nucleus tractus solitarius (NTS) involved in cardiovascular control was studied by injecting nanoliter volumes of excitatory amino acids into the structure. Experiments were performed on urethane-anesthetized, artificially ventilated rats. Multibarrel micropipettes were used for pressure ejection of drugs or a dye for marking ejection sites. Ejected volumes, ranging from 200 pl to 25 nl, were directly monitored for every injection. Injections of as little as 200 fmol of L-glutamate in 200 pl into the medial and lateral NTS region rostral to the obex elicited marked, site-specific decreases in arterial pressure and heart rate. The majority of these responses were eliminated by blockade of parasympathetic and sympathetic neural outflow. At sites caudal to obex, in the commissural region of the NTS, L-glutamate injections produced marked elevations in heart rate and arterial pressure which were sympathetically mediated. Responses to L- glutamate were attenuated by concurrent injection of glutamic acid diethyl ester and DL-2-amino-4-phosphonobutyrate, or lidocaine. These results indicate a heterogeneity in the spatial organization of brain- stem circuitry underlying cardiovascular control that has not been previously described.

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Section: Discussionmentioning

confidence: 66%

Cardiovascular function is altered by picomole injections of glutamate into rat medulla

et al. 1988

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“…However, it is likely that Hcrt-1-activated neurons that primarily projected directly to the nucleus ambiguus (34), the site of origin of vagal cardioinhibitory axons (31), and to a lesser extent, to caudal ventrolateral medullary neurons (5, 34) that inhibit rostral ventrolateral sympathetic premotor neurons (5). This would be consistent with the observation that the bradycardia response is mediated by vagal activation and the depressor response, in part, by sympathoinhibition.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of hypocretin-1 in nucleus of the solitary tract

Oliveira

Rosas‐Arellano

Solano-Flores

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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lar effects of hypocretin-1 in nucleus of the solitary tract. Am J Physiol Heart Circ Physiol 284: H1369-H1377, 2003. First published December 12, 2002 10.1152/ajpheart.00877.2002Experiments were done in male Wistar rats to investigate the effects of microinjection of hypocretin-1 (Hcrt-1) into the nucleus of the solitary tract (NTS) on mean arterial pressure (MAP), heart rate (HR), and the baroreflex. In the first series, the distribution of Hcrt-1-like immunoreactivity (Ir) was mapped within the region of NTS. Hcrt-1 Ir was found throughout the NTS region, predominantly within the caudal dorsolateral (Slt), medial (Sm), and interstitial subnuclei of the NTS. In the second series, in ␣-chloralose or urethaneanesthetized rats, microinjection of Hcrt-1 (0.5-5 pmol) into the caudal NTS elicited a dose-dependent decrease in MAP and HR. A mapping of the caudal NTS region showed that the largest depressor and bradycardia responses elicited by Hcrt-1 were from sites in the Slt and Sm. In addition, doses Ͼ2.5 pmol at a small number of sites localized to the caudal commissural nucleus of NTS elicited pressor and tachycardia responses. Intravenous administration of the muscarinic receptor blocker atropine methyl bromide abolished the bradycardia response and attenuated the depressor response, whereas subsequent administration of the nicotinic receptor blocker hexamethonium bromide abolished the remaining MAP response. Finally, microinjection of Hcrt-1 into the NTS significantly potentiated the reflex bradycardia to activation of arterial baroreceptors as a result of increasing MAP by systemic injections of phenylephrine (2-4 g/kg). These results suggest that Hcrt-1 in the NTS activates neuronal circuits that increases vagal activity to the heart, inhibits sympathetic activity to the heart and vasculature, and alters the excitability of NTS neuronal circuits that reflexly control the circulation.orexin-A; blood pressure; baroreceptor reflex; brain stem; ingestive behavior HYPOCRETIN (Hcrt) neuropeptides have been recently shown to be almost exclusively expressed within neurons of the lateral and perifornical hypothalamic areas (30,33,35,47,49). These peptides, Hcrt-1, a 33 amino-acid peptide with an NH 2 -terminal pyrogutalmyl residue, and Hcrt-2, a 28 amino acid peptide with a COOH-terminal amide (35), are de-

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“…The part of the NA that we stimulated or lesioned (1300 to 1700 fim rostral to the obex) corresponds to the ventrolateral responsive locus described by Nosaka et al, 7 which extends from the level of the obex to 2.000 /xm rostral from obex. The area studied also corresponds to that investigated by Stuesse and Fish,8 who showed that cardioinhibitory cells in the ventral medulla were found in the rostral NA.…”

Section: Discussionmentioning

confidence: 84%

Role of the nucleus ambiguus in the regulation of heart rate and arterial pressure.

Machado

Brody

1988

Hypertension

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SUMMARY The present study examined the effect of lesion of cell bodies in the nucleus ambiguus area on the development of neurogenic hypertension and further explored the cardiovascular responses produced by chemical and electrical stimulation of the nucleus ambiguus and the neighboring Cl region. Three days after chemical lesion of the nucleus ambiguus with kainic acid, arterial pressure and heart rate were unchanged; however, subsequent sinoaortic deafferentation produced a significantly greater increase of arterial pressure (157 ± 7 vs 132 ± 5 mm Hg) and heart rate (436 ± 10 vs 374 ± 10 beats/min) compared with those produced by sham lesion. Glutamate injected into the nucleus ambiguus increased arterial pressure and heart rate at 20 nmol/100 nl and decreased heart rate at 50 nmol/100 nl. Glutamate injected into the Cl area increased arterial pressure and heart rate at both doses. y-Aminobutyric acid at 50 nmol/100 nl produced bradycardia and a fall in arterial pressure when injected into both the nucleus ambiguus and Cl area. The heart rate responses to yaminobutyric acid and glutamate were attenuated in sinoaortic-deafferentated rats. The nucleus ambiguus and the Cl region were mapped using electrical stimulation with microelectrodes. All points stimulated in three anteroposterior sections in the nucleus ambiguus and the Cl area produced increases in arterial pressure, whereas bradycardia was restricted to the middle of three lateral coordinates associated with the center of the nucleus ambiguus and the Cl area ventral to the nucleus ambiguus. These data indicate that 1) chemical lesion of cell bodies of the nucleus ambiguus enhances the increase of arterial pressure after sinoaortic deafferentation and 2) electrical and chemical stimulation of the nucleus ambiguus area produce both bradycardia and increased arterial pressure. The results obtained with kainic acid lesions of the nucleus ambiguus suggest that this area exerts an inhibitory influence on sympathetic vasomotor tone that, when removed, could enhance the increase of arterial pressure after sinoaortic deafferentation. We conclude that the nucleus ambiguus is involved not only in heart rate control but also in central regulation of arterial pressure through pressor systems, and perhaps separately with neuronal projections associated with the baroreceptor reflex. (Hypertension 11: 602-607, 1988) KEY WORDS • cardiovascular regulation • baroreceptor reflex • sinoaortic deafferentation • electrical stimulation • glutamate • y-aminobutyric acid • kainic acid I N previous studies' we observed that electrolytic lesion of the nucleus ambiguus (NA) facilitates the development of hypertension in rats with sinoaortic deafferentation (SAD) and that electrical stimulation of the NA produces a bradycardic effect and an independent pressor response. These results suggested that the NA may be related to autonomic control not

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Localization of vagal cardioinhibitory preganglionic neurons within rat brain stem

Cited by 218 publications

References 30 publications

Cardiovascular function is altered by picomole injections of glutamate into rat medulla

Cardiovascular function is altered by picomole injections of glutamate into rat medulla

Cardiovascular effects of hypocretin-1 in nucleus of the solitary tract

Role of the nucleus ambiguus in the regulation of heart rate and arterial pressure.

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