小清蛋白和钙视网膜蛋白在皮质发育不良大鼠大脑皮质中的表达
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摘要
目的:
了解小清蛋白(PV)、钙视网膜蛋白(CR)在皮质发育不良(CD)大鼠大脑皮质中的表达,探讨其在鉴别不同类型CD和参与癫痫发病机制中的作用。
方法:
孕15d SD大鼠腹腔注射卡莫司汀(BCNU)建立子代鼠CD模型,观察仔鼠脑的生长发育和行为学改变,P30行热水浴诱发惊厥实验,组织病理学技术观察仔鼠皮质结构改变,免疫组化、免疫荧光、RT-PCR技术检测PV、CR在大鼠大脑皮质的表达。
结果:
①模型鼠脑质量较对照组减轻(P <0.05),脑体积减小;热水浴诱发惊厥潜伏期缩短(P <0.05);
②免疫组化显示模型鼠大脑皮质PV阳性细胞数量([37.28±2.72)个/视野]较对照组[(77.50±4.49个)/视野]减少(P <0.05)、空间分布紊乱、皮质浅层出现阳性细胞结节和阳性细胞空白区;CR的表达较对照组无显著差异;
③免疫荧光示模型鼠PV阳性细胞减少,胞体增大;
④RT-PCR检测显示模型鼠PV mRNA表达显著降低,CR mRNA的表达无显著差异。
结论:
1 PV可作为鉴定不同类型CD的指标;
2表达PV的GABA能抑制性中间神经元的损伤可能在CD所致的难治性癫痫中具有重要作用。
Abjective:
To get a message of the expression about parvalbumin and calretinin in the Cortical dysplasia (CD) model rats and investigate the effect in identify different types of CD and the pathogenesy of intractable epilepsy which induced by CD.
Methods:
Sprague-Dawley pregnant rats were given intraperitoneal injections of 1-3-bis-chloroethyl-nitrosourea (BCNU) ,15mg/kg ,on embryonic day 15 (E15) can induce CD in the offspring. We observed the growth and development of the brain and praxiology change in the offspring,used the warm-water-immerse to induce seizure, cortical histopathology was examined in the resulting pups at postnatal 30 day (P30). At the same time, form the results of immunocytochemistry , Immunofluorescence and RT-PCR ,we got the expression of parvalbumin and calretinin in the cortex .
Results:
①Compared to the control group rats,the model rats was lessen of brain weight and volume (P<0.05) ; the latency period before seizure was shorter (P<0.05) ;
②Immunohistochemical Hdemonstrated that the density of parvalbumin-immunoreactive cells in the model rats was 37.28±2.72 cells/ field and 77.50±4.49 cells/ field in the control group rats, which reduced significantly (P<0.05) and have an altered spatial distribution , some parvalbumin-immunoreactive cells nodus appeared in the superficial layers of the cortex, but in the peripheral cortex of it ,the parvalbumin-immunoreactive cells reduced or disappeared .The calretinin-immunoreactive cells were similar to the control group;
③Immunofluorescence technique showed that the density of the parvalbumin-immunoreactive cells was reduced and the size of which was increased in theⅣlayer of the cortex of CD rats;
④Form the RT-PCR results, we got a reduced expression of parvalbumin-mRNA (P<0.05) , but the expression of calretinin -mRNA was similar to the control group.
Conclusions:
1 The parvalbumin can use for index to identify different types of CD;
2 The abnormal density and distribution of GABAergic interneurons which express parvalbumin in the CD model rats may play a pivotal role in the pathophysiologic mechanisms of intractable epilepsy .
了解小清蛋白(PV)、钙视网膜蛋白(CR)在皮质发育不良(CD)大鼠大脑皮质中的表达,探讨其在鉴别不同类型CD和参与癫痫发病机制中的作用。
方法:
孕15d SD大鼠腹腔注射卡莫司汀(BCNU)建立子代鼠CD模型,观察仔鼠脑的生长发育和行为学改变,P30行热水浴诱发惊厥实验,组织病理学技术观察仔鼠皮质结构改变,免疫组化、免疫荧光、RT-PCR技术检测PV、CR在大鼠大脑皮质的表达。
结果:
①模型鼠脑质量较对照组减轻(P <0.05),脑体积减小;热水浴诱发惊厥潜伏期缩短(P <0.05);
②免疫组化显示模型鼠大脑皮质PV阳性细胞数量([37.28±2.72)个/视野]较对照组[(77.50±4.49个)/视野]减少(P <0.05)、空间分布紊乱、皮质浅层出现阳性细胞结节和阳性细胞空白区;CR的表达较对照组无显著差异;
③免疫荧光示模型鼠PV阳性细胞减少,胞体增大;
④RT-PCR检测显示模型鼠PV mRNA表达显著降低,CR mRNA的表达无显著差异。
结论:
1 PV可作为鉴定不同类型CD的指标;
2表达PV的GABA能抑制性中间神经元的损伤可能在CD所致的难治性癫痫中具有重要作用。
Abjective:
To get a message of the expression about parvalbumin and calretinin in the Cortical dysplasia (CD) model rats and investigate the effect in identify different types of CD and the pathogenesy of intractable epilepsy which induced by CD.
Methods:
Sprague-Dawley pregnant rats were given intraperitoneal injections of 1-3-bis-chloroethyl-nitrosourea (BCNU) ,15mg/kg ,on embryonic day 15 (E15) can induce CD in the offspring. We observed the growth and development of the brain and praxiology change in the offspring,used the warm-water-immerse to induce seizure, cortical histopathology was examined in the resulting pups at postnatal 30 day (P30). At the same time, form the results of immunocytochemistry , Immunofluorescence and RT-PCR ,we got the expression of parvalbumin and calretinin in the cortex .
Results:
①Compared to the control group rats,the model rats was lessen of brain weight and volume (P<0.05) ; the latency period before seizure was shorter (P<0.05) ;
②Immunohistochemical Hdemonstrated that the density of parvalbumin-immunoreactive cells in the model rats was 37.28±2.72 cells/ field and 77.50±4.49 cells/ field in the control group rats, which reduced significantly (P<0.05) and have an altered spatial distribution , some parvalbumin-immunoreactive cells nodus appeared in the superficial layers of the cortex, but in the peripheral cortex of it ,the parvalbumin-immunoreactive cells reduced or disappeared .The calretinin-immunoreactive cells were similar to the control group;
③Immunofluorescence technique showed that the density of the parvalbumin-immunoreactive cells was reduced and the size of which was increased in theⅣlayer of the cortex of CD rats;
④Form the RT-PCR results, we got a reduced expression of parvalbumin-mRNA (P<0.05) , but the expression of calretinin -mRNA was similar to the control group.
Conclusions:
1 The parvalbumin can use for index to identify different types of CD;
2 The abnormal density and distribution of GABAergic interneurons which express parvalbumin in the CD model rats may play a pivotal role in the pathophysiologic mechanisms of intractable epilepsy .
引文
[1] Guerrini R ,Sicca F,Parmeggiani L.Epilepsy and malformations of the cerebral cortex[J].Epileptic Disorder,2003,5(Suppl 2):9-26
[2] Sisodiya S M. Malformations of cortical development:burdens and insights from important causes of human epilepsy[J]. Lancet Neurol,2004,3(1):29-38
[3]晏勇.皮质发育障碍的癫痫发作[J].重庆医学,2001,30(5):464-466
[4] Barkovich AJ, Kuzniecky RJ, Jackson GD, et al .A development and genetic classification for malformations of cortical development [J]. Neurology, 2005, 12 : 1873- 1887.
[5] Leventer RJ, Guerrini R, Dobyns WB, et a1.Malformations of cortical development and epilepsy[J].Dialogues Clin Neurosci, 2008, 10(1):47-62
[6] Chen, HX, Steven NR. Reduction of Spontaneous Inhibitory Synaptic Activity in Experimental Heterotopic Gray Matter[J]. Neurophysiol. 2003;89: 150-8
[7] Valencia I, Legido A, Yelin K, et al . Anomalous inhibitory circuits in cortical tubers of human tuberous sclerosis complex associated with refractory epilepsy: aberrant expression of parvalbumin and calbindin-D28k in dysplastic cortex[J].Child Neurol, 2006, 21(12):1058-63
[8] Wu MJ,Lai LW&Lien YH.Efect of calbindin-D28K on cyclosporine toxicity in cultured renal proximal tubular cells[J]. Cell Physiol,2004,200(3):3 95-9
[9] Liu Y’Porta A,Peng X,et a1.Prevention of glucocorticoid.induced apoptosis in osteocytes and osteoblasts by calbindin-D28k[J]. Bone Miner Res,2004,19(3):479-90
[10] Aronica E, Redeker S, Boer K, et al .Inhibitory networks in epilepsy-associated gangliogliomas and in the perilesional epileptic cortex[J].Epilepsy Res ,2007,74(1):33-44.
[11] Hevner RF.Layer-specific markers as probes for neuron type identity in human neocortex and malformations of cortical development[J].Neuropathol Exp Neurol ,2007 ,66(2):101-9.
[12] Lurton D, Yacubian EM, Sanabria EG, et al .Immunohistochemical study of six cases of Taylor's type focal cortical dysplasia: correlation with electroclinical data.[J]. Epilepsia ,2002, 43 Suppl 5:217-9
[13] M. Thom·B. N. Harding·W.-R. Lin , et a1.Sisodiya Cajal-Retzius cells, inhibitory interneuronal populations and neuropeptide Y expression in focal cortical dysplasia and microdysgenesis[J].Acta Neuropathol ,2003,105 : 561–569
[14] Zamecnik J, Krsek P, Druga R, et al . Densities of parvalbumin-immunoreactive neurons in non-malformed hippocampal sclerosis-temporal neocortex and in cortical dysplasias[J].Brain Res Bull ,2006 , 68(6):474-81
[15] Garbelli R, Meroni A, Magnaghi G, et al .Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy[J].Epilepsia, 2006 , 47(6):949-51
[16] AndréVM, Cepeda C, Vinters HV, et al . Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia[J].Neurosci Res ,2008 ,86(14):3151-62
[17] Aronica E, Redeker S, Boer K, et al.Epilepsy Res.Inhibitory networks in epilepsy-associated gangliogliomas and in the perilesional epileptic cortex [J]. Epilepsy Res.2007, 74(1):33-44
[18] M. Thom·B. N. Harding·W.-R. Lin , et al. Cajal-Retzius cells, inhibitory interneuronal populations and neuropeptide Y expression in focal cortical dysplasia and microdysgenesis. [J].Acta Neuropathol ,2003, 105 (6): 561–569.
[19] Zamecnik J, Krsek P, Druga R, et al . Densities of parvalbumin-immunoreactive neurons in non-malformed hippocampal sclerosis-temporal neocortex and in cortical dysplasias[J]. Brain Res Bull, 2006 ,68 (6):474-81
[20] L. Alonso-Nanclares, R. Garbelli, R. G. Sola, et al .Microanatomy of the dysplastic neocortex from epileptic patients. Brain, 2005 ,128(1):158-173.
[21] Stacey A. Trotter,Jaideep Kapur,Matthew J. Anzivino,et al .GABAergic Synaptic Inhibition Is Reduced before Seizure Onset in a Genetic Model of Cortical Malformation[J].Neuroscience, 2006, 26(42):10756-10767
[22] Cai LX, Piao YS, Liu L, et al.Correlation between characteristics of interictal epileptiform discharge and histopathological change in epilepsy patients with focal cortical dysplasia[J].Zhonghua Yi Xue Za Zhi. 2008;88(17):1153-7
[23] Valencia I, Legido A, Yelin K, et al .Anomalous inhibitory circuits in cortical tubers of human tuberous sclerosis complex associated with refractory epilepsy: aberrant expression of parvalbumin and calbindin-D28k in dysplastic cortex[J].Child Neurol ,2006 , (12):1058-63
[24]何选丽,晏勇,马勋泰,等.卡莫司汀诱导大鼠皮质发育障碍模型的研究[J].第三军医大学学报,2007,29(17):1729-1731
[25]官云里,晏勇,马勋泰,等.皮质发育不良模型鼠脑层特异性标志物SMI- 32的表达[J].重庆医科大学学报,2008,33(1):33-36
[26] Racine BJ. Modification of seizure activity by electrical stimulation :Ⅱ.Motor seizure [J]. Electroencephalography and Clinical Neurophysiology,1972(3):281-294
[27] Ueda-Kawamitsu H,Lawson T A,Gwih P R, et a1.In vitro pharrnacokinetics and pharrnacodynamics of 1,3-bis(2-chloroethy1)-1-nitrosourea(BC-NU)[J].Biochem Pharmacol,2002,63(7):1209-1218
[28] Ferrer l, S. Alcdntara a, M. J. Zfijar 1, et al. Structure and pathogenesis of cortical nodules induced by prenatal X-irradiation in the rat [J]. Acta Neuropathol , 1993 ,85(2):205– 212
[29] Spreafico R, Battaglia G, Arcelli P, et a1.Cortical dysplasia: an immunocytochemical study of three patients[J].Neurology. 1998 Jan;50(1):8-10
[30] Benardete EA, Kriegstein AR,Increased excitability and decreased sensitivity to GABA in an animal model of dysplastic cortex[J].Epilepsia.2002 Sep;43(9):970-82
[31] Ramona Frida Moroni, Francesca Inverardi, Maria Cristina Regondi, et al. Altered spatial distribution of PV-cortical cells and dysmorphic neurons in the somatosensory cortex of BCNU-treated rat model of cortical dysplasia[J]. Epilepsia ,2008,49(5):872–887
[32] Gulyás AI, Megías M, Emri Z, et a1.Total Number and Ratio of Excitatory and Inhibitory Synapses Converging onto Single Interneurons of Different Types in the CA1 Area of the Rat Hippocampus [J]. Neuroscience, 1999, 19(22): 10082-10097
[33] Voelker CCJ, Garin N, Taylor JSH, et al. Selective neurofilament (SMI-32, FNP-7 and N200) expression in subpopulations of layer V pyramidal neurons in vivo and in vitro [J]. Cereb Cortex 2004;14:1276-86
[34] Yoneshima H, Yamasaki S, Voelker CCJ, et al. ER81 is expressed in a subpopulation of layer 5 neurons in rodent and primate neocortices [J]. Neuroscience 2006;137:401-12
[35] Molna′r Z, Cheung AFP. Towards the classification of subpopulations of layer V pyramidal projection neurons[J].Neurosci Res 2006;55:105-15
[36] Robert F Hevner, Layer-Specific Markers as Probes for Neuron Type Identity in Human Neocortex and Malformations of Cortical Development [J]. Neuropathology and Experimental Neurology, 2007 ,66(2):101-9
[1] Barkovich AJ, Kuzniecky RJ, Jackson GD, et al .A development and genetic classification for malformations of cortical development[J].Neurology, 2005, 12 : 1873 - 1887
[2] Leventer RJ, Guerrini R, Dobyns WB. Malformations of cortical development and epilepsy[J].Dialogues Clin Neurosci, 2008, 10(1):47-62
[3] Valencia I, Legido A, Yelin K, et al . Anomalous inhibitory circuits in cortical tubers of human tuberous sclerosis complex associated with refractory epilepsy: aberrant expression of parvalbumin and calbindin-D28k in dysplastic cortex[J].Child Neurol, 2006, 21(12):1058-63
[4] Luu K C , Nie G Y , Hampton A , et al . Endometrial expression of calbindin (CaBP-d9k ) but not CaBP‐ 28k in primates implies evolutionary changes and functional redundancy of calbindins at implantation[J]. Reproduction , 2004 ,128(4) :433‐4 41
[5] Aronica E, Redeker S, Boer K, et al .Inhibitory networks in epilepsy-associated gangliogliomas and in the perilesional epileptic cortex[J]. Epilepsy Res , 2007, 74(1):33-44
[6] Hevner RF.Layer-specific markers as probes for neuron type identity in human neocortex and malformations of cortical development[J].Neuropathol Exp Neurol ,2007 ,66(2):101-9
[7] Zecevic N, Chen Y, Filipovic R. Contributions of cortical subventricular zone to the development of the human cerebral cortex[J]. Comp Neurol ,2005 , 91:109-22
[8] Pancoast M, Dobyns W, Golden JA. Interneuron deficits in patients with the Miller-Dieker syndrome[J].Acta Neuropathol ,2005, 109 :400-404
[9] Penschuck S, Flagstad P, Didriksen M ,et al .Decrease in parvalbumin-expressing neurons in the hippocampus and increased phencyclidine-induced locomotor activity in the rat methylazoxymethanol (MAM) model of schizophrenia [J]. Neuroscience ,2006 ,23 (1):279-84
[10] Ramona Frida Moroni,receptors and parvalbumin-positive neurons in intractable epilepsy-related focal cortical dysplasia[J].Zhonghua Bing Li Xue Za Zhi. 2008;37(1):16-20
[15]官云里,晏勇,《大脑皮质特异性层标志物探针与皮质发育畸形研究进展》[J].重庆医学,2008,37(2),202-204
[16] Garbelli R, Meroni A, Magnaghi G, et al .Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy[J].Epilepsia, 2006 , 47(6):949-51
[17] AndréVM, Cepeda C, Vinters HV, et al . Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia[J].Neurosci Res ,2008 ,86(14):3151-62
[18] Zamecnik J, Krsek P, Druga R, et al . Densities of parvalbumin-immunoreactive neurons in non-malformed hippocampal sclerosis-temporal neocortex and in cortical dysplasias[J].Brain Res Bull, 2006 ,68 (6):474-81
[19] L. Alonso-Nanclares1, R. Garbelli3, R. G. Sola2, et al .Microanatomy of the dysplastic neocortex from epileptic patients[J].Brain, 2005 ,128(1):158-173
[20] Stacey A. Trotter,1 Jaideep Kapur,2 Matthew J. Anzivino,1 et al .GABAergic Synaptic Inhibition Is Reduced before Seizure Onset in a Genetic Model of Cortical Malformation[J].Neuroscience, 2006, 26(42):10756-10767
[21] Cai LX, Piao YS, Liu L, et al.Correlation between characteristics of interictal epileptiform discharge and histopathological change in epilepsy patients with focal cortical dysplasia[J].Zhonghua Yi Xue Za Zhi. 2008;88(17):1153-7. [Article in Chinese]
[22] Valencia I, Legido A, Yelin K, et al .Anomalous inhibitory circuits in cortical tubers of human tuberous sclerosis complex associated with refractory epilepsy: aberrant expression of parvalbumin and calbindin-D28k in dysplastic cortex[J].Child Neurol ,2006 , (12):1058-63
[2] Sisodiya S M. Malformations of cortical development:burdens and insights from important causes of human epilepsy[J]. Lancet Neurol,2004,3(1):29-38
[3]晏勇.皮质发育障碍的癫痫发作[J].重庆医学,2001,30(5):464-466
[4] Barkovich AJ, Kuzniecky RJ, Jackson GD, et al .A development and genetic classification for malformations of cortical development [J]. Neurology, 2005, 12 : 1873- 1887.
[5] Leventer RJ, Guerrini R, Dobyns WB, et a1.Malformations of cortical development and epilepsy[J].Dialogues Clin Neurosci, 2008, 10(1):47-62
[6] Chen, HX, Steven NR. Reduction of Spontaneous Inhibitory Synaptic Activity in Experimental Heterotopic Gray Matter[J]. Neurophysiol. 2003;89: 150-8
[7] Valencia I, Legido A, Yelin K, et al . Anomalous inhibitory circuits in cortical tubers of human tuberous sclerosis complex associated with refractory epilepsy: aberrant expression of parvalbumin and calbindin-D28k in dysplastic cortex[J].Child Neurol, 2006, 21(12):1058-63
[8] Wu MJ,Lai LW&Lien YH.Efect of calbindin-D28K on cyclosporine toxicity in cultured renal proximal tubular cells[J]. Cell Physiol,2004,200(3):3 95-9
[9] Liu Y’Porta A,Peng X,et a1.Prevention of glucocorticoid.induced apoptosis in osteocytes and osteoblasts by calbindin-D28k[J]. Bone Miner Res,2004,19(3):479-90
[10] Aronica E, Redeker S, Boer K, et al .Inhibitory networks in epilepsy-associated gangliogliomas and in the perilesional epileptic cortex[J].Epilepsy Res ,2007,74(1):33-44.
[11] Hevner RF.Layer-specific markers as probes for neuron type identity in human neocortex and malformations of cortical development[J].Neuropathol Exp Neurol ,2007 ,66(2):101-9.
[12] Lurton D, Yacubian EM, Sanabria EG, et al .Immunohistochemical study of six cases of Taylor's type focal cortical dysplasia: correlation with electroclinical data.[J]. Epilepsia ,2002, 43 Suppl 5:217-9
[13] M. Thom·B. N. Harding·W.-R. Lin , et a1.Sisodiya Cajal-Retzius cells, inhibitory interneuronal populations and neuropeptide Y expression in focal cortical dysplasia and microdysgenesis[J].Acta Neuropathol ,2003,105 : 561–569
[14] Zamecnik J, Krsek P, Druga R, et al . Densities of parvalbumin-immunoreactive neurons in non-malformed hippocampal sclerosis-temporal neocortex and in cortical dysplasias[J].Brain Res Bull ,2006 , 68(6):474-81
[15] Garbelli R, Meroni A, Magnaghi G, et al .Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy[J].Epilepsia, 2006 , 47(6):949-51
[16] AndréVM, Cepeda C, Vinters HV, et al . Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia[J].Neurosci Res ,2008 ,86(14):3151-62
[17] Aronica E, Redeker S, Boer K, et al.Epilepsy Res.Inhibitory networks in epilepsy-associated gangliogliomas and in the perilesional epileptic cortex [J]. Epilepsy Res.2007, 74(1):33-44
[18] M. Thom·B. N. Harding·W.-R. Lin , et al. Cajal-Retzius cells, inhibitory interneuronal populations and neuropeptide Y expression in focal cortical dysplasia and microdysgenesis. [J].Acta Neuropathol ,2003, 105 (6): 561–569.
[19] Zamecnik J, Krsek P, Druga R, et al . Densities of parvalbumin-immunoreactive neurons in non-malformed hippocampal sclerosis-temporal neocortex and in cortical dysplasias[J]. Brain Res Bull, 2006 ,68 (6):474-81
[20] L. Alonso-Nanclares, R. Garbelli, R. G. Sola, et al .Microanatomy of the dysplastic neocortex from epileptic patients. Brain, 2005 ,128(1):158-173.
[21] Stacey A. Trotter,Jaideep Kapur,Matthew J. Anzivino,et al .GABAergic Synaptic Inhibition Is Reduced before Seizure Onset in a Genetic Model of Cortical Malformation[J].Neuroscience, 2006, 26(42):10756-10767
[22] Cai LX, Piao YS, Liu L, et al.Correlation between characteristics of interictal epileptiform discharge and histopathological change in epilepsy patients with focal cortical dysplasia[J].Zhonghua Yi Xue Za Zhi. 2008;88(17):1153-7
[23] Valencia I, Legido A, Yelin K, et al .Anomalous inhibitory circuits in cortical tubers of human tuberous sclerosis complex associated with refractory epilepsy: aberrant expression of parvalbumin and calbindin-D28k in dysplastic cortex[J].Child Neurol ,2006 , (12):1058-63
[24]何选丽,晏勇,马勋泰,等.卡莫司汀诱导大鼠皮质发育障碍模型的研究[J].第三军医大学学报,2007,29(17):1729-1731
[25]官云里,晏勇,马勋泰,等.皮质发育不良模型鼠脑层特异性标志物SMI- 32的表达[J].重庆医科大学学报,2008,33(1):33-36
[26] Racine BJ. Modification of seizure activity by electrical stimulation :Ⅱ.Motor seizure [J]. Electroencephalography and Clinical Neurophysiology,1972(3):281-294
[27] Ueda-Kawamitsu H,Lawson T A,Gwih P R, et a1.In vitro pharrnacokinetics and pharrnacodynamics of 1,3-bis(2-chloroethy1)-1-nitrosourea(BC-NU)[J].Biochem Pharmacol,2002,63(7):1209-1218
[28] Ferrer l, S. Alcdntara a, M. J. Zfijar 1, et al. Structure and pathogenesis of cortical nodules induced by prenatal X-irradiation in the rat [J]. Acta Neuropathol , 1993 ,85(2):205– 212
[29] Spreafico R, Battaglia G, Arcelli P, et a1.Cortical dysplasia: an immunocytochemical study of three patients[J].Neurology. 1998 Jan;50(1):8-10
[30] Benardete EA, Kriegstein AR,Increased excitability and decreased sensitivity to GABA in an animal model of dysplastic cortex[J].Epilepsia.2002 Sep;43(9):970-82
[31] Ramona Frida Moroni, Francesca Inverardi, Maria Cristina Regondi, et al. Altered spatial distribution of PV-cortical cells and dysmorphic neurons in the somatosensory cortex of BCNU-treated rat model of cortical dysplasia[J]. Epilepsia ,2008,49(5):872–887
[32] Gulyás AI, Megías M, Emri Z, et a1.Total Number and Ratio of Excitatory and Inhibitory Synapses Converging onto Single Interneurons of Different Types in the CA1 Area of the Rat Hippocampus [J]. Neuroscience, 1999, 19(22): 10082-10097
[33] Voelker CCJ, Garin N, Taylor JSH, et al. Selective neurofilament (SMI-32, FNP-7 and N200) expression in subpopulations of layer V pyramidal neurons in vivo and in vitro [J]. Cereb Cortex 2004;14:1276-86
[34] Yoneshima H, Yamasaki S, Voelker CCJ, et al. ER81 is expressed in a subpopulation of layer 5 neurons in rodent and primate neocortices [J]. Neuroscience 2006;137:401-12
[35] Molna′r Z, Cheung AFP. Towards the classification of subpopulations of layer V pyramidal projection neurons[J].Neurosci Res 2006;55:105-15
[36] Robert F Hevner, Layer-Specific Markers as Probes for Neuron Type Identity in Human Neocortex and Malformations of Cortical Development [J]. Neuropathology and Experimental Neurology, 2007 ,66(2):101-9
[1] Barkovich AJ, Kuzniecky RJ, Jackson GD, et al .A development and genetic classification for malformations of cortical development[J].Neurology, 2005, 12 : 1873 - 1887
[2] Leventer RJ, Guerrini R, Dobyns WB. Malformations of cortical development and epilepsy[J].Dialogues Clin Neurosci, 2008, 10(1):47-62
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