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 weeks 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 Muller 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 its 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.

Is it pre- or postsynaptic? used to be the battle cry for workers in the long-term potentiation field. Now its a question for those studying TrkB. Signaling between brain-derived neurotrophic factor and its receptor TrkB contributes to the development of visual pathways. Marshak et al. made use of the alternatively spliced TrkB.T1, which lacks the intracellular kinase domain and thus can act as a dominant-negative inhibitor of TrkB signaling. The authors overexpressed a green fluorescent protein (GFP)TrkB1.T1 fusion protein in their favorite presynaptic cells, Xenopus laevis retinal ganglion cells (RGCs). GFPTrkB.T1 did not disrupt axon pathfinding to the tectum. However, time-lapse
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