Expression of the kcnk3 potassium channel gene lessens the injury from cerebral ischemia, most likely by a general influence on blood pressure
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...
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| Main Authors: | , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
16 February 2010
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| In: |
Neuroscience
Year: 2010, Volume: 167, Issue: 3, Pages: 758-764 |
| ISSN: | 1873-7544 |
| DOI: | 10.1016/j.neuroscience.2010.02.024 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.neuroscience.2010.02.024 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0306452210002204 
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| Author Notes: | S. Muhammad, M.I. Aller, C. Maser-Gluth, M. Schwaninger and W. Wisden |
| Summary: | 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. |
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| Item Description: | Gesehen am 11.05.2023 |
| Physical Description: | Online Resource |
| ISSN: | 1873-7544 |
| DOI: | 10.1016/j.neuroscience.2010.02.024 |