|Table of Contents|

Dynamic changes of glutamate during cerebral ischemia in the cortex of cynomolgus monkeys

(PDF)

《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

Issue:
2017年第17期
Page:
1728-1733
Research Field:
基础医学
Publishing date:

Info

Title:

Dynamic changes of glutamate during cerebral ischemia in the cortex of cynomolgus monkeys

Author(s):

WEI Chen TAO Guoxian TANG Rongping LIU Guolong ZHANG Zhiming YUE Feng

Center for Translational Medicine, Key Laboratory of Longevity and Aging-related Disease of Ministry of Education, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, 530021, China; Wincon Thera Cells Biotechnologies Co. Ltd., Nanning, Guangxi Zhuang Autonomous Region, 530003, China; Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China; Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, 405360098, KY, USA; 5Department of Neurobiology, Xuanwu Hospital of Capital Medical University, Beijing, 100053, China

Keywords:

brain ischemia glutamate acid middle cerebral artery cynomolgus monkeys

PACS:
R341.7;R362;R743.31
DOI:
-
Abstract:

Objective     To explore the dynamic changes of glutamate in the cortex of cynomolgus monkeys during cerebral ischemia. Methods     Proximal M1 segment of middle cerebral artery (MCA) was occluded for 1 h in 3 young cynomolgus monkeys (7.3±1.5 years old) to induce cerebral ischemia. Magnetic resonance imaging and neurologic deficit scoring were used to evaluate the ischemia and observe the manifestations, respectively. Fast Analytical Sensing Technology (FAST) was applied to record the content of cortex glutamate in the same site of ipsilateral primary motor cortex in the periods of pre-, during, and post-occlusion, and at 1 and 2 weeks after surgery. Results         Compared with pre-occlusion, the content of glutamate was increased significantly in the process of occluding in the MCA M1 (P=0.003); No significant difference was observed in the content during occluding and post-occlusion (P=0.877). The content in the first week was decreased obviously as compared with post-occlusion (P=0.004), but it showed no statistical difference with that in the second week (P=0.085). Conclusion     Cerebral ischemia may potentially accelerate the extracellular glutamate release in the cortex, but reperfusion may ameliorate or balance off the glutamate release.

References:

[1]LAI T W, ZHANG S, WANG Y T. Excitotoxicity and stroke: identifying novel targets for neuroprotection[J]. Prog Neurobiol, 2014, 115: 157-188. DOI:10.1016/j.pneurobio.2013.11.006.
[2]FISHER M. New approaches to neuroprotective drug development[J]. Stroke, 2011, 42(1 Suppl): S24-S27. DOI: 10.1161/STROKEAHA.110.592394.
[3]HOQUE A, HOSSAIN M I, AMEEN S S, et al. A beacon of hope in stroke therapyBlockade of pathologically activated cellular events in excitotoxic neuronal death as potential neuroprotective strategies[J]. Pharmacol Ther, 2016, 160: 159-179. DOI:10.1016/j.pharmthera.2016.02.009.
[4]CASTILLO J, LOZA M I, MIRELMAN D, et al. A novel mechanism of neuroprotection: blood glutamate grabber[J]. J Cereb Blood Flow Metab, 2016, 36(2): 292-301. DOI: 10.1177/0271678X15606721.
[5]PASTUKHOV A. KRISANOVA N, MAKSYMENKO V, et al. Personalized approach in brain protection by hypothermia: individual changes in non-pathological and ischemia-related glutamate transport in brain nerve terminals[J]. EPMA J, 2016, 7(1): 26. DOI:10.1186/ s13167016-0075-1.
[6]TALMA N, KOK W F, DE VEIJ MESTDAGH C F, et al. Neuroprotective hypothermiawhy keep your head cool during ischemia and reperfusion[J]. Biochim Biophys Acta, 2016, 1860(11 Pt A): 2521-2528. DOI: 10.1016/j.bbagen.2016.07.024.
[7]SCHAECHTER J D, MOORE C I, CONNELL B D, et al. Structural and functional plasticity in the somatosensory cortex of chronic stroke patients[J]. Brain, 2006, 129(Pt 10): 2722-2733. DOI: 10.1093/ brain/awl214.
[8]CIRSTEA C M, BROOKS W M, CRACIUNAS S C, et al. Primary motor cortex in stroke: a functional MRI-guided proton MR spectroscopic study[J]. Stroke, 2011, 42(4): 1004-1009. DOI: 10.1161/STROKEAHA.110.601047.
[9]QUINTERO J E, DAY B K, ZHANG Z, et al. Amperometric measures of agerelated changes in glutamate regulation in the cortex of rhesus monkeys[J]. Exp Neurol, 2007, 208(2): 238-246. DOI: 10.1016/j.expneurol.2007.08.002.
[10]STEPHENS M L, POMERLEAU F, HUETTL P, et al. Real-time glutamate measurements in the putamen of awake rhesus monkeys using an enzymebased human microelectrode array prototype[J]. J Neurosci Methods, 2010, 185(2): 264-272. DOI: 10.1016/ j.jneumeth. 2009.10.008.
[11]FAN X T, ZHAO F, AI Y, et al. Cortical glutamate levels decrease in a non-human primate model of dopamine deficiency[J]. Brain Res, 2014, 1552: 34-40. DOI:10.1016/j.brainres.2013.12.035.
[12]ZHU H, LI Q, FENG M, et al. A new cerebral hemorrhage model in cynomolgus macaques created by injection of autologous anticoagulated blood into the brain[J]. J Clin Neurosci, 2011, 18(7): 955-960. DOI:10.1016/j.jocn.2010.11.038.
[13]CHEN X, DANG G, DANG C, et al. An ischemic stroke model of nonhuman primates for remote lesion studies: a behavioral and neuroimaging investigation[J]. Restor Neurol Neurosci, 2015, 33(2): 131-142. DOI:10.3233/RNN140440.
[14]WETTERLING F,CHATZIKONSTANTINOU E,TRITSCHLER L, et al. Investigating potentially salvageable penumbra tissue in an in vivo model of transient ischemic stroke using sodium, diffusion, and perfusion magnetic resonance imaging[J]. BMC Neurosci, 2016, 17(1): 82. DOI: 10.1186/s12868-016-0316-1.
[15]COOK D J, TYMIANSKI M. Nonhuman primate models of stroke for translational neuroprotection research[J]. Neurotherapeutics, 2012, 9(2): 371-379. DOI: 10.1007/s13311012-0115-z.
[16]WEST G A, GOLSHANI K J, DOYLE K P, et al. A new model of cortical stroke in the rhesus macaque[J]. J Cereb Blood Flow Metab, 2009, 29(6): 1175-1186. DOI: 10.1038/jcbfm.2009.43.
[17]ROITBERG B, KHAN N, TUCCAR E, et al. Chronic ischemic stroke model in cynomolgus monkeys: behavioral, neuroimaging and anatomical study[J]. Neurol Res, 2003, 25(1): 68-78. DOI: 10.1179/016164103101200950.
[18]MOORE T L, KILLIANY R J, PESSINA M A, et al. Recovery from ischemia in the middleaged brain: a nonhuman primate model[J]. Neurobiol Aging, 2012, 33(3): 619-619. DOI: 10.1016/j.neurobiolaging.2011.02.005.
[19]RODRIGUEZ-MERCADO R, FORD G D, XU Z F, et al. Acute neuronal injury and blood genomic profiles in a nonhuman primate model for ischemic stroke[J]. Comp Med, 2012, 62(5): 427-438.
[20]SUN Z, ZHANG J, CHEN Y, et al. Differential temporal evolution patterns in brain temperature in different ischemic tissues in a monkey model of middle cerebral artery occlusion[J]. J Biomed Biotechnol, 2012, 2012: 980961. DOI: 10.1155/2012/980961.
[21]ZHANG X, TONG F, LI C X, et al. Temporal evolution of ischemic lesions in nonhuman primates: a diffusion and perfusion MRI study[J]. PLoS One, 2015, 10(2): e0117290. DOI: 10.1371/journal.pone.0117290.
[22]武明明, 孙晓川, 吴海涛, 等. 载脂蛋白E基因多态性与星形胶质细胞损伤后兴奋性氨基酸变化的关系[J]. 第三军医大学学报, 2011, 33(9): 928-931.
WU M M, SUN X C, WU H T, et al. In vitro relationship of apolipoprotein e polymorphisms and excitatory amino acids in astrocyte injury[J]. J Third Mil Med Univ,2011, 33(9): 928-931.
[23]HINZMAN J M, DINAPOLI V A, MAHONEY E J, et al. Spreading depolarizations mediate excitotoxicity in the development of acute cortical lesions[J]. Exp Neurol, 2015, 267: 243-253. DOI: 10.1016/j.expneurol.2015.03.014.
[24]SHEN P, HOU S, ZHU M, et al. Cortical spreading depression preconditioning mediates neuroprotection against ischemic stroke by inducing AMP-activated protein kinasedependent autophagy in a rat cerebral ischemic/reperfusion injury model[J]. J Neurochem, 2017, 140(5): 799-813. DOI: 10.1111/jnc.13922.
[25]GONZLEZ R G. Clinical MRI of acute ischemic stroke[J]. J Magn Reson Imaging, 2012, 36(2): 259-271. DOI: 10.1002/jmri.23595.

Memo

Memo:
-
Last Update: 2017-09-04