The Case for the Bulbospinal Respiratory Nitric Oxide Synthase-Immunoreactive Pathway in the Dog

Maršala, J; Lukáčová, Nadežda; Čı́žková, Dáša; Kafka, Jozef; Katsube, Nobuo; Kuchárová, Karolı́na; Maršala, Martin

doi:10.1006/exnr.2002.7978

Cited by 18 publications

(20 citation statements)

References 64 publications

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“…Monosynaptic connections have been demonstrated between the bulbospinal neurons and phrenic motoneurons (1,2). These connections mediate the respiratory drive to respiratory motoneurons (3,4).…”

Section: Introductionmentioning

confidence: 98%

Differential Expression of Adenosine A₁and A_2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Petrov

Kreipke

Alilain

et al. 2007

The Journal of Spinal Cord Medicine

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Background: In an animal model of spinal cord injury, a latent respiratory motor pathway can be pharmacologically activated via adenosine receptors to restore respiratory function after cervical (C2) spinal cord hemisection that paralyzes the hemidiaphragm ipsilateral to injury. Although spinal phrenic motoneurons immunopositive for adenosine receptors have been demonstrated (C3-C5), it is unclear if adenosine receptor protein levels are altered after C2 hemisection and theophylline administration.Objective: To assess the effects of C2 spinal cord hemisection and theophylline administration on the expression of adenosine receptor proteins.Methods: Adenosine A 1 and A 2A receptor protein levels were assessed in adult rats classified as (a) noninjured and theophylline treated, (b) C2 hemisected, (c) C2 hemisected and administered theophylline orally (33 daily) for 3 days only, and (d) C2 hemisected and administered theophylline (33 daily for 3 days) and assessed 12 days after drug administration. Assessment of A 1 protein levels was carried out via immunohistochemistry and A 2A protein levels by densitometry.Results: Adenosine A 1 protein levels decreased significantly (both ipsilateral and contralateral to injury) after C2 hemisection; however, the decrease was attenuated in hemisected and theophylline-treated animals. Attenuation in adenosine A 1 receptor protein levels persisted when theophylline administration was stopped for 12 days prior to assessment. Adenosine A 2A protein levels were unchanged by C2 hemisection; however, theophylline reduced the levels within the phrenic motoneurons. Furthermore, the decrease in A 2A levels persisted 12 days after theophylline was withdrawn.Conclusion: Our findings suggest that theophylline mitigates the effects of C2 hemisection by attenuating the C2 hemisection-induced decrease in A 1 protein levels. Furthermore, A 2A protein levels are unaltered by C2 hemisection but decrease after continuous or interrupted theophylline administration. The effects on protein levels may underlie the stimulant actions of theophylline.

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Section: Introductionmentioning

confidence: 98%

Differential Expression of Adenosine A₁and A_2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Petrov

Kreipke

Alilain

et al. 2007

The Journal of Spinal Cord Medicine

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“…Large NADPH-diaphorase-exhibiting reticulospinal neurons are localized in this region, which is known for its rich network of arterioles and capillaries (Gobel et al, 1990;Richerson et al, 2001). It should be noted that the increase in the number of NADPHdiaphorase-exhibiting neurons was also seen in the dorsal respiratory nuclei forming a part of the premotor descending pathway (Marsala et al, 2002), and are localized in the lateral part of the reticular formation. Greatest increase in NADPH-diaphorasestained neuropil was found in the ventral part of the medullar reticular nucleus (MdV).…”

Section: Discussionmentioning

confidence: 97%

“…An increase in NO production under some neuropathological conditions may result, due to increased activity of nitric oxide synthase which is histochemically detectable, in increased expression of a reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (Xu et al, 2000;Kucharova et al, 2001;Marsala et al, 2002). Nitric oxide may act as a neurotoxic agent in brain ischemia and hypoxia (Aldra et al, 1994;Nakashima et al, 1995).…”

Section: Introductionmentioning

confidence: 96%

Response of NADPH-Diaphorase-Exhibiting Neurons in the Medullar Reticular Formation to High Spinal Cord Injury

et al. 2004

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1. The effect of hemisection of the cervical spinal cord on NADPH-diaphorase staining in the reticular nuclei of the rabbit medulla was investigated using histochemical technique. 2. A quantitative assessment of somal and neuropil NADPH-diaphorase staining was made by an image analyzer in a selected area of each reticular nucleus of the rabbit medulla. 3. On the 7th postsurgery day, the highest up-regulation of somatic NADPH-diaphorase staining was observed in regions regulating cardiorespiratory processes; however, the highest increase of neuropil NADPH-diaphorase staining was found in the reticular nuclei modulating the tonus of postural muscles. 4. The degeneration of non-NADPH-diaphorase-stained neurons was detected throughout the reticular formation of the medulla, but the extent of neuronal death did not correlate with the up-regulation of the NADPH-diaphorase staining in the reticular nuclei of the medulla. 5. The findings provide evidence that NADPH-diaphorase-exhibiting neurons are refractory to the hemisection of the cervical spinal cord and that the neuronal up-regulation of NADPH-diaphorase at the medullar level is probably not a causative factor leading to the death of the reticulospinal neurons.

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“…However, in sepsis, overproduction of NO, and as a result the excessive opening of K ATP in vascular smooth muscles and diaphragm, has been well known to be related to the genesis of hypotension [28][29][30][31] and diaphragmatic dysfunction [32][33][34] ; and inhibition of NO production and/or blockade of K ATP opening have been suggested as prospective procedures for sepsis treatment. Neuronal NOS (nNOS) expression in local neurons or neuronal terminals has been identified in almost all respiratory-related medullary/spinal nuclei such as the rhythmogenesis center pre-Bötzinger complex [5] , respiratory motoneurons [5,8] , and the sensory relay nuclei of the nucleus of solitary tract (NTS) [5][6][7][8] .…”

Section: Discussionmentioning

confidence: 99%

“…Neuroinflammatory factors may also contribute to abnormalities in respiratory movement, including nitric oxide (NO) and prostaglandins, and some cytokines may be upregulated in the brain in several diseases, such as meningitis and septic encephalopathy. Some of these factors such as NO [5][6][7][8][9][10][11][12][13][14][15][16][17][18] and prostaglandins [19][20][21] have been found to alter the frequency and the output intensity of central respiratory activity under both physiological and pathological conditions. Lipopolysaccharide (LPS) and interleukin-1 ␤ induced meningitis will result in disruption of blood brain barrier (BBB), blood-cerebrospinal fluid barrier (BCSFB) and blood-arachnoid barrier (BAB), as demonstrated by gadolinium-enhancement ratio imaging [22] .…”

mentioning

confidence: 99%

Nitric Oxide and ATP-Sensitive Potassium Channels Mediate Lipopolysaccharide-Induced Depression of Central Respiratory-Like Activity in Brain Slices

Wang

Chen

et al. 2012

Neurosignals

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Infection may result in early abnormalities in respiratory movement, and the mechanism may involve central and peripheral factors. Peripheral mechanisms include lung injury and alterations in electrolytes and body temperature, but the central mechanisms remain unclear. In the present study, brainstem slices harvested from rats were stimulated with lipopolysaccharide at different doses. Central respiratory activities as demonstrated by electrophysiological activity of the hypoglossal rootlets were examined and the mechanisms were investigated by inhibiting nitric oxide synthase and ATP-sensitive potassium channels. As a result, 0.5 µg/ml lipopolysaccharide mainly caused inhibitory responses in both the frequency and the output intensity, while 5 µg/ml lipopolysaccharide caused an early frequency increase followed by delayed decreases in both the frequency and the output intensity. At both concentrations the inhibitory responses were fully reversed by inhibition of nitric oxide synthase with Nω-nitro-L-arginine methyl ester hydrochloride (20 µM), and by inhibition of ATP- sensitive potassium channels with glybenclamide (100 µM). These results show that direct lipopolysaccharide challenge altered central respiratory activity in dose- and time- related manners. Nitric oxide synthase and ATP-sensitive potassium channels may be involved in the respiratory changes.

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The Case for the Bulbospinal Respiratory Nitric Oxide Synthase-Immunoreactive Pathway in the Dog

Cited by 18 publications

References 64 publications

Differential Expression of Adenosine A₁and A_2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Differential Expression of Adenosine A₁and A_2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Response of NADPH-Diaphorase-Exhibiting Neurons in the Medullar Reticular Formation to High Spinal Cord Injury

Nitric Oxide and ATP-Sensitive Potassium Channels Mediate Lipopolysaccharide-Induced Depression of Central Respiratory-Like Activity in Brain Slices

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The Case for the Bulbospinal Respiratory Nitric Oxide Synthase-Immunoreactive Pathway in the Dog

Cited by 18 publications

References 64 publications

Differential Expression of Adenosine A1and A2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Differential Expression of Adenosine A1and A2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Response of NADPH-Diaphorase-Exhibiting Neurons in the Medullar Reticular Formation to High Spinal Cord Injury

Nitric Oxide and ATP-Sensitive Potassium Channels Mediate Lipopolysaccharide-Induced Depression of Central Respiratory-Like Activity in Brain Slices

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Differential Expression of Adenosine A₁and A_2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats

Differential Expression of Adenosine A₁and A_2AReceptors After Upper Cervical (C2) Spinal Cord Hemisection in Adult Rats