Contribution of the delayed-rectifier potassium channel Kv2.1 to acute spinal cord injury in rats

• Published in: BMB reports Vol. 43; no. 11; pp. 756 - 760
• Main Authors: Song, M.Y., Kyung Hee University School of Medicine, Seoul, Republic of Korea, Moon, Y.J., Kyung Hee University School of Medicine, Seoul, Republic of Korea, Shin, S.K., Kyung Hee University School of Medicine, Seoul, Republic of Korea, Kim, T.Y., Kyung Hee University School of Medicine, Seoul, Republic of Korea, Yune, T.Y., Kyung Hee University School of Medicine, Seoul, Republic of Korea, Park, K.S., Kyung Hee University School of Medicine, Seoul, Republic of Korea
• Format: Journal Article
• Language: English
• Published: Korea (South) 생화학분자생물학회 01.11.2010
• Subjects: Acute Disease; Animals; APOPTOSE; APOPTOSIS; Delayed-rectifier Kv channel; Immunohistochemistry; Kv1.2 Potassium Channel - genetics; Kv1.2 Potassium Channel - metabolism; Neuron; Rats; RNA, Messenger - metabolism; Shab Potassium Channels - genetics; Shab Potassium Channels - metabolism; Shaw Potassium Channels - genetics; Shaw Potassium Channels - metabolism; Spinal Cord Injuries - etiology; Spinal Cord Injuries - metabolism; Spinal cord injury; Time Factors; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2010.43.11.756

Recent studies have reported that delayed-rectifier Kv channels regulate apoptosis in the nervous system. Herein, we investigated changes in the expression of the delayed-rectifier Kv channels Kv1.2, Kv2.1, and Kv3.1 after acute spinal cord injury (SCI) in rats. We performed RT-PCR analysis and found an increase in the level of Kv2.1 mRNA after SCI but no significant changes in the levels of Kv1.2 and Kv3.1 mRNA. Western blot analysis revealed that Kv2.1 protein levels rapidly decreased and then dramatically increased from 1 day, whereas Kv3.1b protein levels gradually and sharply decreased at 5 days. Kv1.2 protein levels did not change significantly. In addition, Kv2.1 clusters were disrupted in the plasma membranes of motor neurons after SCI. Interestingly, the expressional changes and translocation of Kv2.1 were consistent with the apoptotic changes on day 1. Therefore, these results suggest that Kv2.1 channels probably contribute to neuronal cell responses to SCI.