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Anterior thalamic nuclei deep brain stimulation reduces disruption of the blood–brain barrier, albumin extravasation, inflammation and apoptosis in kainic acid-induced epileptic rats.

Authors :
Chen, Ying-Chuan
Zhu, Guan-Yu
Wang, Xiu
Shi, Lin
Du, Ting-Ting
Liu, De-Feng
Liu, Yu-Ye
Jiang, Yin
Zhang, Xin
Zhang, Jian-Guo
Source :
Neurological Research; Dec2017, Vol. 39 Issue 12, p1103-1113, 11p
Publication Year :
2017

Abstract

ObjectiveThe therapeutic efficacy of anterior thalamic nuclei deep brain stimulation (ATN-DBS) against seizures has been largely accepted; however, the effects of ATN-DBS on disruption of the blood–brain barrier (BBB), albumin extravasation, inflammation and apoptosis still remain unclear. MethodsRats were distributed into four treatment groups: physiological saline (PS, N = 12), kainic acid (KA, N = 12), KA-sham-DBS (N = 12) and KA-DBS (N = 12). Seizures were monitored using video-electroencephalogram (EEG). One day after surgery, all rats were sacrificed. Then, samples were prepared for quantitative real-time PCR (qPCR), western blot, immunofluorescence (IF) staining, and transmission electron microscopy to evaluate the disruption of the BBB, albumin extravasation, inflammation, and apoptosis. ResultBecause of the KA injection, the disruption of the BBB, albumin extravasation, inflammation and apoptosis were more severe in the KA and the KA-sham-DBS groups compared to the PS group (all Ps < 0.05 or < 0.01). The ideal outcomes were observed in the KA-DBS group. ATN-DBS produced a 46.3% reduction in seizure frequency and alleviated the disruption of the BBB, albumin extravasation, inflammatory reaction and apoptosis in comparison to the KA-sham-DBS group (all Ps < 0.05 or < 0.01). Conclusion(1) Seizures can be reduced using ATN-DBS in the epileptogenic stage. (2) ATN-DBS can reduce the disruption of the BBB and albumin extravasation. (3) ATN-DBS has an anti-inflammatory effect in epileptic models. [ABSTRACT FROM PUBLISHER]

Details

Language :
English
ISSN :
01616412
Volume :
39
Issue :
12
Database :
Complementary Index
Journal :
Neurological Research
Publication Type :
Academic Journal
Accession number :
126361508
Full Text :
https://doi.org/10.1080/01616412.2017.1379241