Neurotransmitters in the Nucleus Tractus Solitarius Mediating Cardiovascular Function

Sapru, Hreday N.

doi:10.1007/978-1-4419-9054-9_4

Cited by 20 publications

(22 citation statements)

References 67 publications

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“…Based on the available information regarding medullo-spinal cardiovascular regulatory areas (Coote, 2007;Gordon and Sved, 2002;Guyenet, 2006;Sapru, 2002Sapru, , 2004Talman et al, 1984), the following mechanism may be involved in mediating the cardiovascular responses elicited by MCH microinjections into the mNTS. MCH stimulates mNTS neurons as shown by direct pressure micro-applications of this peptide to these neurons.…”

Section: Discussionmentioning

confidence: 99%

“…The nucleus tractus solitarius (NTS) is one of the medullary structures that plays an important role in the central regulation of cardiovascular function (for reviews see: Coote, 2007;Gordon and Sved, 2002;Guyenet, 2006;Sapru, 2002Sapru, , 2004Talman et al, 1984). The presence of MCH containing fibers and MCH-1 receptors has been demonstrated in the NTS (Hervieu et al, 2000;Zamir et al, 1986a,b).…”

Section: Introductionmentioning

confidence: 99%

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Microinjections of melanin concentrating hormone into the nucleus tractus solitarius of the rat elicit depressor and bradycardic responses

et al. 2007

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The presence of melanin-concentrating hormone (MCH) containing processes, projecting from the lateral hypothalamus to the medial nucleus tractus solitarius (mNTS), has been reported in the rat. It was hypothesized that MCH acting within the mNTS may modulate the central regulation of cardiovascular function. This hypothesis was tested in urethane-anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (100 nl) of MCH (0.25, 0.5, 0.75, and 1 mM) into the mNTS of anesthetized rats elicited decreases in mean arterial pressure (20.4 ± 1.6, 50.7 ± 3.3, 35.7 ± 2.8 and 30.0 ± 2.6 mmHg, respectively). The decreases in heart rate in response to these concentrations of MCH were 40.0 ± 8.7, 90.0 ± 13.0, 48.0 ± 7.3 and 48.0 ± 8.0 beats/min, respectively. Maximum cardiovascular responses were elicited by a 0.5 mM concentration of MCH. Cardiovascular responses to MCH were similar in unanesthetized mid-collicular decerebrate rats. Control microinjections of normal saline (100 nl) did not elicit any cardiovascular response. Ipsilateral or bilateral vagotomy significantly attenuated MCH-induced bradycardia. Prior microinjections of PMC-3881-PI (2 mM; MCH-1 receptor antagonist) into the mNTS blocked the cardiovascular responses to microinjections of MCH. Microinjection of MCH (0.5 mM) into the mNTS decreased efferent greater splanchnic nerve activity. Direct application of MCH (0.5 mM; 4 nl) to barosensitive NTS neurons increased their firing rate. These results indicate that: 1) MCH microinjections into the mNTS activate MCH-1 receptors and excite barosensitive NTS neurons, causing a decrease in efferent sympathetic activity and blood pressure, and 2) MCH-induced bradycardia is mediated via the activation of the vagus nerves.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Microinjections of melanin concentrating hormone into the nucleus tractus solitarius of the rat elicit depressor and bradycardic responses

et al. 2007

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“…The nucleus tractus solitarius (NTS) is another area that is important in cardiovascular regulation (Sapru, 2004). It is well established that peripheral baroreceptor, chemoreceptor and cardiopulmonary afferents make their first synapse in the NTS.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of heart rate responses elicited by chemical stimulation of the hypothalamic paraventricular nucleus in the rat

et al. 2009

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This study was designed to examine the mechanism of heart rate (HR) responses elicited by the stimulation of hypothalamic paraventricular nucleus (PVN). Experiments were done in urethaneanesthetized, barodenervated, adult, male Wistar rats. Chemical stimulation of the PVN by unilateral microinjections of N-methyl-D-aspartic acid (NMDA) elicited increases in HR which were attenuated by bilateral vagotomy. PVN-induced tachycardia was also attenuated by the blockade of the spinal ionotropic glutamate receptors (iGLURs) which was accomplished by intrathecal injections at T9-T10 or direct application at T1-T4 of iGLUR antagonists. The blockade of spinal iGLURs combined with bilateral vagotomy completely blocked PVN-induced tachycardia. Blockade of GABA receptors in the medial nucleus tractus solitarius (mNTS) also attenuated the PVN-induced tachycardia. Complete blockade of PVN-induced tachycardia was also observed after the blockade of iGLURs in both the spinal cord and mNTS. Combination of the blockade of mNTS GABA receptors and spinal iGLURs also abolished PVN-induced tachycardia. PVN-induced tachycardia was not altered by the blockade of spinal vasopressin or oxytocin receptors at T1-T4. These results suggested that in barodenervated rats: 1) tachycardia elicited by the chemical stimulation of the PVN was mediated via both inhibition of vagal and activation of sympathetic outflows to the heart, 2) the vagal inhibition contributing to the PVN-induced tachycardia was mediated by the iGLURs and GABARs in the mNTS, 3) sympathetic activation contributing to the PVN-induced tachycardia was mediated via spinal iGLURs, and 4) spinal vasopressin and oxytocin receptors were not involved in the mediation of PVN-induced tachycardia.

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“…Inhibition of neurons in the NTS blocks several cardiovascular reflexes and produces increases in arterial pressure and sympathetic outflow, indicating a tonic sympathoinhibitory influence of the NTS (13,38,44,49). Similar to other brain regions, glutamate appears to be the primary excitatory neurotransmitter and GABA appears to be the primary inhibitory neurotransmitter in the NTS (2,26,37,43). Reductions in glutamatergic and enhancement of GABAergic neurotransmission in the NTS would tend to increase sympathetic nervous system activity and have been implicated in various forms of experimental hypertension (32,40,46).…”

mentioning

confidence: 95%

“…The nucleus tractus solitarius (NTS) is the primary termination site for cardiovascular afferents (9) and is an important brain region involved in both resting and reflex control of arterial pressure and sympathetic nervous system activity (2,37,43). Inhibition of neurons in the NTS blocks several cardiovascular reflexes and produces increases in arterial pressure and sympathetic outflow, indicating a tonic sympathoinhibitory influence of the NTS (13,38,44,49).…”

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confidence: 99%

Putative role of the NTS in alterations in neural control of the circulation following exercise training in rats

Mueller

Hasser

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Exercise training (ExTr) has been associated with alterations in neural control of the circulation, including effects on arterial baroreflex function. The nucleus tractus solitarius (NTS) is the primary termination site of cardiovascular afferents and critical in the regulation of baroreflex-mediated changes in heart rate (HR) and sympathetic nervous system outflow. The purpose of the present study was to determine whether ExTr is associated with alterations in neurotransmitter regulation of neurons involved in control of cardiovascular function at the level of the NTS. We hypothesized that ExTr would increase glutamatergic and reduce GABAergic transmission in the NTS and that, collectively, these changes would result in a greater overall sympathoinhibitory drive from the NTS in ExTr animals. To test these hypotheses, male Sprague-Dawley rats were treadmill trained or maintained under sedentary conditions for 8-10 wk. NTS microinjections were performed in Inactin-anesthetized animals instrumented to record mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Generalized activation of the NTS with unilateral microinjections of glutamate (1-10 mM, 30 nl) produced dose-dependent decreases in MAP, HR, and LSNA that were unaffected by ExTr. Bilateral inhibition of NTS with the GABAA agonist muscimol (1 mM, 90 nl) produced increases in MAP and LSNA that were blunted by ExTr. In contrast, pressor and sympathoexcitatory responses to bilateral microinjections of the ionotropic glutamate receptor antagonist, kynurenate (40 mM, 90 nl), were similar between groups. Bradycardic responses to bilateral microinjections of the GABAA antagonist bicuculline (0.1 mM, 90 nl) were attenuated by ExTr. These data indicate that alterations in neurotransmission at the level of the NTS contribute importantly to regulation of HR and LSNA in ExTr animals. In addition to alterations at NTS, these experiments suggest indirectly that changes in other cardiovascular nuclei contribute to the observed alterations in neural control of the circulation following ExTr.

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Neurotransmitters in the Nucleus Tractus Solitarius Mediating Cardiovascular Function

Cited by 20 publications

References 67 publications

Microinjections of melanin concentrating hormone into the nucleus tractus solitarius of the rat elicit depressor and bradycardic responses

Microinjections of melanin concentrating hormone into the nucleus tractus solitarius of the rat elicit depressor and bradycardic responses

Mechanism of heart rate responses elicited by chemical stimulation of the hypothalamic paraventricular nucleus in the rat

Putative role of the NTS in alterations in neural control of the circulation following exercise training in rats

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