Evidence for a kynurenate-insensitive glutamate receptor in nucleus tractus solitarii

Pawloski-Dahm, Corinn M.; Gordon, Frank J.

doi:10.1152/ajpheart.1992.262.5.h1611

Cited by 44 publications

(45 citation statements)

References 19 publications

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“…On the other hand, (1S,3R)-ACPD injected in the CVLM produced dose-dependent decreases in blood pressure and SNA that are characteristic of stimulation of sympathoinhibitory neurons of this region. These observations bear a striking resemblance to the findings of Pawloski-Dahm and Gordon, 9 who showed that (rans-ACPD injected in the NTS evoked depressor responses. Although our data represent the first observations in rats that mGluR in the ventrolateral medulla may participate in cardiovascular regulation, our findings are in agreement with the preliminary report of McManigle et al 19 that trans-ACPD injected in the CVLM of cats decreased blood pressure and HR.…”

Section: Discussionsupporting

confidence: 85%

“…4 - 5 The pharmacological and functional characteristics of mGluR have been disclosed by using a selective mGluR agonist, (±)-l-aminocyclopentane-fran.s-l,3-dicarboxylic acid (frans-ACPD*). 6 - 8 Recently, Pawloski-Dahm and Gordon 9 showed that activation of mGluR by trans-ACPD injected in the nucleus tractus solitarii (NTS) evoked cardiovascular effects that were similar to those produced by Glu.…”

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confidence: 99%

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Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Tsuchihashi

Averill

1993

Hypertension

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We investigated the hypothesis that stimulation of metabotropic excitatory amino acid receptors in the ventrolateral medulla evokes cardiovascular responses. Thus, (15,3/?)-l-aminocyclopentane-l,3-dicarboxylic acid [(1S,3/J)-ACPD], a selective agonist of metabotropic excitatory amino acid receptors, was microinjected into the rostral or caudal ventrolateral medulla of halothane-anesthetized Sprague-Dawley rats. Microinjections of (lS,3/f)-ACPD (100 pmol-1 nmol) into the rostral ventrolateral medulla produced dose-dependent increases in mean arterial pressure (+20±4 mm Hg by 100 praol and +35±2 mm Hg by 1 nmol, p< 0.01 versus artificial cerebrospinal fluid) and integrated splanchnic sympathetic nerve activity (+17±3% and +46±4%, respectively, p<0.01), whereas (15,3/f)-ACPD microinjected into the caudal ventrolateral medulla decreased mean arterial pressure (-28±2 mm Hg by 100 pmol and -48±6 mm Hg by 1 nmol, p<0.01 versus artificial cerebrospinal fluid) and splanchnic sympathetic nerve activity (-24±4% and -49±5%, p<0.01). The blockade of ionotropic excitatory amino acid receptors by the combined injection of 2-amino-7-phosphonoheptanoic acid (200 pmol) and 6,7-dinitroquinoxaline-2,3-dione ( t is well appreciated that L-glutamate (Glu) is a primary excitatory neurotransmitter in the central nervous system. Glu or other excitatory amino acids (EAA) may act at receptors that are ligand-gated ion channels and are referred to as ionotropic EAA receptors.1 These receptors exhibit selective responsiveness to 7V-methyl-D-aspartic acid (NMDA), kainic acid, or a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA);

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Section: Discussionsupporting

confidence: 85%

mentioning

confidence: 99%

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Tsuchihashi

Averill

1993

Hypertension

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“…A possible explanation is that the increase in AP was presumably due to vasoconstriction in mesenteric arteries [4,13] but also partly in consequence of a rise in cardiac output (tachycardia). The increase in AP baseline following suramin or kynurenate microinjected into the NTS was similar to reports in previous studies [35][36][37][38]. Although the cardiovascular changes reverted to resting values prior to injections after ∼20-30 min, the receptors remained blocked by the antagonists that were tested by respective agonists.…”

Section: Hindlimb Vasodilation In Alerting-defense Responses Is Mediasupporting

confidence: 89%

Interaction of medullary P2 and glutamate receptors mediates the vasodilation in the hindlimb of rat

Korim

Ferreira-Neto

Pedrino

et al. 2012

Purinergic Signalling

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In the nucleus tractus solitarii (NTS) of rats, blockade of extracellular ATP breakdown to adenosine reduces arterial blood pressure (AP) increases that follow stimulation of the hypothalamic defense area (HDA). The effects of ATP on NTS P2 receptors, during stimulation of the HDA, are still unclear. The aim of this study was to determine whether activation of P2 receptors in the NTS mediates cardiovascular responses to HDA stimulation. Further investigation was taken to establish if changes in hindlimb vascular conductance (HVC) elicited by electrical stimulation of the HDA, or activation of P2 receptors in the NTS, are relayed in the rostral ventrolateral medulla (RVLM); and if those responses depend on glutamate release by ATP acting on presynaptic terminals. In anesthetized and paralyzed rats, electrical stimulation of the HDA increased AP and HVC. Blockade of P2 or glutamate receptors in the NTS, with bilateral microinjections of suramin (10 mM) or kynurenate (50 mM) reduced only the evoked increase in HVC by 75 % or more. Similar results were obtained with the blockade combining both antagonists. Blockade of P2 and glutamate receptors in the RVLM also reduced the increases in HVC to stimulation of the HDA by up to 75 %. Bilateral microinjections of kynurenate in the RVLM abolished changes in AP and HVC to injections of the P2 receptor agonist α,β-methylene ATP (20 mM) into the NTS. The findings suggest that HDA-NTS-RVLM pathways in control of HVC are mediated by activation of P2 and glutamate receptors in the brainstem in alerting-defense reactions.

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“…Perhaps compensatory mechanisms in the contralateral NTS prevent the baseline BP from rising. Consistent with this explanation are the reports that bilateral blockade of glutamate receptors in the NTS are necessary to increase the baseline BP (24). Furthermore, blockade of ionotropic as well as metabotropic glutamate receptors in the NTS may be necessary to elevate baseline BP (11).…”

Section: Discussionmentioning

confidence: 58%

Mechanism of cardiovascular effects of nociceptin microinjected into the nucleus tractus solitarius of the rat

Chitravanshi

Sapru

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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.62, and 1.25 mmol/l of nociceptin into the medial nucleus tractus solitarius (mNTS) elicited decreases in mean arterial pressure (11 Ϯ 1.8, 20 Ϯ 2.1, 21.5 Ϯ 3.1, and 15.5 Ϯ 1.9 mmHg, respectively) and heart rate (14 Ϯ 2.7, 29 Ϯ 5.5, 39 Ϯ 5.2, and 17.5 Ϯ 3.1 beats/min, respectively). Because maximal responses were elicited by microinjections of 0.62 mmol/l nociceptin, this concentration was used for other experiments. Repeated microinjections of nociceptin (0.62 mmol/l) into the mNTS, at 20-min intervals, did not elicit tachyphylaxis. Bradycardia induced by microinjections of nociceptin into the mNTS was abolished by bilateral vagotomy. The decreases in mean arterial pressure and heart rate elicited by nociceptin into the mNTS were blocked by prior microinjections of the specific ORL1-receptor antagonist [N-Phe 1 ]-nociceptin-(1-13)-NH2 (9 mmol/l). Microinjections of the ORL1-receptor antagonist alone did not elicit a response. Prior combined microinjections of GABA A and GABAB receptor antagonists (2 mmol/l gabazine and 100 mmol/l 2-hydroxysaclofen, respectively) into the mNTS blocked the responses to microinjections of nociceptin at the same site. Prior microinjections of ionotropic glutamate receptor antagonists (2 mmol/l NBQX and 5 mmol/l D-AP7) also blocked responses to nociceptin microinjections into the mNTS. These results were confirmed by direct neuronal recordings. It was concluded that 1) nociceptin inhibits GABAergic neurons in the mNTS, 2) GABAergic neurons may normally inhibit the release of glutamate from the terminals of peripheral afferents in the mNTS, and 3) inhibition of GABAergic neurons by nociceptin results in an increase in the release of glutamate in the mNTS, which in turn elicits depressor and bradycardic responses via activation of ionotropic glutamate receptors on secondary mNTS neurons. bradycardia; depressor responses; opioid peptides THE PRESENCE OF A NOVEL G-protein-coupled receptor [opioid receptor-like receptor (ORL1) or OP 4 receptor] throughout the central nervous system has been repeatedly demonstrated (1, 3, 6, 12, 18, 20 -22). There is a high sequence similarity of this receptor with other opioid receptors (e.g., -, ␦-, and -receptors) (3,6,21,36). Nociceptin (orphanin FQ) (4, 25, 26), a heptadecapeptide, has been demonstrated to be an endogenous ligand of ORL1 receptor because of its high and selective affinity for this receptor and a very poor affinity for -, ␦-, and -opioid receptors. One notable difference between other opioid receptor agonists (e.g., endomorphins, enkephalins, and dynorphin A) and nociceptin is that naloxone blocks the effects of these opioid receptor agonists but not those of nociceptin (4,5,13,16,29).The presence of an endogenous ligand for ORL1 receptors (nociceptin or orphanin FQ) has been demonstrated throughout the central nervous system, including the nucleus tractus solitarius (NTS) (10, 23, 35). There are very few reports in which the cardiovascular effects of ORL1 receptor activation by nociceptin in the medial nucleus tractus solitarius (m...

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Evidence for a kynurenate-insensitive glutamate receptor in nucleus tractus solitarii

Cited by 44 publications

References 19 publications

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Interaction of medullary P2 and glutamate receptors mediates the vasodilation in the hindlimb of rat

Mechanism of cardiovascular effects of nociceptin microinjected into the nucleus tractus solitarius of the rat

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