Expression of the kcnk3 potassium channel gene lessens the injury from cerebral ischemia, most likely by a general influence on blood pressure

• Verfasst von: Muḥammad, Sajjad [VerfasserIn]
• Verfasst von: Aller, M. I. [VerfasserIn]
• Verfasst von: Maser-Gluth, Christiane [VerfasserIn]
• Verfasst von: Schwaninger, Markus [VerfasserIn]
• Verfasst von: Wisden, William [VerfasserIn]
• Titel: Expression of the kcnk3 potassium channel gene lessens the injury from cerebral ischemia, most likely by a general influence on blood pressure
• Verf.angabe: S. Muhammad, M.I. Aller, C. Maser-Gluth, M. Schwaninger and W. Wisden
• E-Jahr: 2010
• Jahr: 16 February 2010
• Umfang: 7 S.
• Fussnoten: Gesehen am 11.05.2023
• Titel Quelle: Enthalten in: Neuroscience
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1976
• Jahr Quelle: 2010
• Band/Heft Quelle: 167(2010), 3, Seite 758-764
• ISSN Quelle: 1873-7544
• DOI: doi:10.1016/j.neuroscience.2010.02.024
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: cerebral ischemia
• Sach-SW: middle cerebral artery occlusion
• Sach-SW: stroke
• Sach-SW: TASK-1
• Sach-SW: TASK-3
• K10plus-PPN: 1845251466

Abstract

We examined the possible protective effect of TASK-1 (TWIK-related acid-sensitive potassium channel-1, kcnk3) and -3 potassium channels during stroke. TASK-1 and TASK-3, members of the two pore domain (K2P or kcnk) potassium channel family, form hetero or homodimers and help set the resting membrane potential. We used male TASK-1 and TASK-3 knockout mice in a model of focal cerebral ischemia, permanent middle cerebral artery occlusion (pMCAO). Infarct volume was measured 48 h after pMCAO. The TASK-1 knockout brains had larger infarct volumes (P=0.004), and those in TASK-3 knockouts were unchanged. As the TASK-1 gene is expressed in adrenal gland, heart and possibly blood vessels, the higher infarct volumes in the TASK-1 knockout mice could be due to TASK-1 regulating blood vessel tone and hence blood pressure or influencing blood vessel microarchitecture and blood flow rate. Indeed, we found that male TASK-1 knockout mice had reduced blood pressure, likely explaining the increased brain injury seen after pMCAO. Thus to make precise conclusions about how TASK-1 protects neurons, neural- or organ-specific deletions of the gene will be needed. Nevertheless, a consequence of having TASK-1 channels expressed (in various non-neuronal tissues and organs) is that neuronal damage is lessened when stroke occurs.