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Acid‐sensing ion channel 1 is expressed in cerebral arteries and located near neuronal nitric oxide synthase
Author(s) -
Lin LiHsien,
Talman William T.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.604.6
Subject(s) - acid sensing ion channel , cerebral arteries , middle cerebral artery , nitric oxide synthase , ischemia , anterior cerebral artery , basilar artery , medicine , posterior cerebral artery , neuronal nitric oxide synthase , neuroscience , anatomy , ion channel , nitric oxide , biology , receptor
Dramatic tissue acidosis is a common feature of ischemic brain. Responses to acid may be mediated through acid‐sensing ion channels (ASICs), a family of proteins that are activated by acid or modulate acid‐gated subunits. One ASICs subtype, ASIC type 1 (ASIC1), has been implicated in ischemic brain injury. Although ASIC1 is found in many areas of the brain, it is not known if it is expressed in cerebral arteries. Nitric oxide (NO) may modulate ASICs activity and upregulation of neuronal NO synthase (nNOS) in the parasympathetic innervation of cerebral vessels may protect the brain from ischemia. Therefore, we sought to examine the expression of ASIC1 as well as the anatomical relationship between ASIC1 and nNOS in rat cerebral arteries. Confocal images of immunofluorescent stained brain sections showed that ASIC1‐immunoreactivity (IR) was present in smooth muscle layers of the anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior communicating artery (PCA) and basilar artery (BA). This layer was confirmed to be positive for alpha‐smooth muscle actin, a marker for smooth muscle. nNOS‐IR was noted in immediately adjacent endothelial and adventitial layers of ACA, MCA, PCA and BA. The close anatomical location of ASIC1 and nNOS suggests a possible interaction between ASIC1 and nNOS in regulating vasomotor tone and in mediating brain injury induced by ischemia. Support: NIH R01 HL59593 and R01 HL088090.