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Article: Reduction by naloxone of lipopolysaccharide-induced neurotoxicity in mouse cortical neuron-glia co-cultures

TitleReduction by naloxone of lipopolysaccharide-induced neurotoxicity in mouse cortical neuron-glia co-cultures
Authors
Issue Date2000
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 2000, v. 97 n. 4, p. 749-756 How to Cite?
AbstractAn inflammatory response in the CNS mediated by activation of microglia is a key event in the early stages of the development of neurodegenerative diseases. Using mouse cortical mixed glia cultures, we have previously demonstrated that the bacterial endotoxin lipopolysaccharide induces the activation of microglia and the production of proinflammatory factors. Naloxone, an opioid receptor antagonist, inhibits the lipopolysaccharide- induced activation of microglia and the production of proinflammatory factors. Using neuron-glia co-cultures, we extended our study to determine if naloxone has a neuroprotective effect against lipopolysaccharide-induced neuronal damage and analysed the underlying mechanism of action for its potential neuroprotective effect. Pretreatment of cultures with naloxone (1 μM) followed by treatment with lipopolysaccharide significantly inhibited the lipopolysaccharide-induced production of nitric oxide and the release of tumor necrosis factor-α, and significantly reduced the lipopolysaccharide- induced damage to neurons. More importantly, both naloxone and its opioid- receptor ineffective enantiomer (+)-naloxone were equally effective in inhibiting the lipopolysaccharide-induced generation of proinflammatory factors and the activation of microglia, as well as in the protection of neurons. These results indicate that the neuroprotective effect of naloxone is mediated by its inhibition of microglial activity and may be unrelated to its binding to the classical opioid receptors.
Persistent Identifierhttp://hdl.handle.net/10722/149591
ISSN
2015 Impact Factor: 3.231
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Ben_US
dc.contributor.authorDu, Len_US
dc.contributor.authorKong, LYen_US
dc.contributor.authorHudson, PMen_US
dc.contributor.authorWilson, BCen_US
dc.contributor.authorChang, RCen_US
dc.contributor.authorAbel, HHen_US
dc.contributor.authorHong, JSen_US
dc.date.accessioned2012-06-26T05:55:40Z-
dc.date.available2012-06-26T05:55:40Z-
dc.date.issued2000en_US
dc.identifier.citationNeuroscience, 2000, v. 97 n. 4, p. 749-756en_US
dc.identifier.issn0306-4522en_US
dc.identifier.urihttp://hdl.handle.net/10722/149591-
dc.description.abstractAn inflammatory response in the CNS mediated by activation of microglia is a key event in the early stages of the development of neurodegenerative diseases. Using mouse cortical mixed glia cultures, we have previously demonstrated that the bacterial endotoxin lipopolysaccharide induces the activation of microglia and the production of proinflammatory factors. Naloxone, an opioid receptor antagonist, inhibits the lipopolysaccharide- induced activation of microglia and the production of proinflammatory factors. Using neuron-glia co-cultures, we extended our study to determine if naloxone has a neuroprotective effect against lipopolysaccharide-induced neuronal damage and analysed the underlying mechanism of action for its potential neuroprotective effect. Pretreatment of cultures with naloxone (1 μM) followed by treatment with lipopolysaccharide significantly inhibited the lipopolysaccharide-induced production of nitric oxide and the release of tumor necrosis factor-α, and significantly reduced the lipopolysaccharide- induced damage to neurons. More importantly, both naloxone and its opioid- receptor ineffective enantiomer (+)-naloxone were equally effective in inhibiting the lipopolysaccharide-induced generation of proinflammatory factors and the activation of microglia, as well as in the protection of neurons. These results indicate that the neuroprotective effect of naloxone is mediated by its inhibition of microglial activity and may be unrelated to its binding to the classical opioid receptors.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscienceen_US
dc.relation.ispartofNeuroscienceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCerebral Cortex - Cytology - Physiologyen_US
dc.subject.meshCoculture Techniquesen_US
dc.subject.meshEmbryo, Mammalianen_US
dc.subject.meshL-Lactate Dehydrogenase - Analysisen_US
dc.subject.meshLipopolysaccharides - Antagonists & Inhibitors - Toxicityen_US
dc.subject.meshMiceen_US
dc.subject.meshNaloxone - Pharmacologyen_US
dc.subject.meshNeuroglia - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshNeurons - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshNeuroprotective Agentsen_US
dc.subject.meshNeurotoxins - Toxicityen_US
dc.subject.meshNitrites - Metabolismen_US
dc.subject.meshStereoisomerismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Secretionen_US
dc.titleReduction by naloxone of lipopolysaccharide-induced neurotoxicity in mouse cortical neuron-glia co-culturesen_US
dc.typeArticleen_US
dc.identifier.emailChang, RC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0306-4522(00)00057-9en_US
dc.identifier.pmid10842020-
dc.identifier.scopuseid_2-s2.0-0034072541en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034072541&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume97en_US
dc.identifier.issue4en_US
dc.identifier.spage749en_US
dc.identifier.epage756en_US
dc.identifier.isiWOS:000087641700015-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridLiu, B=36079151900en_US
dc.identifier.scopusauthoridDu, L=7201905705en_US
dc.identifier.scopusauthoridKong, LY=7201533114en_US
dc.identifier.scopusauthoridHudson, PM=35566903000en_US
dc.identifier.scopusauthoridWilson, BC=35243580200en_US
dc.identifier.scopusauthoridChang, RC=7403713410en_US
dc.identifier.scopusauthoridAbel, HH=7103073193en_US
dc.identifier.scopusauthoridHong, JS=7404117981en_US

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