2006
Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons
Yuan H, Gerencser A, Liot G, Lipton S, Ellisman M, Perkins G, Bossy-Wetzel E. Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons. Cell Death & Differentiation 2006, 14: 462-471. PMID: 17053808, DOI: 10.1038/sj.cdd.4402046.Peer-Reviewed Original ResearchConceptsMitochondrial fissionNitric oxideFoci formationCortical neuronsMitochondrial fission machineryBcl-2 familyNitrosative stressAntiapoptotic Bcl-xLNeuronal cell deathFission machineryMitofusin 1Puncta formationBioenergetic crisisBax accumulationMitochondrial inhibitorsNeuronal demiseBcl-xLCell deathMitochondrial dysfunctionMitochondriaNeurodegenerative disordersNO donorNeuronsScission siteFission
1996
Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures
Pan Z, Segal M, Lipton S. Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 15423-15428. PMID: 8986827, PMCID: PMC26420, DOI: 10.1073/pnas.93.26.15423.Peer-Reviewed Original ResearchConceptsMiniature excitatory postsynaptic currentsSpontaneous miniature excitatory postsynaptic currentsSpontaneous miniature synaptic currentsExcitatory postsynaptic currentsMiniature synaptic currentsPure NO donorPostsynaptic currentsSynaptic activitySynaptic currentsNeuronal culturesNO donorNitric oxideNO donor moleculesNeurotransmissionNitric oxide-related speciesParadoxical observationEPSCsDonorsBCL-2 delay apoptosis and PARP cleavage induced by NO donors in GT1-7 cells
Bonfoco E, Zhivotovsky B, Rossi A, Aguilar-Santelises M, Orrenius S, Lipton S, Nicotera P. BCL-2 delay apoptosis and PARP cleavage induced by NO donors in GT1-7 cells. Neuroreport 1996, 8: 273-276. PMID: 9051794, DOI: 10.1097/00001756-199612200-00054.Peer-Reviewed Original ResearchCytoskeletal Breakdown and Apoptosis Elicited by NO Donors in Cerebellar Granule Cells Require NMDA Receptor Activation
Bonfoco E, Leist M, Zhivotovsky B, Orrenius S, Lipton S, Nicotera P. Cytoskeletal Breakdown and Apoptosis Elicited by NO Donors in Cerebellar Granule Cells Require NMDA Receptor Activation. Journal Of Neurochemistry 1996, 67: 2484-2493. PMID: 8931482, DOI: 10.1046/j.1471-4159.1996.67062484.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAstrocytesCalciumCells, CulturedCerebellumCysteineCytoskeletonDizocilpine MaleateDNA FragmentationEnzyme InhibitorsExcitatory Amino Acid AntagonistsNitric OxidePenicillaminePotassiumRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateS-Nitroso-N-AcetylpenicillamineS-NitrosothiolsSignal TransductionTyrosineConceptsCultured cerebellar granule cellsNMDA receptor activationCerebellar granule cellsCytoskeletal breakdownGranule cellsReceptor activationUncompetitive NMDA receptor antagonistsD-aminophosphonovaleric acidNecrosis of neuronsS-nitrosocysteineNO donor S-nitrosocysteineNMDA receptor antagonistNitric oxide donorTyrosine nitrationReceptor antagonistMK-801Astroglial cellsOxide donorIntracellular Ca2NO donorBreakdown of microtubulesCerebellar astroglial cellsApoptosisUnderwent apoptosisCytoskeletal alterations