The effect of nitric oxide on synaptic vesicle proton gradient and mitochondrial potential of brain nerve terminals

Tarasenko, A. S.

doi:10.15407/ubj87.06.064

Cited by 4 publications

(7 citation statements)

References 36 publications

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“…Howe-ver, the picture drastically changed in the presence of 1 mM DTT in the incubation medium. According to the literature and our data, the biological effect of S-nitrosothiols, including SNAP, is significantly enhanced in the presence of low molecular mass thiols that is associated with the formation of the highly reactive intermediates and additional NO release due to fast SNAP cleavage [15,16]. As it is seen in Fig.…”

Section: Resultssupporting

confidence: 80%

“…It is known that the accumulation of neurotransmitters in the synaptic vesicles is coupled with proton transfer into the vesicles, so the increase in cytoplasmic GABA concentration might be due to disruption in the function of a vesicular H + -ATPase, which forms the H + -gradient. Previously, we have shown that the addition of SNAP/+DTT to synaptosomes caused a dissipation of the synaptic vesicle proton gradient that is most likely the result of cytosolic ATP depletion owing to inhibition of mitochondrial respiration by nitric oxide [15]. The maximum of H + -gradient dissipation was observed at the 10 th min that is fully correlated in time with the maximum of [ 3 H]GABA release from cytosol pool.…”

Section: Resultsmentioning

confidence: 77%

“…1, A), 10 min after addition of SNAP (100 µM) to [ 3 H]GABA-loaded synaptosome, the amount of the extrasynaptosomal neurotransmitter (minus basal release) was insignificant (1.1 ± 0.52%). This indicates that SNAP itself, which at this concentration spontaneously releases NO in a concentration of several nM [15], had little effect on the inhibitory neurotransmission. Howe-ver, the picture drastically changed in the presence of 1 mM DTT in the incubation medium.…”

Section: Resultsmentioning

confidence: 87%

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Effect of nitric oxide donor SNAP on GABA release from rat brain nerve terminals

Tarasenko¹

2016

Ukr.Biochem.J.

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In this work we investigated the effect of nanomolar concentrations of nitric oxide on the release of gamma-aminobutyric acid (GABA) from rat brain nerve terminals using a radioisotope method with [3H]GABA and a spectrofluorimetric method with Ca2+-sensitive probe Fluo-4 AM. It was shown that in the presence of dithiothreitol (DTT), nitric oxide donor SNAP at concentration, in which it produces NO in the nanomolar range, caused Ca2+-independent [3H]GABA release from nerve terminals. The applications of 4-aminopyridine (4-AP) and nipecotic acid (NA), as the inducers of GABA release from vesicular and cytoplasmic pools, showed that the maximum of SNAP/+DTT-induced [3H]GABA release was registered at 10th min of incubation and coincided in time with significant increase (almost double) in NA-induced [3H]GABA release. At this time point, 4-AP-induced release of [3H]GABA was drastically reduced. At the 15th min of incubation of nerve terminals with SNAP/+DTT, the opposite picture was observed: the decrease in NA- and increase in 4-AP-induced [3H]GABA release. Thus, nitric oxide in the form of S-nitrosothiols at nanomolar concentrations causes Ca2+-independent GABA leakage from synaptic vesicles into cytosol with subsequent release from nerve terminals. The reuptake of the neurotransmitter and its re-accumulation in synaptic vesicles occur later.

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Section: Resultssupporting

confidence: 80%

Section: Resultsmentioning

confidence: 77%

Section: Resultsmentioning

confidence: 87%

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Effect of nitric oxide donor SNAP on GABA release from rat brain nerve terminals

Tarasenko¹

2016

Ukr.Biochem.J.

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“…Stereoselectivity of effects of L-CSNO may involve its ability to enter cells via L-amino acid transporter (L-AT) systems, which do not transport D-CSNO ( Nemoto et al, 2003 ; Li and Whorton, 2007 ). Intracellular entry of L-CSNO via L-AT would allow it to modulate the activities/functions of signaling pathways ( Matsumoto et al, 2003 ; Burwell et al, 2006 ; Whalen et al, 2007 ; Forrester et al, 2009 ; Broniowska and Hogg, 2010 ; Iwakiri, 2011 ; Seth and Stamler, 2011 ; Piantadosi, 2012 ; Dejanovic and Schwarz, 2014 ; Tarasenko, 2015 ; Lin et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

“…Endogenous S-nitrosothiols (SNOs) regulate a variety of neural systems within the central ( Lei et al, 1992 ; Lipton et al, 1993 ; Lipton et al, 1994 ; Takahashi et al, 2007 ; Tegeder et al, 2011 ; Raju et al, 2015 ; Tarasenko, 2015 ; Nakamura and Lipton, 2016 ) and peripheral nervous systems ( Meller et al, 1990 ; Matsuda et al, 1995 ; Savidge, 2011 ; Lee et al, 2013 ; Tooker and Vigh, 2015 ; Gaston et al, 2020 ). SNOs exert their effects by mechanisms involving breakdown to nitric oxide (NO) followed by formation of dinitrosothiol-iron complexes that activate intracellular soluble guanylate cyclase and protein kinase G cell signaling ( Mellion et al, 1983 ; Travis et al, 1996 ; Severina et al, 2003 ; Lima et al, 2010 ; Martínez-Ruiz et al, 2013 ; Marozkina and Gaston, 2015 ; Vanin, 2019 ), and by S-nitrosylation (transfer of NO + ) of sulfur atoms within functional proteins ( Jaffrey et al, 2001 ; Joksovik et al, 2007 ; Foster et al, 2009 ; Lima et al, 2010 ; Rudkouskaya et al, 2010 ; Marozkina and Gaston, 2012 ; Anand et al, 2014 ; Pires da Silva et al, 2016 ; Wynia-Smith and Smith, 2017 ; Stomberski et al, 2019 ; Marozkina and Gaston, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

S-Nitroso-L-Cysteine Stereoselectively Blunts the Deleterious Effects of Fentanyl on Breathing While Augmenting Antinociception in Freely-Moving Rats

Getsy

Baby²,

Gruber³

et al. 2022

Front. Pharmacol.

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Endogenous and exogenously administered S-nitrosothiols modulate the activities of central and peripheral systems that control breathing. We have unpublished data showing that the deleterious effects of morphine on arterial blood-gas chemistry (i.e., pH, pCO2, pO2, and sO2) and Alveolar-arterial gradient (i.e., index of gas exchange) were markedly diminished in anesthetized Sprague Dawley rats that received a continuous intravenous infusion of the endogenous S-nitrosothiol, S-nitroso-L-cysteine. The present study extends these findings by showing that unanesthetized adult male Sprague Dawley rats receiving an intravenous infusion of S-nitroso-L-cysteine (100 or 200 nmol/kg/min) markedly diminished the ability of intravenous injections of the potent synthetic opioid, fentanyl (10, 25, and 50 μg/kg), to depress the frequency of breathing, tidal volume, and minute ventilation. Our study also found that the ability of intravenously injected fentanyl (10, 25, and 50 μg/kg) to disturb eupneic breathing, which was measured as a marked increase of the non-eupneic breathing index, was substantially reduced in unanesthetized rats receiving intravenous infusions of S-nitroso-L-cysteine (100 or 200 nmol/kg/min). In contrast, the deleterious effects of fentanyl (10, 25, and 50 μg/kg) on frequency of breathing, tidal volume, minute ventilation and non-eupneic breathing index were fully expressed in rats receiving continuous infusions (200 nmol/kg/min) of the parent amino acid, L-cysteine, or the D-isomer, namely, S-nitroso-D-cysteine. In addition, the antinociceptive actions of the above doses of fentanyl as monitored by the tail-flick latency assay, were enhanced by S-nitroso-L-cysteine, but not L-cysteine or S-nitroso-D-cysteine. Taken together, these findings add to existing knowledge that S-nitroso-L-cysteine stereoselectively modulates the detrimental effects of opioids on breathing, and opens the door for mechanistic studies designed to establish whether the pharmacological actions of S-nitroso-L-cysteine involve signaling processes that include 1) the activation of plasma membrane ion channels and receptors, 2) selective intracellular entry of S-nitroso-L-cysteine, and/or 3) S-nitrosylation events. Whether alterations in the bioavailability and bioactivity of endogenous S-nitroso-L-cysteine is a key factor in determining the potency/efficacy of fentanyl on breathing is an intriguing question.

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S-nitroso-L-cysteine stereoselectively blunts the adverse effects of morphine on breathing and arterial blood gas chemistry while promoting analgesia

Getsy

Young

Bates

et al. 2022

Biomedicine & Pharmacotherapy

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The effect of nitric oxide on synaptic vesicle proton gradient and mitochondrial potential of brain nerve terminals

Cited by 4 publications

References 36 publications

Effect of nitric oxide donor SNAP on GABA release from rat brain nerve terminals

Effect of nitric oxide donor SNAP on GABA release from rat brain nerve terminals

S-Nitroso-L-Cysteine Stereoselectively Blunts the Deleterious Effects of Fentanyl on Breathing While Augmenting Antinociception in Freely-Moving Rats

S-nitroso-L-cysteine stereoselectively blunts the adverse effects of morphine on breathing and arterial blood gas chemistry while promoting analgesia

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