Research on expression and function of phosphorylated DARPP-32 on pentylenetetrazol-induced epilepsy model of rat.
- Author:
Weiwen WANG
;
Xiaoyang LIAO
;
Zhenghui YANG
;
Hang LIN
;
Qingsong WANG
;
Yuxian WU
;
Yu LIU
- Publication Type:Journal Article
- MeSH:
Animals;
Cerebral Cortex;
metabolism;
Corpus Striatum;
metabolism;
Dopamine and cAMP-Regulated Phosphoprotein 32;
metabolism;
Hippocampus;
metabolism;
Male;
Neurons;
metabolism;
Pentylenetetrazole;
Rats;
Rats, Sprague-Dawley;
Status Epilepticus;
chemically induced;
metabolism
- From:
Journal of Biomedical Engineering
2014;31(3):637-641
- CountryChina
- Language:Chinese
-
Abstract:
The present study is to explore the change process and distribution of phosphorylated DARPP-32 (p-DARPP-32) in rat brain including cortex, hippocampus and striatum and to further deduce whether p-DARPP-32 was possibly involved in epilepsy induced by repetitive low doses of pentylenetetrazol (PTZ). PTZ-induced epilepsy model in rat was established with 30 male SD rats randomly divided into 6 groups, control group and five trial groups [PTZ 1 h, PTZ 6 h, PTZ 24 h, PTZ 48 h and PTZ 72 h respectively, after onset of status epilepticus (SE)]. Immunohistochemistry and immunofluorescence double-labeling were used to detect the temporal time change and distribution of p-DARPP-32 expression and to analyze the coexpression of DARPP-32 and p-DARPP-32 in rat brain after the onset of PTZ-induced generalized SE. The results showed that there was a temporal time change of p-DARPP-32 expression in rat brain after the onset of SE. The number of p-DARPP-32-positive cells increased significantly and reached the peaks at the ends of 1 hour and 6 hours after the onset of SE, but decreased at the end of 24 hours. The moderate to strong p-DARPP-32-immunopositive neurons were observed in cortex, hippocampus and striatum, and located in cell cytoplasm and cell nucleus. Further immunofluorescence double-labeling revealed that denser colocalization of p-DARPP-32 and DARPP-32 in the neurons existed in the area mentioned above. Therefore, PTZ-induced SE may cause phosphorylation of DARPP-32 in rat brain. The temporal time change and distribution of p-DARPP-32 suggest that phosphorylation of DARPP-32 may be involved in PTZ-induced epilepsy in rat brain including cortex, hippocampus and striatum, and p-DARPP-32 may play a central role in the onset of SE.
