Possible involvement of nitric oxide in the modulation of photolytic flash‐induced intercellular calcium waves in cultured astrocytes

Kikuchi, Kôichi; Iwabuchi, Sadahiro

doi:10.1002/nrc.10073

Cited by 3 publications

(3 citation statements)

References 15 publications

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“…We have also found that NO modulates the propagation of astrocytic Ca 2+ waves induced by the local photolysis of a caged Ca 2+ ionophore (22,23). In addition, Yun et al (24) have recently demonstrated that the activation of p21 RAS induced by NO derived from nNOS is responsible for the PC-induced tolerance of neurons, suggesting that NO is a key mediator in the process leading to resistance against lethal ischemia.…”

Section: Discussionsupporting

confidence: 56%

Nitric Oxide Produced During Sublethal Ischemia Is Crucial for the Preconditioning-Induced Down-Regulation of Glutamate Transporter GLT-1 in Neuron/Astrocyte Co-Cultures

et al. 2006

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Running head: nitric oxide and preconditioning-induced ischemic tolerance ------------------------------------------------------------------- AbstractIn the brain, prior sublethal ischemia (preconditioning, PC) produces tolerance of neurons to subsequent lethal ischemia. This study aims at elucidating whether and how nitric oxide (NO) produced during PC is involved in the PC-induced ischemic tolerance of neurons in neuron/astrocyte co-cultures. The rise in the extracellular concentration of glutamate during ischemia caused by the reversed uptake of glutamate (Glu) by the astrocytic Glu transporter GLT-1 was markedly suppressed by the prior PC treatment, but the suppression was reversed by treatment with an inhibitor of nitric oxide synthase (NOS) during PC. Immunocytochemical and Western blot analyses demonstrated that the expression of GLT-1 was down-regulated after the PC insult, and this down-regulation was also antagonized by treatment with NOS inhibitors during PC.Here we show that nNOS-derived NO produced during PC was crucial for the down-regulation of astrocytic GLT-1, and this down-regulation coincided with an increased survival rate of neurons.

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Section: Discussionsupporting

confidence: 56%

Nitric Oxide Produced During Sublethal Ischemia Is Crucial for the Preconditioning-Induced Down-Regulation of Glutamate Transporter GLT-1 in Neuron/Astrocyte Co-Cultures

et al. 2006

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“…Recently, we have demonstrated that the activity of NOS varies with cell differentiation, suggesting that NO functions as an important signaling molecule in differentiated cells (Kawahara et al, 2002b). We have also demonstrated in cultured astrocytes that propagating Ca 2+ waves can be evoked by the local photolysis of caged calcium ionophore (Iwabuchi et al, 2002), and wave propagation is modulated by endogenously produced NO (Kawahara et al, 2003a). In the heart, NO plays a physiological role in mediating the effect of vagal stimulation in the autonomic regulation of heart functions (Brady et al, 1992).…”

Section: Introductionmentioning

confidence: 85%

Carbachol-induced Suppression of Contraction Rhythm in Spontaneously Beating Cultured Cardiac Myocytes From Neonatal Rats

Kohashi¹,

Kikuchi²,

Yamauchi³

2003

Biological Rhythm Research

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Nitric oxide (NO) and reactive oxygen species (ROS) are known to play various functional and pathophysiological roles as an intracellular messenger in the heart. In this study, we investigated whether the increased production of NO and/or ROS was involved in the cholinergic regulation of rhythmic contraction in spontaneously beating cultured cardiac myocytes from neonatal rats.Exposure of cultures to carbachol, an agonist of muscarinic acetylcholine receptors (mAchR), produced a dose-dependent decrease in the beat rate of cultured cardiac myocytes, and such a effect was significantly attenuated by pre-treatment with an NOS inhibitor, as well as an NO scavenger. In addition, exposure to an NO donor (SNAP) also decreased the beat rate dose-dependently. Carbachol -or SNAP-induced suppression of the contraction rhythm was significantly attenuated by co-treatment with 5-hydroxydecanoate (5-HD). In contrast, treatment with diazoxide decreased the beat rate dose-dependently.Carbachol treatment increased the intensity of 2',7'-dichlorodihydrofluorescein fluorescence, suggesting that the production of ROS was enhanced by the treatment. In addition, the carbachol-or diazoxide-induced suppression of contraction rhythm was attenuated by co-treatment with 2-mercaptopropionyl glycine, a scavenger of ROS. The present study has suggested that the mAchR-NO-mitoK ATP -ROS pathway is a factor responsible for 1 carbachol-induced suppression of contraction rhythm in cultured cardiac myocytes.

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“…Recently, we have 3 demonstrated that the activity of nitric oxide synthase (NOS) varies associated with the differentiation of a neuronal cell line (NG108-15 cells), suggesting that NO functions as an important signaling molecule in differentiated NG108-15 cells (8). We have also found that NO modulates the propagation of astrocytic Ca 2+ waves induced by the local photolysis of caged Ca 2+ ionophore (9,10). In addition, Yun et al (11) have recently demonstrated that the activation of p21 RAS induced by NO derived from nNOS is responsible for the PC-induced tolerance of neurons, suggesting that NO is a key mediator in the process leading to tolerance against lethal ischemia.…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Produced During Ischemia Is Toxic but Crucial to Preconditioning-Induced Ischemic Tolerance of Neurons in Culture

et al. 2004

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The present study investigated the roles of nitric oxide (NO) in preconditioning (PC)-induced neuronal ischemic tolerance in cortical cultures. Ischemia in vitro was simulated by subjecting cultures to both oxygen and glucose deprivation (OGD). A sublethal OGD (PC) significantly increased the survival rate of neurons when cultures were exposed to a lethal OGD 24 hr later. Both the inhibition of nitric oxide synthase (NOS) and scavenging of NO during PC significantly attenuated the PC-induced neuronal tolerance. In addition, exposure to an NO donor emulated the PC. In contrast, the inhibition of NOS and the scavenging of NO during lethal OGD tended to increase the survival rate of neurons. This study suggested that NO produced during ischemia was fundamentally toxic, but critical to the development of PC-induced neuronal tolerance.

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Possible involvement of nitric oxide in the modulation of photolytic flash‐induced intercellular calcium waves in cultured astrocytes

Cited by 3 publications

References 15 publications

Nitric Oxide Produced During Sublethal Ischemia Is Crucial for the Preconditioning-Induced Down-Regulation of Glutamate Transporter GLT-1 in Neuron/Astrocyte Co-Cultures

Nitric Oxide Produced During Sublethal Ischemia Is Crucial for the Preconditioning-Induced Down-Regulation of Glutamate Transporter GLT-1 in Neuron/Astrocyte Co-Cultures

Carbachol-induced Suppression of Contraction Rhythm in Spontaneously Beating Cultured Cardiac Myocytes From Neonatal Rats

Nitric Oxide Produced During Ischemia Is Toxic but Crucial to Preconditioning-Induced Ischemic Tolerance of Neurons in Culture

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