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Isoflurane preconditioning decreases glutamate receptor overactivation-induced Purkinje neuronal injury in rat cerebellar slices.
Brain Res. 2005 Aug 30; 1054(2):143-51.BR

Abstract

A brain slice model was used to test the hypothesis that preconditioning with isoflurane, a commonly used volatile anesthetic in clinical practice, reduces neuronal injury caused by overstimulation of glutamate receptors. Glutamate receptors were stimulated by various concentrations of glutamate for 20 min, N-methyl-d-aspartate (NMDA) for 15 min or alpha-amino-3-hydroxy-5-methyl-4-isoxazol propionic acid (AMPA) for 15 min. Morphology of Purkinje neurons in the cerebellar slices of adult male Sprague-Dawley rats was evaluated 5 h after the agonist stimulation. Glutamate, NMDA and AMPA induced a dose-dependent decrease in the percentage of morphologically normal Purkinje neurons. The concentration to induce the maximal neurotoxic effect was 300 microM for glutamate, 300 microM for NMDA and 30 microM for AMPA. Isoflurane preconditioning (2% isoflurane for 30 min and then a 15-min rest period before the agonist stimulation) significantly reduced the neurotoxicity induced by 300 microM glutamate, 300 microM NMDA or 30 microM AMPA. Isoflurane preconditioning-induced protection against glutamate neurotoxicity was abolished by two protein kinase C (PKC) inhibitors, calphostin C (0.5 microM) and chelerythrine (5 microM), or a nitric oxide synthase (NOS) inhibitor, l-nitro(G)-arginine methyl ester (l-NAME, 1.5 mM), but was not affected by an adenosine A1 receptor inhibitor, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 300 nM), or a Gi protein inhibitor, pertussis toxin (PTX, 200 ng/ml). Isoflurane preconditioning-induced protection against NMDA neurotoxicity was also abolished by calphostin C, chelerythrine or l-NAME. Thus, isoflurane preconditioning reduced glutamate receptor overstimulation-induced neuronal injury/death. This neuroprotection may be PKC- and NOS-dependent.

Authors+Show Affiliations

Department of Anesthesiology, University of Virginia Health System, One Hospital Drive, P.O. Box 800710, Charlottesville, VA 22908-0710, USA.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

16081051

Citation

Zheng, Shuqiu, and Zhiyi Zuo. "Isoflurane Preconditioning Decreases Glutamate Receptor Overactivation-induced Purkinje Neuronal Injury in Rat Cerebellar Slices." Brain Research, vol. 1054, no. 2, 2005, pp. 143-51.
Zheng S, Zuo Z. Isoflurane preconditioning decreases glutamate receptor overactivation-induced Purkinje neuronal injury in rat cerebellar slices. Brain Res. 2005;1054(2):143-51.
Zheng, S., & Zuo, Z. (2005). Isoflurane preconditioning decreases glutamate receptor overactivation-induced Purkinje neuronal injury in rat cerebellar slices. Brain Research, 1054(2), 143-51.
Zheng S, Zuo Z. Isoflurane Preconditioning Decreases Glutamate Receptor Overactivation-induced Purkinje Neuronal Injury in Rat Cerebellar Slices. Brain Res. 2005 Aug 30;1054(2):143-51. PubMed PMID: 16081051.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Isoflurane preconditioning decreases glutamate receptor overactivation-induced Purkinje neuronal injury in rat cerebellar slices. AU - Zheng,Shuqiu, AU - Zuo,Zhiyi, PY - 2005/01/20/received PY - 2005/06/20/revised PY - 2005/06/25/accepted PY - 2005/8/6/pubmed PY - 2005/12/22/medline PY - 2005/8/6/entrez SP - 143 EP - 51 JF - Brain research JO - Brain Res VL - 1054 IS - 2 N2 - A brain slice model was used to test the hypothesis that preconditioning with isoflurane, a commonly used volatile anesthetic in clinical practice, reduces neuronal injury caused by overstimulation of glutamate receptors. Glutamate receptors were stimulated by various concentrations of glutamate for 20 min, N-methyl-d-aspartate (NMDA) for 15 min or alpha-amino-3-hydroxy-5-methyl-4-isoxazol propionic acid (AMPA) for 15 min. Morphology of Purkinje neurons in the cerebellar slices of adult male Sprague-Dawley rats was evaluated 5 h after the agonist stimulation. Glutamate, NMDA and AMPA induced a dose-dependent decrease in the percentage of morphologically normal Purkinje neurons. The concentration to induce the maximal neurotoxic effect was 300 microM for glutamate, 300 microM for NMDA and 30 microM for AMPA. Isoflurane preconditioning (2% isoflurane for 30 min and then a 15-min rest period before the agonist stimulation) significantly reduced the neurotoxicity induced by 300 microM glutamate, 300 microM NMDA or 30 microM AMPA. Isoflurane preconditioning-induced protection against glutamate neurotoxicity was abolished by two protein kinase C (PKC) inhibitors, calphostin C (0.5 microM) and chelerythrine (5 microM), or a nitric oxide synthase (NOS) inhibitor, l-nitro(G)-arginine methyl ester (l-NAME, 1.5 mM), but was not affected by an adenosine A1 receptor inhibitor, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 300 nM), or a Gi protein inhibitor, pertussis toxin (PTX, 200 ng/ml). Isoflurane preconditioning-induced protection against NMDA neurotoxicity was also abolished by calphostin C, chelerythrine or l-NAME. Thus, isoflurane preconditioning reduced glutamate receptor overstimulation-induced neuronal injury/death. This neuroprotection may be PKC- and NOS-dependent. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/16081051/Isoflurane_preconditioning_decreases_glutamate_receptor_overactivation_induced_Purkinje_neuronal_injury_in_rat_cerebellar_slices_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(05)00963-7 DB - PRIME DP - Unbound Medicine ER -