In vivo electrochemical detection of nitric oxide release in the dorsal motor nucleus of the vagus after intracisternal administration of bombesin

Galanin plays an important role in the regulation of food intake, energy balance, and body weight. Many galanin-positive fibers as well as galanin-positive neurons were seen in the dorsal vagal complex, suggesting that galanin produces its effects by actions involving vagal neurons. In the present experiment, we used tract-tracing and neurophysiological techniques to evaluate the origin of the galaninergic fibers and the effect of galanin on neurons in the dorsal vagal complex. Our results reveal that the nucleus of the solitary tract is the major source of the galanin terminals in the dorsal vagal complex. In vivo experiments demonstrated that galanin inhibited the majority of gut-related neurons in the dorsal motor nucleus of the vagus. In vitro experiments demonstrated that galanin inhibited the majority of stomach-projecting neurons in the dorsal motor nucleus of the vagus by suppressing spontaneous activity and/or producing a fully reversible dose-dependent membrane hyperpolarization and outward current. The galanin-induced hyperpolarization and outward current persisted after synaptic input was blocked, suggesting that galanin acts directly on receptors of neurons in the dorsal motor nucleus of the vagus. The reversal potential induced by galanin was close to the potassium ion potentials of the Nernst equation and was prevented by the potassium channel blocker tetraethylammonium, indicating that the inhibitory effect of galanin was mediated by a potassium channel. These results indicate that the dorsal motor nucleus of the vagus is inhibited by galanin derived predominantly from neurons in the nucleus of the solitary tract projecting to the dorsal motor nucleus of the vagus nerve. Galanin is one of the neurotransmitters involved in the vago-vagal reflex.

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Methodological variables during analysis of in vivo cerebellar cyclic GMP, an indirect marker of nitric oxide release

Journal of Pharmacological and Toxicological Methods ◽

10.1016/1056-8719(94)90050-7 ◽

1994 ◽

Vol 31 (2) ◽

pp. 107-112 ◽

Cited By ~ 8

Author(s):

M. Bansinath ◽

B. Arbabha ◽

H. Turndorf ◽

U.C. Garg

Keyword(s):

Nitric Oxide ◽

Cyclic Gmp ◽

Nitric Oxide Release

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The inhibition by central bombesin of peripheral stimulation of gastric secretion involves the release of nitric oxide in the dorsal motor nucleus of the vagus

Gastroenterology ◽

10.1016/s0016-5085(98)80287-4 ◽

1998 ◽

Vol 114 ◽

pp. A72

Author(s):

B. Beltrán ◽

M.D. Barrachina ◽

R. Bello ◽

S. Calatayud ◽

J.V. Esplugues

Keyword(s):

Nitric Oxide ◽

Gastric Secretion ◽

Motor Nucleus ◽

Peripheral Stimulation ◽

Dorsal Motor Nucleus ◽

Stimulation Of

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P129. In vivo nitric oxide release is associated with lowered circulating cholesterol and albumin levels

Nitric Oxide ◽

10.1016/j.niox.2006.04.196 ◽

2006 ◽

Vol 14 (4) ◽

pp. 60

Author(s):

William Roediger ◽

C. Koh ◽

Irene Kanter ◽

Ray Morris

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Release

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Nitric oxide-mediated excitatory effect on neurons of dorsal motor nucleus of vagus

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1994.266.1.g154 ◽

1994 ◽

Vol 266 (1) ◽

pp. G154-G160 ◽

Cited By ~ 10

Author(s):

R. A. Travagli ◽

R. A. Gillis

Keyword(s):

Nitric Oxide ◽

Guanylate Cyclase ◽

Soluble Guanylate Cyclase ◽

Spontaneous Discharge ◽

Motor Nucleus ◽

Excitatory Effect ◽

Dorsal Motor Nucleus ◽

Ly 83583 ◽

Spontaneous Firing Rate

The purpose of our study was to explore whether nitric oxide was involved as an intercellular messenger in the dorsal motor nucleus of the vagus (DMV). To achieve this purpose we examined DMV motoneurons of the rat in vitro with the use of the extracellular cell-attached recording technique. The motoneurons, in general, exhibit a spontaneous discharge and when exposed to NO-producing drugs (i.e., 3-300 microM L-arginine and 10-100 microM S-nitroso-N-acetylpenicillamine) exhibit a concentration-related increase in their spontaneous firing rate. Because NO activates soluble guanylate cyclase and increases guanosine 3',5'-cyclic monophosphate (cGMP), we tested dibutyryl-cGMP (30-300 microM) and found that it also excites DMV neurons. Perfusion of the DMV neurons with N omega-nitro-L-arginine (300 microM), an inhibitor of NO synthase (NOS), and with NO scavenger, reduced hemoglobin (1 microM), counteracted the excitatory effect of L-arginine and N-methyl-D-aspartate (NMDA). Perfusion of the preparation with LY-83583 (10 microM), an inhibitor of guanylate cyclase, also counteracted the effects of L-arginine and NMDA. These data indicate that NOS is present in DMV neurons, and that the excitatory effect of NMDA on these neurons is due in part to formation of NO and the resulting accumulation of cGMP in DMV neurons.

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Stereoselective Differences in the Vasorelaxing Effects of S(+) and R(-) Ketamine on Rat Isolated Aorta

Anesthesiology ◽

10.1097/00000542-199803000-00023 ◽

1998 ◽

Vol 88 (3) ◽

pp. 718-724 ◽

Cited By ~ 5

Author(s):

Adriani Kanellopoulos ◽

Gunther Lenz ◽

Bernd Muhlbauer

Keyword(s):

Nitric Oxide ◽

Adenosine Triphosphate ◽

Blocking Agent ◽

Rat Aorta ◽

K Channel ◽

Nitric Oxide Synthase Inhibitor ◽

Nitric Oxide Release ◽

Racemic Ketamine ◽

Synthase Inhibitor

Background S(+) ketamine, because of its higher anesthetic potency and lower risk of psychotomimetic reactions, has been suggested to be superior to presently available racemic ketamine. The racemate is a direct vasodilator in vivo, and thus the authors investigated the vasorelaxing effects of ketamine enantiomers on rat aorta. Methods Rat isolated aortic rings with and without endothelium were contracted with 3 x 10(-7) M norepinephrine. Then 10(-5) to 3 x 10(-3) M S(+), R(-), or racemic ketamine were added cumulatively. Vascular responses to ketamine were further studied in rings pretreated with the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine (NNLA), the adenosine triphosphate-sensitive K+ channel antagonist glibenclamide, and the L-type calcium channel blocking agent D888. Results Ketamine enantiomers and the racemate produced concentration-dependent vasorelaxation. The relaxing effect of S(+) ketamine was significantly weaker compared with R(-) ketamine and the racemate reflected by the half-maximum effective concentration (EC50) values of 11.6 x 10(-4), 4.8 x 10(-4), and 6 x 10(-4) M, respectively. Removal of the endothelium and NNLA or glibenclamide pretreatment did not significantly alter the vasorelaxing effect of ketamine. In contrast, D888 pretreatment significantly shifted the concentration-effect curves of both S(+) and R(-) ketamine rightward (EC50 values of 18.9 x 10(-4) and 8.5 x 10(-4) M, respectively), whereas the difference between the isomers was not affected. Conclusions Vasorelaxation by ketamine enantiomers is quantitatively stereoselective: The effect of S(+)ketamine is significantly weaker compared with that of the racemate and R(-) ketamine. This stereoselective difference is not due to nitric oxide release, activation of adenosine triphosphate-sensitive potassium channels, or differential inhibition of L-type calcium channels.

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