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Glutamate preconditioning prevents neuronal death induced by combined oxygen-glucose deprivation in cultured cortical neurons.
Eur J Pharmacol. 2008 Jul 28; 589(1-3):85-93.EJ

Abstract

The study of ischemic tolerance is critical in the development of strategies for the treatment of ischemic stroke. We used the oxygen and glucose deprivation (OGD) paradigm in cultured cortical neurons as an in vitro approach to elucidate the mechanism of protection conferred by glutamate preconditioning. Pretreatment of neurons with N-methyl-d-aspartate (NMDA) receptor antagonists prevented OGD-induced cell death whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor and voltage-dependent Ca(++) channel (VDCC) blockers were without effect. Neurons preconditioned with glutamate exhibited resistant to damage induced by OGD. The ischemic tolerance depended on the duration of preconditioning exposure and the interval between preconditioning exposure and test challenge. Protective efficacy was blocked by the NMDA or AMPA receptor antagonists but not by the VDCC blocker. Furthermore, neuroprotective effect was not seen if extracellular Ca(++) was omitted or removed with EGTA. Pretreatment with staurosporin and 2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)] amino-N-(4-chlorocinnamyl)-N-methylbenzylamine (KN93) but not 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one (LY294002) or 1,4-diamino-2,3-dicyano-1, 4-bis[2-aminophenylthio] butadiene (U0126) significantly reduced ischemic tolerance. Preconditioning increased phosphorylated levels of cAMP responsive element binding protein (CREB) and pretreatment with CRE-decoy oligonucleotide completely blocked preconditioning-induced increase in cell viability. Importantly, glutamate preconditioning increased Bcl-2 expression that was blocked by KN93, staurosporin and CRE-decoy oligonucleotide. These results suggest that preconditioning with glutamate conferred neuroprotection against subsequent OGD by inducing p-CREB-mediated Bcl-2 expression.

Authors+Show Affiliations

Department of Pharmacology, Center for Gene Regulation and Signal Transduction Research, National Cheng-Kung University, Tainan, Taiwan.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18589412

Citation

Lin, Chia-Ho, et al. "Glutamate Preconditioning Prevents Neuronal Death Induced By Combined Oxygen-glucose Deprivation in Cultured Cortical Neurons." European Journal of Pharmacology, vol. 589, no. 1-3, 2008, pp. 85-93.
Lin CH, Chen PS, Gean PW. Glutamate preconditioning prevents neuronal death induced by combined oxygen-glucose deprivation in cultured cortical neurons. Eur J Pharmacol. 2008;589(1-3):85-93.
Lin, C. H., Chen, P. S., & Gean, P. W. (2008). Glutamate preconditioning prevents neuronal death induced by combined oxygen-glucose deprivation in cultured cortical neurons. European Journal of Pharmacology, 589(1-3), 85-93. https://doi.org/10.1016/j.ejphar.2008.05.047
Lin CH, Chen PS, Gean PW. Glutamate Preconditioning Prevents Neuronal Death Induced By Combined Oxygen-glucose Deprivation in Cultured Cortical Neurons. Eur J Pharmacol. 2008 Jul 28;589(1-3):85-93. PubMed PMID: 18589412.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutamate preconditioning prevents neuronal death induced by combined oxygen-glucose deprivation in cultured cortical neurons. AU - Lin,Chia-Ho, AU - Chen,Po-See, AU - Gean,Po-Wu, Y1 - 2008/06/06/ PY - 2008/04/05/received PY - 2008/04/17/revised PY - 2008/05/20/accepted PY - 2008/7/1/pubmed PY - 2008/10/25/medline PY - 2008/7/1/entrez SP - 85 EP - 93 JF - European journal of pharmacology JO - Eur. J. Pharmacol. VL - 589 IS - 1-3 N2 - The study of ischemic tolerance is critical in the development of strategies for the treatment of ischemic stroke. We used the oxygen and glucose deprivation (OGD) paradigm in cultured cortical neurons as an in vitro approach to elucidate the mechanism of protection conferred by glutamate preconditioning. Pretreatment of neurons with N-methyl-d-aspartate (NMDA) receptor antagonists prevented OGD-induced cell death whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor and voltage-dependent Ca(++) channel (VDCC) blockers were without effect. Neurons preconditioned with glutamate exhibited resistant to damage induced by OGD. The ischemic tolerance depended on the duration of preconditioning exposure and the interval between preconditioning exposure and test challenge. Protective efficacy was blocked by the NMDA or AMPA receptor antagonists but not by the VDCC blocker. Furthermore, neuroprotective effect was not seen if extracellular Ca(++) was omitted or removed with EGTA. Pretreatment with staurosporin and 2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)] amino-N-(4-chlorocinnamyl)-N-methylbenzylamine (KN93) but not 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one (LY294002) or 1,4-diamino-2,3-dicyano-1, 4-bis[2-aminophenylthio] butadiene (U0126) significantly reduced ischemic tolerance. Preconditioning increased phosphorylated levels of cAMP responsive element binding protein (CREB) and pretreatment with CRE-decoy oligonucleotide completely blocked preconditioning-induced increase in cell viability. Importantly, glutamate preconditioning increased Bcl-2 expression that was blocked by KN93, staurosporin and CRE-decoy oligonucleotide. These results suggest that preconditioning with glutamate conferred neuroprotection against subsequent OGD by inducing p-CREB-mediated Bcl-2 expression. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/18589412/Glutamate_preconditioning_prevents_neuronal_death_induced_by_combined_oxygen_glucose_deprivation_in_cultured_cortical_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(08)00584-0 DB - PRIME DP - Unbound Medicine ER -