Literature DB >> 16054513

A simplified procedure for the quantitative measurement of neurological deficits after forebrain ischemia in mice.

Rodolfo Rodriguez1, Jacinto Santiago-Mejia, Claudia Gomez, Eduardo Ramirez San-Juan.   

Abstract

This study describes a comprehensive method to assess neurological deficits after brain ischemia produced by sequential common carotid artery sectioning (SCAS) in aged mice, and a scale to determine the degree of functional incapacity of ischemic animals. The method involves an initial phase of undisturbed observation and a later manipulative phase during which each animal is subjected to a sequence of very simple manipulations. Sham-operated animals demonstrated 96% survival throughout the study period (72 h), whereas the 24, 48 and 72 h survival rates of SCAS-mice were 48, 38 and 36%, respectively. In the surviving SCAS-mice, we detected a total of 23 neurological alterations throughout the observation period (72 h); the most frequent alterations were: motor incoordination, abnormal body position, hypomobility, decreased body tone and muscular strength, tremor, hunched back, passivity, forelimb flexion and ataxic gait. Based on these alterations, we used a global scale that comprises 10 progressive grades beyond 0 (normal), extending to status 10 (death due to SCAS), with higher scores indicating greater deficit. The median neurological scores for sham-operated animals were 1.36, 1.48 and 1.32 at 24, 48 and 72 h, respectively, whereas total neurological scores in SCAS-mice of 6.1, 6.8 and 7.4, at 24, 48 and 72 h, respectively, were substantially greater than those observed in sham-operated animals. The simplicity of the procedure, herein described, to measure the functional neurological condition of ischemic animals, and the remarkable level of functional impairment produced by SCAS offer the possiblity to test the efficacy of putative stroke therapies and to monitor progress of deficits over time in groups of animals.

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Year:  2005        PMID: 16054513     DOI: 10.1016/j.jneumeth.2005.02.013

Source DB:  PubMed          Journal:  J Neurosci Methods        ISSN: 0165-0270            Impact factor:   2.390


  19 in total

1.  Altered responsiveness of the guinea-pig isolated ileum to smooth muscle stimulants and to electrical stimulation after in situ ischemia.

Authors:  Rodolfo Rodriguez; Rosa Ventura-Martinez; Jacinto Santiago-Mejia; Maria R Avila-Costa; Teresa I Fortoul
Journal:  Br J Pharmacol       Date:  2006-02       Impact factor: 8.739

2.  Nicotinamide Mononucleotide Adenylyltransferase 1 Protects Neural Cells Against Ischemic Injury in Primary Cultured Neuronal Cells and Mouse Brain with Ischemic Stroke Through AMP-Activated Protein Kinase Activation.

Authors:  Jia Liang; Peng Wang; Jia Wei; Cuifen Bao; Donghe Han
Journal:  Neurochem Res       Date:  2015-04-05       Impact factor: 3.996

3.  Role of protease-activated receptor-1 in brain injury after experimental global cerebral ischemia.

Authors:  Jinhu Wang; Hang Jin; Ya Hua; Richard F Keep; Guohua Xi
Journal:  Stroke       Date:  2012-07-17       Impact factor: 7.914

4.  Determination of Brain-Regional Blood Perfusion and Endogenous cPKCγ Impact on Ischemic Vulnerability of Mice with Global Ischemia.

Authors:  Shuiqiao Liu; Qingqing Dai; Rongrong Hua; Ting Liu; Song Han; Shujuan Li; Junfa Li
Journal:  Neurochem Res       Date:  2017-06-08       Impact factor: 3.996

5.  5-HMF attenuates striatum oxidative damage via Nrf2/ARE signaling pathway following transient global cerebral ischemia.

Authors:  Bai-Liu Ya; Hong-Fang Li; Hai-Ying Wang; Fei Wu; Qing Xin; Hong-Ju Cheng; Wen-Juan Li; Na Lin; Zai-Hua Ba; Ru-Juan Zhang; Qian Liu; Ya-Nan Li; Bo Bai; Feng Ge
Journal:  Cell Stress Chaperones       Date:  2016-11-03       Impact factor: 3.667

6.  MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway.

Authors:  Peng Wang; Xinyu Liang; Yijun Lu; Xingjian Zhao; Jia Liang
Journal:  Neurochem Res       Date:  2016-06-14       Impact factor: 3.996

7.  The DREAM protein negatively regulates the NMDA receptor through interaction with the NR1 subunit.

Authors:  Ying Zhang; Ping Su; Ping Liang; Tao Liu; Xu Liu; Xin-Ying Liu; Bo Zhang; Tao Han; Yan-Bing Zhu; Dong-Min Yin; Junfa Li; Zhuan Zhou; Ke-Wei Wang; Yun Wang
Journal:  J Neurosci       Date:  2010-06-02       Impact factor: 6.167

8.  Inhibition of neuron-specific CREB dephosphorylation is involved in propofol and ketamine-induced neuroprotection against cerebral ischemic injuries of mice.

Authors:  Luowa Shu; Tianzuo Li; Song Han; Fang Ji; Chuxiong Pan; Bingxi Zhang; Junfa Li
Journal:  Neurochem Res       Date:  2011-09-03       Impact factor: 3.996

9.  Down-regulation of miRNA-30a alleviates cerebral ischemic injury through enhancing beclin 1-mediated autophagy.

Authors:  Peng Wang; Jia Liang; Yun Li; Jiefei Li; Xuan Yang; Xinxin Zhang; Song Han; Shujuan Li; Junfa Li
Journal:  Neurochem Res       Date:  2014-04-26       Impact factor: 3.996

10.  cPKCγ-Modulated Autophagy in Neurons Alleviates Ischemic Injury in Brain of Mice with Ischemic Stroke Through Akt-mTOR Pathway.

Authors:  Haiping Wei; Yun Li; Song Han; Shuiqiao Liu; Nan Zhang; Li Zhao; Shujuan Li; Junfa Li
Journal:  Transl Stroke Res       Date:  2016-08-10       Impact factor: 6.829

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