Passing potassium with and without gap junctions.

Editor's Note: These short reviews of a recent paper in the Journal, written exclusively by graduate students or postdoctoral fellows, are intended to mimic the journal clubs that exist in your own departments or institutions. For more information on the format and purpose of the Journal Club, please see Review of Wallraff et al. Glia, originally thought to play a passive role in the CNS, are now recognized as active regulators of CNS activity. For example , astrocytes are essential for the maintenance of extracellular ion concentrations , notably K ϩ , at physiological levels (Orkand et al., 1966). Any deviation of extracellular K ϩ concentration ([K ϩ ] o) from ϳ3 mM can affect neural activity. Elevated [K ϩ ] o occurs during seizure activity , ischemia, and spreading depression, in which [K ϩ ] o can reach 10 –50 mM (Walz, 2000; Somjen, 2002), with consequent effects on neuronal excitability and ultimately on cell viability. To limit increased [K ϩ ] o , astrocytes are equipped with a variety of K ϩ uptake mechanisms, including the Na ϩ-K ϩ-ATPase, Na ϩ-K ϩ-2Cl Ϫ cotransporters and voltage-activated K ϩ channels. Furthermore, local elevations in [K ϩ ] o shift the K ϩ equilibrium potential (E K) to more positive values relative to the membrane potential (V m), thus driving K ϩ into these cells along an electrochemical gradient. K ϩ can also be spatially buffered via diffusion through the astrocytic cytoplasm to areas of lower [K ϩ ] o , and then K ϩ is driven back out of the cell at distal sites at which E K is still more negative than the V m. Spatial redistribution of K ϩ is believed to be enhanced by gap junction coupling between astrocytes, although the experimental evidence for this mechanism is minimal (Walz, 2000; Kofuji and Newman, 2004). In their recent paper in The Journal of Neuroscience, Wallraff et al. (2006) examined the role of gap junction coupling between astrocytes in K ϩ buffer-ing and its subsequent physiological effect. Using hippocampal slices, the authors examined coupling in transgenic mice from which connexin43 (Cx43), the most abundant astrocytic Cx, had been conditionally deleted. Cx43/Cx30 double knockout (dko) mice were also used because Cx30 is the other major connexin in astrocytes. Dye coupling of the gap junction-permeable tracer biocytin was reduced in the Cx43 knockout and abolished in the dko [Wallraff et …