Journal
NEUROSCIENCE
Volume 268, Issue -, Pages 276-283Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2014.03.030
Keywords
NDEL1; DISC1; p-ERK; spontaneous seizures; status epilepticus; hippocampus
Categories
Funding
- National Natural Science Foundation of China [81100967, 81071048, 81000553]
- Specialized Research Fund for the Doctoral Program of Higher Education [20110162120002]
- Fundamental Research Funds for the Central Universities of China [2011QNZT152]
- Hunan Provincial Innovation Foundation For Postgraduate [2501-71380100001]
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Nuclear distribution factor E homolog like 1 (NDEL1) plays an important role in mitosis, neuronal migration, and microtubule organization during brain development by binding to disrupted-in-schizophrenia-1 (DISC1) or lissencephaly (LIS1). Although some evidence has suggested that DISC1 expression is altered in epilepsy, few studies have reported the relationship between NDEL1 and the etiology of epilepsy. In present study, we first investigated the expression of NDEL1 and its binding protein DISC1 after pilocarpine-induced epilepsy in male C57BL/6 mice. Data revealed that the mRNA and protein expression of NDEL1 and DISC1 in the whole hippocampus increased during the spontaneous seizure period after status epilepticus (SE). Interestingly, however, the expression of NDEL1 was decreased in the cornu ammonis 3 (CA3) and dentate gyrus (DG) regions. Moreover, SE also increased the number of blood vessels that fed the CA3 and DG regions of the hippocampus and increased the incidence of abnormalities in capillary network formation where NDEL1 protein was expressed positively. Meanwhile, the expression of phosphorylated ERK (p-ERK) was also increased during the spontaneous seizure period, with a similar expression pattern as NDEL1 and DISC1. Based on these results, we hypothesize that NDEL1 might interact with DISC1 to activate ERK signaling and function as a potential protective factor during the spontaneous seizure period after pilocarpine-induced SE. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
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