Involvement of nitric oxide in realization of the NMDA influence on the respiratory rhythm generated by medullo-spinal preparations of early postnatal rats

1998 ◽  
Vol 30 (1) ◽  
pp. 48-54
Author(s):  
D. V. Volgin
Keyword(s):  
Nitric Oxide ◽  
Respiratory Rhythm ◽  
Postnatal Rats

Involvement of NMDA receptors in the control of respiratory rhythm generated by medullo-spinal preparations of early postnatal rats

1998 ◽  
Vol 30 (2) ◽  
pp. 101-106
Author(s):  
D. V. Volgin ◽  
V. A. Marchenko ◽  
M. M. Seredenko ◽  
D. A. Vasilenko
Keyword(s):  
Nmda Receptors ◽  
Respiratory Rhythm ◽  
Postnatal Rats

Endogenous oestrogens do not regulate endothelial nitric oxide production in early postnatal rats

2015 ◽  
Vol 765 ◽  
pp. 598-605 ◽  
Author(s):  
Svetlana I. Sofronova ◽  
Dina K. Gaynullina ◽  
Andrey A. Martyanov ◽  
Olga S. Tarasova
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Endothelial Nitric Oxide ◽  
Postnatal Rats

Nitric oxide and respiratory rhythm in mammals: a new modulator of phase transition?

2007 ◽  
Vol 35 (5) ◽  
pp. 1258-1263 ◽  
Author(s):  
O. Pierrefiche ◽  
A.P.L. Abdala ◽  
J.F.R. Paton
Keyword(s):  
Nitric Oxide ◽  
Phase Transition ◽  
Soluble Guanylate Cyclase ◽  
Respiratory Rhythm ◽  
Central Pattern Generators ◽  
Cellular Level ◽  
Respiratory Neurons ◽  
No Donor ◽  
Respiratory Rhythmogenesis ◽  
Pattern Generators

NO (nitric oxide) modulates several central pattern generators, but its role in respiratory rhythmogenesis and its mode of action on medullary respiratory neurons during normoxia are unknown. We analysed the actions of NO on the mammalian respiratory network at the system and cellular levels. Given systemically, the NO donor diethylamine NONOate increased post-inspiratory duration in vagus, phrenic and hypoglossal nerves, whereas blockade of NO generation with L-NAME (NG-nitro-L-arginine methyl ester) produced the opposite response. At the cellular level, we pressure-ejected the NO donor on to respiratory neurons. NO had both inhibitory and excitatory effects on all types of respiratory neurons. Inhibitory effects involved soluble guanylate cyclase, as they were blocked with ODQ (1H-[1,2,4]oxadiazolo[4,3a]quinoxalin-1-one), whereas excitations were antagonized by uric acid and possibly mediated via peroxynitrite. Importantly, NO facilitated both GABA (γ-aminobutyric acid)- and NMDA (N-methyl-D-aspartate)-induced neuronal responses, but this was restricted to post-inspiratory and pre-inspiratory neurons; other neuron types showed additive effects only. Our results support NO as modulator of centrally generated respiratory activity and specifically of ligand-mediated responses in respiratory neuron types involved in respiratory phase transition.

Distribution and colocalization of neurotransmitters and receptors in the pre-Bötzinger complex of rats

2001 ◽  
Vol 91 (3) ◽  
pp. 1387-1395 ◽  
Author(s):  
Ying-Ying Liu ◽  
Gong Ju ◽  
Margaret T. T. Wong-Riley
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Respiratory Rhythm ◽  
Nucleus Ambiguus ◽  
Acid Decarboxylase ◽  
Adult Rats ◽  
Neurokinin 1 Receptor ◽  
Synaptic Interactions ◽  
Bötzinger Complex ◽  
Neurokinin 1

The pre-Bötzinger complex (PBC), thought to be the center of respiratory rhythm generation, is a cell column ventrolateral to the nucleus ambiguus. The present study analyzed its cellular and neurochemical composition in adult rats. PBC neurons were mainly oval, fusiform, or multipolar in shape and small to medium in size. Neurokinin-1 receptor, a marker of the PBC, was present in the plasma membrane of mostly medium and small neurons and their associated processes and boutons. Among neurons immunoreactive for different neurotransmitter or receptor candidates, various numbers were colocalized with neurokinin-1 receptor. The highest ratio was with nitric oxide synthase (52.72%), and the lowest was with glycine receptors (31.93%). Glutamic acid decarboxylase- and glycine transporter 2-immunoreactive boutons, as well as GABAA receptor-immunoreactive plasma membrane processes and boutons, were also identified in the PBC. PBC neurons exhibited different levels of cytochrome oxidase activity, indicating their various energy demands. Our results suggest that synaptic interactions within the PBC of adult rats involve a variety of neurotransmitter and receptor types and that nitric oxide may play an important role in addition to glutamate, GABA, glycine, and neurokinin.

Nitric Oxide Synthase Inhibitors Alter Ventilation in Isoflurane Anesthetized Rats 

1998 ◽  
Vol 88 (5) ◽  
pp. 1240-1248 ◽  
Author(s):  
Gaurav M. Patel ◽  
Damian J. Horstman ◽  
Milton J. Adams ◽  
George F. Rich
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Minute Ventilation ◽  
Respiratory Rhythm ◽  
Anesthetic Depth ◽  
Ventilatory Responses ◽  
Nos Inhibitors ◽  
Carbon Dioxide Levels ◽  
End Tidal ◽  
Oxide Synthase

Background Nitric oxide (NO) is present in medullary structures and can modulate respiratory rhythm. The authors determined if spontaneous ventilation at rest and in response to increased carbon dioxide is altered by selective neuronal NO synthase (NOS; 7-nitro-indazole, 7-NI) or nonselective (neuronal plus endothelial) NOS (NG-L-arginine methyl ester [L-NAME] and NG-monomethyl L-arginine [L-NMMA]) inhibitors in rats anesthetized with isoflurane. Methods Fifty-four rats received either L-NAME or L-NMMA (1, 10, and 30 mg/kg) or 7-NI (20, 80, and 400 mg/kg) and were compared with time controls (isoflurane = 1.4%), with isoflurane concentrations (1.6%, 1.8%, and 2%) increased consistent with the increased anesthetic depth caused by NOS inhibitors, or with L-arginine (300 mg/kg). Tidal volume (VT), respiratory frequency (f), minute ventilation (VE), and ventilatory responses to increasing carbon dioxide were determined. Results L-NAME and L-NMMA decreased resting VT and VE, whereas 7-NI had no effect. Increasing concentrations of isoflurane decreased resting f, VT, and VE. L-NAME and L-NMMA decreased VT and VE, whereas 7-NI had no effect at 8%, 9%, and 10% end-tidal carbon dioxide (ETCO2). Increasing concentrations of isoflurane decreased f, VT, and VE at 8%, 9%, and 10% ETCO2. The slope of VE versus ETCO2 was decreased by isoflurane but was unaffected by L-NAME, L-NMMA, or 7-NI. L-arginine alone had no effect on ventilation. Conclusions Nonselective NOS inhibitors decreased VT and VE at rest and at increased carbon dioxide levels but did not alter the slope of the carbon dioxide response. Selective neuronal NOS inhibition had no effect, suggesting that endothelial NOS may be the isoform responsible for altering ventilation. Finally, the cause of the decreased ventilation is not a result of the enhanced anesthetic depth caused by NOS inhibitors.

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