TY - JOUR T1 - K+ at concentrations reached in the extracellular space during neuronal activity promotes a Ca2+-dependent glycogen hydrolysis in mouse cerebral cortex JF - The Journal of Neuroscience JO - J. Neurosci. SP - 1922 LP - 1928 DO - 10.1523/JNEUROSCI.08-06-01922.1988 VL - 8 IS - 6 AU - PR Hof AU - E Pascale AU - PJ Magistretti Y1 - 1988/06/01 UR - http://www.jneurosci.org/content/8/6/1922.abstract N2 - The effect of increasing [K+]0 on 3H-glycogen levels was examined in mouse cerebral cortical slices. K+ stimulates in a time- and concentration-dependent manner the hydrolysis of 3H-glycogen. Over 70% of the maximal effect is reached within 30 sec and the EC50 for the glycogenolytic action of K+ is 11 mM. Significant 3H-glycogen hydrolysis occurs at 5–12 mM [K+]0, concentrations reached by the ion in the extracellular space during neuronal activity. The K+-evoked glycogenolysis is Ca2+-dependent, and is inhibited by Ca2+-channel blockers such as Ni2+ and Mn2+, but not by Cd2+, nifedipine, and omega- conotoxin. Furthermore, the effect of K+ is not enhanced by the Ca2+- channel agonist Bay K 8644. This type of pharmacological profile suggests that the activation of voltage-sensitive Ca2+ channels of the T subtype mediates the glycogenolytic action of K+. This set of observations suggests that K+ released in the extracellular space by active neurons may promote the mobilization of energy substrates and therefore play a role in the coupling between neuronal activity and energy metabolism. ER -