Neocortical in vivo focal and spreading potassium responses and the influence of astrocytic gap junctional coupling.

Raised extracellular potassium ion (K) concentration is associated with several disorders including migraine, stroke, neurotrauma and epilepsy. K spatial buffering is a well-known mechanism for extracellular K regulation/distribution. Astrocytic gap junction-mediated buffering is a controversial candidate for K spatial buffering. To further investigate the existence of a K spatial buffering and to assess the involvement of astrocytic gap junctional coupling in K redistribution, we hypothesized that neocortical K and concomitant spreading depolarization (SD)-like responses are controlled by powerful local K buffering mechanisms and that K buffering/redistribution occurs partially through gap junctional coupling. Herein, we show, in vivo, that a threshold amount of focally applied KCl is required to trigger local and/or distal K responses, accompanied by a SD-like response. This observation indicates the presence of powerful local K buffering which mediates a rapid return of extracellular K to the baseline. Application of gap junctional blockers, carbenoxolone and Gap27, partially modulated the amplitude and shape of the K response and noticeably decreased the velocity of the spreading K and SD-like responses. Opening of gap junctions by trimethylamine, slightly decreased the amplitude of the K response and markedly increased the velocity of redistribution of K and SD-like events. We conclude that spreading K responses reflect powerful local K buffering mechanisms which are partially modulated by gap junctional communication. Gap junctional coupling mainly affected the velocity of the K and SD-like responses.