Localization of nitric oxide synthase-immunoreactive neurons in the solitary nucleus and ventrolateral medulla oblongata of the rat: their relation to catecholaminergic neurons

Ohta, Akihiko; Takagi, Hiroshi; Matsui, Toshiyasu; Hamai, Yoko; Iida, Sachio; Esumi, Hiroyasu

doi:10.1016/0304-3940(93)90605-k

Cited by 90 publications

(45 citation statements)

References 16 publications

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“…Since NO was first discovered as an elusive endothelial-derived relaxing factor in 1987, extensive research efforts have been devoted to studying the function of NO in physiology and pathology [3][4][5] . To comprehensively understand the physiological roles of NO and to design new strategies to manipulate NO regulatory pathways for therapeutic purposes, it is desirable to probe the production and diffusion processes of NO in biological systems in real time.…”

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confidence: 99%

Real-time electrical detection of nitric oxide in biological systems with sub-nanomolar sensitivity

et al. 2013

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Real-time monitoring of nitric oxide concentrations is of central importance for probing the diverse roles of nitric oxide in neurotransmission, cardiovascular systems and immune responses. Here we report a new design of nitric oxide sensors based on hemin-functionalized graphene field-effect transistors. With its single atom thickness and the highest carrier mobility among all materials, graphene holds the promise for unprecedented sensitivity for molecular sensing. The non-covalent functionalization through p-p stacking interaction allows reliable immobilization of hemin molecules on graphene without damaging the graphene lattice to ensure the highly sensitive and specific detection of nitric oxide. Our studies demonstrate that the graphene-hemin sensors can respond rapidly to nitric oxide in physiological environments with a sub-nanomolar sensitivity. Furthermore, in vitro studies show that the graphene-hemin sensors can be used for the detection of nitric oxide released from macrophage cells and endothelial cells, demonstrating their practical functionality in complex biological systems.

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confidence: 99%

Real-time electrical detection of nitric oxide in biological systems with sub-nanomolar sensitivity

et al. 2013

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“…Vincent and Kimura (1992) first demonstrated the presence of NOS-immunoreactive neurons in the RVLM of rats, which was further confirmed by Ohta et al (1993) and Simonian and Herbison (1996). This morphological evidence implies a potentially functional involvement of RVLM local NO in the regulation of sympathetic outflow.…”

Section: Discussionmentioning

confidence: 53%

Simvastatin Inhibits Central Sympathetic Outflow in Heart Failure by a Nitric-Oxide Synthase Mechanism

Gao¹,

Wang²,

Zucker³

2008

J Pharmacol Exp Ther

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Our previous study demonstrated that oral treatment with simvastatin (SIM) suppressed renal sympathetic nerve activity (RSNA) in the rabbits with chronic heart failure (CHF). The purpose of this experiment was to determine the effects of direct application of SIM to the central nervous system on RSNA and its relevant mechanisms. Experiments were carried out on 21 male New Zealand White rabbits with pacing-induced CHF. The CHF rabbits received infusion of vehicle, SIM, or SIM ϩ N -nitro-L-arginine methyl ester into the lateral cerebral ventricle via osmotic minipump for 7 days. We found that 1) in CHF rabbits, intracerebroventricular infusion of SIM significantly suppressed basal RSNA (1st day 69.5 Ϯ 8.9% maximum; 7th day 26.0 Ϯ 6.0% maximum; P Ͻ 0.05, n ϭ 7) and enhanced arterial baroreflex function starting from the 2nd day and lasting through the following 5 days; 2) statin treatment significantly up-regulated neuronal nitric-oxide synthase (nNOS) protein expression in the rostral ventrolateral medulla (RVLM) (control, n ϭ 6, 0.12 Ϯ 0.04; SIMtreated, n ϭ 7, 0.31 Ϯ 0.05. P Ͻ 0.05); 3) in CATH.a neurons, incubation with SIM significantly up-regulated the nNOS mRNA expression, which was blocked by coincubation with mevalonate, farnesyl-pyrophosphate, or geranylgeranyl-pyrophosphate; and 4) incubation with Y-27632 [(R)-(ϩ)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide] significantly up-regulated nNOS mRNA expression in these neurons. These results suggest that central treatment with SIM decreased sympathetic outflow in CHF rabbits via up-regulation of nNOS expression in RVLM, which may be due to the inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase and a decrease in Rho kinase by SIM.Chronic heart failure (CHF) is characterized by both sympatho-excitation (Packer, 1992) and blunted arterial baroreflex function (DiBona and Sawin, 1995). Our previous studies demonstrated that oral treatment with the HMG-CoA reductase inhibitor, simvastatin (SIM), improved baroreflex function and normalized sympathetic outflow in the rabbits with CHF (Pliquett et al., 2003). In previous experiments, we have demonstrated that these therapeutic effects of SIM correlated with changes in several important signaling molecules in the rostral ventrolateral medulla (RVLM) of rabbits with CHF (Gao et al., 2005a). These experiments were based on systemic (oral) administration of SIM. Therefore, it is difficult to determine whether these effects were mediated by central or peripheral mechanisms following oral administration of SIM. Because SIM has been demonstrated to permeate the blood-brain barrier (Saheki et al., 1994), we postulated that the above effects of oral SIM were mediated, at least partially, by central mechanisms. Our first hypothesis in the current experiment was that direct administration of SIM into the brain would reduce sympathetic nerve activity in the CHF state.There is considerable evidence suggesting that nitric oxide (NO) in the central nervous system, especially in the brain stem, plays an imp...

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“…[25,26,[30][31][32][33]. Numerous NOS-immunoreactive neurons have been detected throughout the NTS in the rostrocaudal direction.…”

Section: Anatomical Distribution Of Nitric Oxide Synthase In the Brainmentioning

confidence: 99%

“…It has been found that NOS and neuronal nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) at many brain sites are identical [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36]. [25,26,[30][31][32][33].…”

Section: Anatomical Distribution Of Nitric Oxide Synthase In the Brainmentioning

confidence: 99%

“…Figure 1 presents a schematic illustration of the formation of NO and the action of NO on target cells. NO synthase (NOS) is distributed throughout the central nervous system [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] including regions related to the regulation of cardiovascular functions. NO has been inferred not only to act directly on vascular vessels, but also to regulate circulation within the brain.…”

mentioning

confidence: 99%

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Central Control Mechanisms of Circulation in the Medulla Oblongata by Nitric Oxide.

Maeda¹,

Inoue²,

Takao³

et al. 1999

JJP

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reported that the relaxation of isolated rabbit aorta and other arteries induced by acetylcholine and other agonists for muscarinic receptors was dependent on the presence of endothelial cells within the preparations [2]. After removal of these cells, acetylcholine could no longer induce relaxation. Endothelium-dependent relaxation by acetylcholine results from the release of a diffusable relaxing substance, which was later termed endothelium-dependent relaxing factor (EDRF) [3,4]. It has been shown that this EDRF is nitric oxide (NO) [5][6][7]. Moreover, NO is involved in numerous physiological functions [8][9][10][11][12][13][14][15][16][17][18][19][20]. It inhibits platelet aggregation and adhesion and leukocyte adhesion, and modulates smooth muscle cell proliferation [8]. In the peripheral nervous system, NO is a mediator released by a widespread network of nerves [9][10][11]. It contributes to cytotoxicity against tumor cells, bacteria, viruses and microorganisms in activated macrophages [12][13][14]. In the brain, it has been shown that NO plays a physiological role in synaptic transmission by elevating the cyclic GMP (cGMP)

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Localization of nitric oxide synthase-immunoreactive neurons in the solitary nucleus and ventrolateral medulla oblongata of the rat: their relation to catecholaminergic neurons

Cited by 90 publications

References 16 publications

Real-time electrical detection of nitric oxide in biological systems with sub-nanomolar sensitivity

Real-time electrical detection of nitric oxide in biological systems with sub-nanomolar sensitivity

Simvastatin Inhibits Central Sympathetic Outflow in Heart Failure by a Nitric-Oxide Synthase Mechanism

Central Control Mechanisms of Circulation in the Medulla Oblongata by Nitric Oxide.

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