Quantitative study of variation of number of neurons in cortical dysplasia rat hippocampus by stereological method
FENG Fei, CHEN Xiao-Shan, HE Xin, ZHANG Jian-Gang, WEN Meng, TANG Yong, YAN Yong
Chinese Journal of Clinical Anatomy ›› 2013, Vol. 31 ›› Issue (1) : 85-88.
Quantitative study of variation of number of neurons in cortical dysplasia rat hippocampus by stereological method
Objective To investigate the variation of number and volume of hippocampus neuron in CA1,CA3 and DG region of rats with cortical dysplasia induced by X-ray using stereological method. Methods 5 normal rats and 5 model rats with 2 months old were used in this study with their brain subsequently and sequentially taken out, embedded in paraffin blocks and being subject to coronal section in thickness of 8 ?滋m. The sections were uniformly and randomly sampled from the consecutive sections of the hippocampus according to the principles of systematic，uniform and random sampling．The sections were stained for Nissl substance for quantification of neuron number in CA1，CA3 ,DG region and volume of the hippocampus using stereological device. Results The number of unilateral hippocampus neurons in CA1，and DG region in normal rats was 8.35×104±1.44×104、8.23×104±1.60×104 and 1.43×105±2.24×104, respectively，and was 3.70×104±1.96×104、3.57×104±1.47×104 and 6.86×104±4.85×104 in model rats with cortical dysplasia, respectively. The volume of the unilateral hippocampus in normal rats and rats with disorders of cortical development was (14.18±1.52) mm3 and (8.49±3.41) mm3, respectively. Compared to normal rats, the number of neurons in CA1,CA3 and DG region and the volume of hippocampus in model rats decreased(P<0.05). Conclusion Compared with normal rats, the number and volume of hippocampus neuron in CA1, CA3 and DG regions of rats with cortical dysplasia induced by X-ray is significantly reduced.
Cortical dysplasia / Epilepsy / Neuron / Hippocampus / Stereology
[1] Montenegro MA, Kinay D, Cendes F, et al. Patterns of hippocampal abnormalities in malformations of cortical development
[J]. J Neurol Neurosurg Psychiatry, 2006, 77(3): 367-371.
[2] Kuruba R, Hattiangady B, Shetty AK. Hippocampal neurogenesis and neural stem cells in temporal lobe epilepsy
[J]. Epilepsy Behav, 2009, 14( Suppl 1): 65-73.
[3]张建刚, 宋延波, 张毅, 等. X射线照射致皮质发育障碍模型大鼠致癫性的研究
[J]. 第三军医大学学报, 2011, 33(1): 74-77.
[4]师晓燕, 赵圆宇, 卢伟, 等. 运用新的体视学方法定量研究大鼠海马结构神经元和突触数目
[J]. 第三军医大学学报, 2011, 33(13): 1328-1332.
[5] 杨正伟. 均匀随机方向上的体视学测试：各向同性随机测试
[J]. 川北医学院学报, 2006, 21(5): 399-412.
[6] West MJ, Slomianka L, Gundersen HJ. Unbiased stereological estimation of the total number of neurons inthesubdivisions of the rat hippocampus using the optical fractionator
[J]. Anat Rec, 1991, 231(4): 482-497.
[7] 周铨, 周列民, 朱丹. 颞叶癫痫患者海马硬化神经元脱失的亚群特点
[J]. 中华神经医学杂志, 2005, 4(7): 677-679.
[8] Mathern GW, Babb TL, Mischel PS, et al. Childhood generalized and mesial temporal epilepsies demonstrate differentamounts and patterns of hippocampal neuron loss and mossy fibre synapticreorganization
[J]. Brain, 1996, 119 ( Pt 3): 965-987.
[9] Bocti C, Robitaille Y, Diadori P, et al. The pathological basis of temporal lobe epilepsy in childhood
[J]. Neurology, 2003, 60(2): 191-195.
[10]McHugh JC, Delanty N. Epidemiology and classification of epilepsy: gender comparisons
[J]. Int Rev Neurobiol, 2008, 83(1): 11-26.
[11]Migliore M, Novara G, Tegolo D. Single neuron binding properties and the magical number 7
[J]. Hippocampus, 2008, 18(11): 1122-1130.
[12]Hattiangady B, Shetty AK. Decreased neuronal differentiation of newly generated cells underlies reducedhippocampal neurogenesis in chronic temporal lobe epilepsy
[J]. Hippocampus, 2010, 20(1): 97-112.
[13]Mathern GW, Babb TL, Vickrey BG, et al. The clinical-pathogenic mechanisms of hippocampal neuron loss and surgicaloutcomes in temporal lobe epilepsy
[J]. Brain, 1995, 118 ( Pt 1): 105-118.
[14]Bazelot M, Simonnet J, Dinocourt C, et al. Cellular anatomy, physiology and epileptiform activity in the CA3 region of Dcx knockout mice: a neuronal lamination defect and its consequences
[J]. Eur J Neurosci, 2012, 35(2): 244-256.
[15]Kappeler C, Dhenain M, Phan DTF, et al. Magnetic resonance imaging and histological studies of corpus callosal and hippocampal abnormalities linked to doublecortin deficiency
[J]. J Comp Neurol, 2007, 500(2): 239-254.
[16]Feng ZH, Hao J, Ye L, et al. Overexpression of mu-calpain in the anterior temporal neocortex of patients with intractable epilepsy correlates with clinicopathological characteristics
[J]. Seizure, 2011, 20(5): 395-401.
[17]张建刚, 宋延波, 张毅, 等. 生长抑素受体1在皮质发育障碍大鼠海马的异常表达
[J]. 中国实用神经疾病杂志, 2011, 14(21): 12-14.
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