Inhibition of nitric oxide synthase increases extracellular cerebral glutamate concentration after global ischemia
Zhang J, Benveniste H, Piantadosi C. Inhibition of nitric oxide synthase increases extracellular cerebral glutamate concentration after global ischemia. Neuroscience Letters 1993, 157: 179-182. PMID: 7694195, DOI: 10.1016/0304-3940(93)90731-y.Peer-Reviewed Original ResearchConceptsGlutamate releaseGlutamate concentrationNitric oxide synthase inhibitionCerebral glutamate concentrationsOxide synthase inhibitionGlobal brain ischemiaInhibition of NOSNitric oxide synthaseExtracellular glutamate releaseCerebral microdialysisBrain ischemiaForebrain ischemiaControl ratsGlobal ischemiaNOS inhibitorOxide synthaseSynthase inhibitionCarotid arteryBrain flowDialysis probeIschemiaDialysate concentrationsControl valuesRatsReperfusionIschemia as an Excitotoxic Lesion: Protection Against Hippocampal Nerve Cell Loss by Denervation
Diemer N, Johansen F, Benveniste H, Bruhn T, Berg M, Valente E, Jørgensen M. Ischemia as an Excitotoxic Lesion: Protection Against Hippocampal Nerve Cell Loss by Denervation. Acta Neurochirurgica Supplement 1993, 57: 94-101. PMID: 8380675, DOI: 10.1007/978-3-7091-9266-5_14.Peer-Reviewed Original ResearchConceptsPyramidal neuronsIschemic neuron damageVulnerable nerve cellsTransient cerebral ischemiaGABA-ergic interneuronsNerve cell lossMin of ischemiaHippocampal pyramidal neuronsRelease of glutamateExtracellular glutamate releaseKainate/Neuroexcitatory mechanismsNeuron damagePostischemic periodCerebral ischemiaHilus cellsPostischemic hypoperfusionCalcium blockersGlutamate releaseIntact innervationIschemic animalsDenervated ratsDentate hilusReceptor autoradiographyCA1 neurons