Nitric oxide (NO): in vivo electrochemical monitoring in the dorsal horn of the spinal cord of the rat

Rivot, J.P.; Barraud, Jérémie; Montécot, Céline; Jost, Bernard; Besson, Jean‐Marie

doi:10.1016/s0006-8993(97)00898-6

Cited by 30 publications

(22 citation statements)

References 47 publications

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“…The present data further concur with a recent report by Rivot et al [21] who showed that continuous NO production occurs within the nervous tissue, is enhanced by NMDA, and can be modified by NOS inhibitors and NO donors. Similarly, using the calibration curve obtained from in vitro experiments, the mean amplitude of the oxidation current generated during basal conditions within the tissue would correspond to F0.15 ÌM in the young pups and F0.4-0.5 ÌM in the adult rat, the latter values being strikingly similar to those previously reported in the rat [18].…”

Section: Discussionsupporting

confidence: 82%

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Gozal

Torres²

2001

Neonatology

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Gasping is an important mechanism for survival that appears to be developmentally modulated by the glutamate-nitric oxide (NO) pathway. However, the temporal characteristics of NO brain tissue levels during gasping are unknown. We hypothesized that during anoxia-induced gasping, the gasping frequency would be closely correlated with caudal brainstem tissue NO concentrations in developing rats. Brainstem and cortical tissue NO levels were measured during anoxia using a voltammetric electrode in adult rats and 5-day-old pups during control conditions and following pretreatment with the NMDA receptor antagonist MK-801 (1 mg/kg) or the neuronal NO synthase inhibitor 7-nitro-indazole (7-NI; 100 mg/kg). In young animals, NO tissue levels followed a triphasic trajectory coincident with gasp frequency which was markedly altered by MK-801 and 7-NI, albeit with preservation of gasp frequency-NO tissue level relationships. In adult rats, 40-fold higher NO tissue levels occurred and followed a monophasic trajectory coincident with gasp patterning. In the cortex, monophasic increases in NO levels occurred at all ages. We conclude that anoxia-induced gasping neurogenesis is modulated via NMDA-NO mechanisms in the developing rat. We postulate that higher NO brainstem concentrations may favor early autoresuscitation, but limit anoxic tolerance.

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Section: Discussionsupporting

confidence: 82%

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Gozal

Torres²

2001

Neonatology

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“…In rat cerebellar slices, electrical stimulation elevated NO by ϳ6 -60 nM (Shibuki, 1990;Maffei et al, 2003). In contrast, Rivot et al (1997) estimated a basal extracellular NO concentration of ϳ0.5 M in rat dorsal horn, and concentrations exceeding 3 M were reported after electrical stimulation of sensory neurons (Schulte and Millar, 2003). These discrepancies may reflect different production rates and/or different methods used to measure NO.…”

Section: Robustness Of Predicted Spread To Altering the Parameter Valuesmentioning

confidence: 90%

Modeling Cooperative Volume Signaling in a Plexus of Nitric Oxide Synthase-Expressing Neurons

Philippides¹,

Ott²,

Husbands³

et al. 2005

J. Neurosci.

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Invertebrateandinvertebratebrains,nitricoxide(NO)synthase(NOS)isfrequentlyexpressedinextensivemeshworks(plexuses)ofexceedingly fine fibers. In this paper, we investigate the functional implications of this morphology by modeling NO diffusion in fiber systems of varying fineness and dispersal. Because size severely limits the signaling ability of an NO-producing fiber, the predominance of fine fibers seems paradoxical. Our modeling reveals, however, that cooperation between many fibers of low individual efficacy can generate an extensive and strong volume signal. Importantly, the signal produced by such a system of cooperating dispersed fibers is significantly more homogeneous in both space and time than that produced by fewer larger sources. Signals generated by plexuses of fine fibers are also better centered on the active region and less dependent on their particular branching morphology. We conclude that an ultrafine plexus is configured to target a volume of the brain with a homogeneous volume signal. Moreover, by translating only persistent regional activity into an effective NO volume signal, dispersed sources integrate neural activity over both space and time. In the mammalian cerebral cortex, for example, the NOS plexus would preferentially translate persistent regional increases in neural activity into a signal that targets blood vessels residing in the same region of the cortex, resulting in an increased regional blood flow. We propose that the fineness-dependent properties of volume signals may in part account for the presence of similar NOS plexus morphologies in distantly related animals.

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“…The oxidation current from NO was monitored with carbon fiber microelectrodes 15 implanted into the frontal cortex. Variations in the height of the NO peak were continuously monitored (one measurement every 2 minutes) with a Biopulse system (Tacussel, France) and computerized (analog/digital interface; National Instruments).…”

Section: Cortical No Detectionmentioning

confidence: 99%

“…The effect of iNO was associated with increased arterial blood flow velocities and cortical CBF in the ischemic penumbra during ischemia. In contrast, iNO exposure during reperfusion was detrimental to the P7 rat brain.Using the same voltammetric device, 15,17,18 we first observed that in control P7 rat pups, iNO was able to increase NO concentrations in the cerebral cortex, where significant amounts of NO seem to be produced continuously even under basal conditions. 19 This increase in NO availability, despite long-lasting inhalation (over 90 minutes), reached a steady state, whereas an NO donor continually increases NO concentrations during its administration.…”

mentioning

confidence: 97%

Inhaled Nitric Oxide Reduces Brain Damage by Collateral Recruitment in a Neonatal Stroke Model

Charriaut‐Marlangue

Bonnin

Gharib

et al. 2012

Stroke

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N eonatal hypoxia-ischemia is a common cause of neonatal brain injury and results in cerebral palsy, learning disabilities, and epilepsy.1 In addition to global cerebral ischemia arising from systemic asphyxia, recent data suggest a higher incidence of focal ischemia-reperfusion leading to stroke in near-term neonates.2 Tissue-type plasminogen activator is the only approved agent capable of improving reperfusion after ischemia in the adult brain. 3 However, no safe neuroprotective molecule is currently available to protect the immature brain.Among vasoactive molecules, nitric oxide (NO) is a small, highly diffusible and reactive molecule produced by the NO synthases and released from endothelial cells 4 and perivascular nitrergic neurons. 5,6 Endogenous NO is widely recognized as an important messenger and effector molecule for vascular tone and tolerance to damage as well as a mediator in a variety of acute and chronic inflammatory systems. 7 NO is also involved in several critical processes in the developing brain; indeed, exposure to inhaled NO (iNO) during the first week of postnatal life has recently been shown to play a key role in myelination in the developing brain 8 and to significantly reduce the size of excitotoxic lesions in neonatal rat pups. 9 We recently demonstrated, by using 2-dimensional color-coded pulsed ultrasound imaging, that collateral recruitment or failure during ischemia, as revealed by changes in blood flow velocities in the basilar trunk (BT), determined the extent of the ischemic lesion in P7 rats 10 and wasBackground and Purpose-We recently demonstrated that endogenous nitric oxide (NO) modulates collateral blood flow in a neonatal stroke model in rats. The inhalation of NO (iNO) has been found to be neuroprotective after ischemic brain damage in adults. Our objective was to examine whether iNO could modify cerebral blood flow during ischemiareperfusion and reduce lesions in the developing brain. Methods-In vivo variations in cortical NO concentrations occurring after 20-ppm iNO exposure were analyzed using the voltammetric method in P7 rat pups. Inhaled NO-mediated blood flow velocities were measured by ultrasound imaging with sequential Doppler recordings in both internal carotid arteries and the basilar trunk under basal conditions and in a neonatal model of ischemia-reperfusion. The hemodynamic effects of iNO (5 to 80 ppm) were correlated with brain injury 48 hours after reperfusion. Results-Inhaled NO (20 ppm) significantly increased NO concentrations in the P7 rat cortex and compensated for the blockade of endogenous NO synthesis under normal conditions. Inhaled NO (20 ppm) during ischemia increased blood flow velocities and significantly reduced lesion volumes by 43% and cellular damage. In contrast, both 80 ppm iNO given during ischemia and 5 or 20 ppm iNO given 30 minutes after reperfusion were detrimental. Blood flow increases in the BT mirror the efficiency of collateral support through the circle of Willis and the opening of cortical arterial anastomoses among anter...

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Nitric oxide (NO): in vivo electrochemical monitoring in the dorsal horn of the spinal cord of the rat

Cited by 30 publications

References 47 publications

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Modeling Cooperative Volume Signaling in a Plexus of Nitric Oxide Synthase-Expressing Neurons

Inhaled Nitric Oxide Reduces Brain Damage by Collateral Recruitment in a Neonatal Stroke Model

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