期刊
BIOSCIENCE REPORTS
卷 41, 期 6, 页码 -出版社
PORTLAND PRESS LTD
DOI: 10.1042/BSR20210736
关键词
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资金
- Swedish Research Council
- Swedish HeartLung Foundation
- Swedish Society of Medicine
- Swedish Stroke Association
- Magnus Bergvall foundation
- Stiftelsen Langmanska kulturfonden
- Stiftelsen Gamla tjanarinnor
- Lars Hiertas foundation
- Ake Wiberg foundation
- OE and Edla Johanssons vetenskapliga stiftelse
- Stiftelsen Tornspiran
- Emil and Wera Cornells foundation
- Dr. Felix Neuberghs Foundation
- Emelle Foundation
- Wilhelm and Martina Lundgren foundation
- Stohnes foundation
- Mary von Sydow foundation
- Swedish government [ALF GBG723131]
- county councils [ALF GBG723131]
The study investigated the expression of alpha 7nAChR in different brain regions and evaluated the potential effect of the alpha 7nAChR agonist AR-R17779 on ischemia-reperfusion brain injury in mice. It was found that alpha 7nAChR expression varies in different brain regions, and despite a decrease in white blood cells in sham mice receiving AR-R17779, this compound does not affect stroke-induced brain injury.
Inflammation plays a central role in stroke-induced brain injury. The alpha7 nicotinic acetylcholine receptor (alpha 7nAChR) can modulate immune responses in both the periphery and the brain. The aims of the present study were to investigate alpha 7nAChR expression in different brain regions and evaluate the potential effect of the selective alpha 7nAChR agonist AR-R17779 on ischemia-reperfusion brain injury in mice. Droplet digital PCR (ddPCR) was used to evaluate the absolute expression of the gene encoding alpha 7nAChR (Chrna7) in hippocampus, striatum, thalamus and cortex in adult, naive mice. Mice subjected to transient middle cerebral artery occlusion (tMCAO) or sham surgery were treated with alpha 7nAChR agonist AR-R17779 (12 mg/kg) or saline once daily for 5 days. Infarct size and microglial activation 7 days after tMCAO were analyzed using immunohistochemistry. Chrna7 expression was found in all analyzed brain regions in naive mice with the highest expression in cortex and hippocampus. At sacrifice, white blood cell count was significantly decreased in AR-R17779 treated mice compared with saline controls in the sham groups, although, no effect was seen in the tMCAO groups. Brain injury and microglial activation were evident 7 days after tMCAO. However, no difference was found between mice treated with saline or AR-R17779. In conclusion, alpha 7nAChR expression varies in different brain regions and, despite a decrease in white blood cells in sham mice receiving AR-R17779, this compound does not affect stroke-induced brain injury.
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