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Int J Med Sci. 2019 Jan 1;16(1):60-67. doi: 10.7150/ijms.27442. eCollection 2019.

A Novel Model for Studying Voltage-Gated Ion Channel Gene Expression during Reversible Ischemic Stroke.

Author information

1
Department of Surgery, E-Da Hospital, Kaohsiung, Taiwan.
2
Department of Orthopedic Surgery, E-Da Hospital, Kaohsiung, Taiwan.
3
Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA.
4
School of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan.
5
Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung, Taiwan.
6
Department of Neurology, China Medical University Hospital, Taichung, Taiwan.
7
School of Medicine, China Medical University, Taichung, Taiwan.
8
Department of Neurology, China Medical University, An-Nan Hospital, Tainan, Taiwan.
9
Department of Medical Research, E-Da Hospital/ E-Da Cancer Hospital, Kaohsiung, Taiwan.

Abstract

The dysfunction of voltage-gated ion channels contributes to the pathology of ischemic stroke. In this study, we developed rat models of transient ischemic attack (TIA) and reversible ischemic neurological deficit (RIND) that was induced via the injection of artificial embolic particles during full consciousness, that allow us to monitor the neurologic deficit and positron emission tomography (PET) scans in real-time. We then evaluated the infarction volume of brain tissue was confirmed by 2,3,5-triphenyl tetrazolium chloride (TTC) staining, and gene expressions were evaluated by quantitative real-time PCR (qPCR). We found that rats with TIA or RIND exhibited neurological deficits as determined by negative TTC and PET findings. However, the expression of voltage-gated sodium channels in the hippocampus was significantly up-regulated in the qPCR array study. Furthermore, an altered expression of sodium channel β-subunits and potassium channels, were observed in RIND compared to TIA groups. In conclusion, to our knowledge, this is the first report of the successful evaluation of voltage-gated ion channel gene expression in TIA and RIND animal models. This model will aid future studies in investigating pathophysiological mechanisms, and in developing new therapeutic compounds for the treatment of TIA and RIND.

KEYWORDS:

animal model; embolic stroke; reversible ischemic neurological deficit; transient ischemic attack; voltage-gated ion channels

Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

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