A Siphon Hypothesis Goes Down the Tube
نویسندگان
چکیده
So-called neurovascular coupling reflects local blood flow changes that accompany neuronal activity. Not only is this a homeostatic metabolic mechanism, but it also serves as the basis for functional brain imaging. The theory goes that glia cells siphon activity-generated extracellular potassium ions to glial endfeet abutting small blood vessels, leading to vessel relaxation. Not so, say Metea et al. in this week’s Journal. In a rat retina preparation, light stimulation evoked vasodilation as did increases in extracellular potassium. However, long and large depolarizations of single astrocytes or Müller cells did not produce changes in arteriole diameter. In mice lacking Kir4.1, the potassium channel that is expressed at glial endfeet adjacent to arterioles, light-evoked vasodilation was similar to wild-type mice. If it’s not potassium siphoning, what is it? The authors suggest that glial-derived arachidonic acid metabolites, known to contribute to vasomotor response, may be the culprit.
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