Department of Pharmacology, University of Vermont, Burlington, VT 05405, USA.
Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3811-6. doi: 10.1073/pnas.0914722107. Epub 2010 Feb 2.
Neuronal activity is thought to communicate to arterioles in the brain through astrocytic calcium (Ca(2+)) signaling to cause local vasodilation. Paradoxically, this communication may cause vasoconstriction in some cases. Here, we show that, regardless of the mechanism by which astrocytic endfoot Ca(2+) was elevated, modest increases in Ca(2+) induced dilation, whereas larger increases switched dilation to constriction. Large-conductance, Ca(2+)-sensitive potassium channels in astrocytic endfeet mediated a majority of the dilation and the entire vasoconstriction, implicating local extracellular K(+) as a vasoactive signal for both dilation and constriction. These results provide evidence for a unifying mechanism that explains the nature and apparent duality of the vascular response, showing that the degree and polarity of neurovascular coupling depends on astrocytic endfoot Ca(2+) and perivascular K(+).
神经元活动被认为通过星形胶质细胞钙（Ca(2+))信号传递到脑内的小动脉，从而引起局部血管舒张。矛盾的是，在某些情况下，这种通讯可能导致血管收缩。在这里，我们表明，无论星形胶质细胞终足 Ca(2+)升高的机制如何，适度增加 Ca(2+)诱导舒张，而较大的增加则将舒张转变为收缩。星形胶质细胞终足中的大电导、Ca(2+)-敏感钾通道介导了大部分的舒张和全部的血管收缩，提示局部细胞外 K(+)作为舒张和收缩的血管活性信号。这些结果为解释血管反应的性质和明显的双重性提供了统一的机制证据，表明神经血管耦联的程度和极性取决于星形胶质细胞终足 Ca(2+)和血管周 K(+)。
