Correlation study on expression of CaMKⅡ and ERK in Cerebral Cortex of autism mouse model

doi:10.11852/zgetbjzz2017-25-07-09

Abstract

Abstract: Objective To explore the role of calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ )and extracellular signal-regulated kinase ( ERK) in the pathogenesis of autism spectrum disorders. Methods Female Sprague-Dawley rats were given a single intraperitoneal injection of sodium valproate (VPA,600 mg/kg) on 12.5 d after pregnancy,and their offspring were as the model group; while the other pregnancy rats were given normal saline,and their offspring were as the control group.Both groups were observed with the HE staining,immunohistochemistry of CaMK Ⅱ and ERK and image analysis 1,7,14 d and 28 d after birth. Results Compared with the control group,HE staining showed the number of cortical neurons decreased on 1 d and 7 d after birth in the model group,rapidly increased on 14 d after birth,and maintained in high level on 28d after birth.For immunohistochemistry,the integrated optical density (IOD) of CaMKⅡ and ERK were increased in cortex on 1~14 d after birth (P<0.001) in both groups,and were stable 28 d after birth (P>0.05).Compared with the control group,the IOD of CaMK Ⅱ and ERK increased much more at every time point (P<0.001) in the model group.CaMK Ⅱ and ERK were increased on 1 d,7 d (P<0.001),significantly increased on 14 d (P<0.001),and tended to be stable on 28 d after birth (P>0.05). Conclusion The expression of CaMKⅡ and ERK of cerebral cortex neurons increases in the autism model rats,especially in the early time.

Key words: autistic spectrum disorders, pathogenesis, signal pathway, calmodulin-dependent protein kinase Ⅱ, extracellular signal-regulated kinase, rat model

摘要： 目的探讨钙调蛋白激酶Ⅱ(CaMK Ⅱ)和细胞外信号调节激酶(ERK)在孤独症谱系障碍发病中的作用。方法孕12.5 d Sprague-Dawley孕鼠腹腔注射丙戊酸钠600 mg/kg建立子代孤独症谱系障碍模型大鼠,对照组注射同等剂量生理盐水。利用HE染色、免疫组化和图像分析技术观察比较出生后1、7、14 d和28 d两组大鼠脑部CaMK Ⅱ、ERK表达情况。结果 HE染色:出生后1 d、7 d模型组神经元数量较少,出生14 d后剧增,出生后28 d仍高于对照组。免疫组化:出生后1~14 d两组CaMKⅡ、ERK表达均显著升高(P<0.001),出生28 d后表达趋于稳定(P>0.05);与对照组相比,模型组各日龄大鼠CaMK Ⅱ、ERK表达水平均增高(P<0.001);CaMK Ⅱ、ERK于出生后1 d、7 d表达显著升高(P<0.001),出生后14 d表达量最多(P<0.001),出生28 d后趋于稳定(P>0.05)。结论孤独症谱系障碍模型大鼠大脑皮层CaMK Ⅱ、ERK的表达增加,尤其是在出生后早期。

关键词: 孤独症谱系障碍, 发病机制, 信号通路, 钙调蛋白激酶Ⅱ, 细胞外信号调节激酶, 鼠模型

CLC Number:

R179

SUN Yan-qiu, JIANG Zhi-mei, NIE Ying, GUO Lan-min, LI Xue-mei, WANG Can. Correlation study on expression of CaMKⅡ and ERK in Cerebral Cortex of autism mouse model[J]. journal1, 2017, 25(7): 679-682.

孙艳秋, 姜志梅, 聂颖, 郭岚敏, 李雪梅, 王灿. 孤独症鼠模型脑组织CaMKⅡ和ERK表达的相关研究[J]. 中国儿童保健杂志, 2017, 25(7): 679-682.

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URL: https://manu41.magtech.com.cn/Jwk_zgetbjzz/EN/10.11852/zgetbjzz2017-25-07-09

https://manu41.magtech.com.cn/Jwk_zgetbjzz/EN/Y2017/V25/I7/679

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