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Anat Cell Biol. 2011 Mar;44(1):50-59. English. Original Article. https://doi.org/10.5115/acb.2011.44.1.50
Yeo SI , Ryu HJ , Kim JE , Chun W , Seo CH , Lee BC , Choi IG , Sheen SH , Kang TC .
Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chuncheon, Korea. tckang@hallym.ac.kr
Institute of Epilepsy Research, College of Medicine, Hallym University, Chuncheon, Korea.
Department of Surgery, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.
Department of Rehabilitation, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.
Department of Psychiatry, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.
Department of Neurosurgery, Graduate School, School of Medicine, Kyung Hee University, Seoul, Korea.
Abstract

We analyzed aquaporin (AQP) expression in the rat spinal cord following an electrical shock (ES) to elucidate the roles of AQP in spinal cord injury (SCI) induced by an electrical burn. In control animals, AQP1 immunoreactivity was observed in the small diameter dorsal horn fibers of laminae I and II and in astrocytes and neurons in the spinal cord. Both AQP4 and AQP9 immunoreactivity were detected in astrocytes. One week after the ES, AQP1 immunoreactivity in dorsal horn fibers was downregulated to 83, 61, and 33% of control levels following a 1-, 4-, or 6-second ES, respectively. However, AQP1 immunoreactivity in ventral horn neurons increased to 1.3-, 1.5-, and 2.4-fold of control levels following a 1-, 4-, or 6-second ES, respectively. AQP4 immunoreactivity was upregulated after an ES in laminae I and II astrocytes in a stimulus-intensity independent manner. Unlike AQP1 and AQP4, AQP9 immunoreactivity was unaffected by the ES. These findings indicate that altered AQP immunoreactivity may be involved in SCI following an ES.

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