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

Neocortical in vivo focal and spreading potassium responses and the influence of astrocytic gap junctional coupling. Neurobiol Dis. 2020 Nov 02;:105160 Authors: EbrahimAmini A, Bazzigaluppi P, Aquilino MS, Stefanovic B, Carlen PL Abstract 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+...
Source: Neurobiology of Disease - Category: Neurology Authors: Tags: Neurobiol Dis Source Type: research