Inhibition of nitric oxide synthase increases extracellular cerebral glutamate concentration after global ischemia

Zhang, Jing; Benveniste, Helene; Piantadosi, Claude A.

doi:10.1016/0304-3940(93)90731-y

Cited by 21 publications

(6 citation statements)

References 15 publications

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“…Since evidence was presented that NOS inhibitors prevent the neurotoxicity elicited by NMDA and EAAs, 6) the involvement of NO in neurotoxicity has been investigated intensively. 5,10,18,26,30,[33][34][35] Some of the resulting data suggest that the administration of NOS inhibitors dramatically reduces the volume of brain edema and/or subsequent cerebral infarction following ischemic insult, which implicates NO in the mediation of neuronal death. 21) On the other hand, conflicting results indicate that NOS inhibitors enhance neuronal death.…”

Section: Discussionmentioning

confidence: 99%

“…11) Blockade of NO synthesis causes a dramatic reduction in the volume of the cortical infarct induced by irreversible focal cerebral ischemia in the mouse, 21) so application of NOS inhibitors to the cerebral ischemic insults should provide some neuroprotection from any associated neuronal damages. A number of laboratory-based trials testing several types of NOS inhibitors on animal models have now been carried out, 5,6,10,18,26,30,[33][34][35] but no conclusion has been reached in the debate about the efficacy of NOS inhibitors as protectors against cerebral ischemic insult. Activation of N-methyl-D-aspartate (NMDA) receptors, overstimulation of which causes massive influx of calcium ions at toxic levels in neurons, has been recently found to be associated with an increase in intracellular NO levels in rat cerebellar slices.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective Effects of Ebselen Following Forebrain Ischemia: Involvement of Glutamate and Nitric Oxide

Koizumi

Fujisawa

Suehiro

et al. 2011

Neurol. Med. Chir.(Tokyo)

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Ebselen is a mimic of glutathione peroxidase that reacts with peroxynitrite and inhibits nitric oxide (NO) synthase. Ebselen has beneficial effects on the neurological outcome of patients with stroke. In this study, the mechanisms by which ebselen can elicit neuroprotective effects against ischemic brain injury were investigated in male Wistar rats. Experimental forebrain ischemia was induced by bilateral common carotid artery occlusion with hemorrhagic hypotension. Ebselen was administered to animals in the treatment group 2 hours prior to the induction of forebrain ischemia, and placebo was administered in the control group. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. Cortical extracellular levels of excitatory amino acids (EAAs) and NO were evaluated using in vivo microdialysis. Neuronal damage in the CA1 subfield of the hippocampus was assessed in brains harvested after a 24-hour period of survival. CBF did not recover to normal physiological levels after ischemic insults in either the control or treatment groups. The differences in the sequential changes in extracellular EAA and NO levels between groups were not statistically significant. There was a significantly larger mean density of intact, undamaged neurons in the CA1 subfield in the treatment group than in the control group. The neuroprotective effects of ebselen were reflected in the histological findings, without significant inhibition of glutamate release or NO synthesis during the acute phase of experimentally induced cerebral ischemia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Ebselen Following Forebrain Ischemia: Involvement of Glutamate and Nitric Oxide

Koizumi

Fujisawa

Suehiro

et al. 2011

Neurol. Med. Chir.(Tokyo)

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“…Nitric oxide synthase inhibitors have been described as both providing protection against cerebral ischemic infarction 1,3,25,32,35,55,59 and increasing postischemic damage. 9,44,54,57,58 In addition, NO precursors, L-arginine, and nitrovasodilators have been shown to reduce damage. 26,31,56 Consistent with the latter observations, NO confers protection against ROS damage 51 and does not cause cell death.…”

Section: Discussionmentioning

confidence: 99%

Production of reactive oxygen species after reperfusion in vitro and in vivo: protective effect of nitric oxide

Mason¹,

Pluta²,

Walbridge³

et al. 2000

Journal of Neurosurgery

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“…In focal ischemia, it was found that an NOS inhibitor suppressed the increase in extracellular glutamate (Buisson et a!., 1993). In forebrain ischemia, however, an NOS in hibitor increased extracellular glutamate concentra tion during ischemia (Nanri et a!., 1994) or on reper fusion (Zhang et a!., 1993(Zhang et a!., , 1995, although the mechanism involved is unclear. Therefore, our find ing of an increase in glutamate concentration by Zn PP-9 in forebrain ischemia may reflect the inhibi tory effect on NOS activity.…”

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide, a Novel Neural Messenger, Does Not Modulate Extracellular Glutamate Concentration in Forebrain Ischemia

Takizawa

Fujita

Ogawa

et al. 1996

J Cereb Blood Flow Metab

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We investigated the role of carbon monoxide as a neural modulator of extracellular glutamate concentration in rat hippocampus CA1 in transient forebrain ischemia by using metalloporphyrins, which block the production of carbon monoxide through the inhibition of heme oxygenase (HO) activity. Infusion of 10 and 100 microM zinc protoporphyrin IX, which inhibits nitric oxide synthase activity as well as HO activity, significantly increased glutamate concentration compared with that on the vehicle-treated side. However, infusion of 100 microM tin mesoporphyrin IX, which inhibits only HO activity, did not affect glutamate concentration in ischemia. Our results therefore do not support the hypothesis that carbon monoxide acts as a neural messenger through the modulation of extracellular glutamate concentration in ischemia.

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Inhibition of nitric oxide synthase increases extracellular cerebral glutamate concentration after global ischemia

Cited by 21 publications

References 15 publications

Neuroprotective Effects of Ebselen Following Forebrain Ischemia: Involvement of Glutamate and Nitric Oxide

Neuroprotective Effects of Ebselen Following Forebrain Ischemia: Involvement of Glutamate and Nitric Oxide

Production of reactive oxygen species after reperfusion in vitro and in vivo: protective effect of nitric oxide

Carbon Monoxide, a Novel Neural Messenger, Does Not Modulate Extracellular Glutamate Concentration in Forebrain Ischemia

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