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Altered expression of Dscam in temporal lobe tissue from human and experimental animals
Author(s) -
Shen Lan,
Xiao Zheng,
Pan Yumin,
Fang Min,
Li Chengshan,
Chen Dan,
Wang Liang,
Xi Zhiqin,
Xiao Fei,
Wang Xuefeng
Publication year - 2011
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20924
Subject(s) - axon guidance , blot , biological neural network , immunohistochemistry , biology , temporal lobe , neuroscience , immunofluorescence , cell adhesion molecule , neural cell adhesion molecule , epilepsy , axon , pathology , microbiology and biotechnology , medicine , immunology , cell , cell adhesion , antibody , gene , genetics
Down syndrome cell adhesion molecule (Dscam) is a neural adhesion molecule that plays an essential role in the establishment of neural circuits. Considerable evidence suggests that Dscam is required for axon guidance and dendritic arborization. Our aim was to investigate the expression of Dscam in the temporal lobes of patients with intractable epilepsy (IE) and of experimental animals. In this study, we used immunohistochemistry, immunofluorescence, and western blotting to examine Dscam expression in thirty‐five surgical samples from brains of IE patients and 15 control brain samples. We also measured the levels of Dscam during the entire epileptic process in a rat model of temporal lobe epilepsy. Dscam expression in IE patients was significantly higher compared with that in the controls. In addition, Dscam was also highly expressed in the rat brain during the different phases of the epileptic process. It is the first time to find abnormal expression of Dscam in the brain tissues in patients with IE. And this finding provides an experimental evidence for the study of neuronal circuit remodeling and synaptic plasticity in IE, furthermore, our results also suggest that Dscam may be involved in the generation and the development of IE. Synapse, 2011. © 2011 Wiley‐Liss, Inc.