Potassium Outflux From Rabbit Cortex During Spreading Depression

Mechanisms involved in spreading depression

“…The increase in Na+ permeability caused by the presence of K f in the extracellular space will produce depolarization and an additional release of K +, which may further increase the Na + permeability. That potassium is released during SD was shown by the demonstration of K f in the washings of the surface of cortex invaded by SD (Brinley et al, 1960;Ki'ivAnek and Bures, 1960) and by its effect on the conduction in nerve tracts passing through a region invaded by SD (FifkovA and BureS, 1966;BureS, Hartmann and Lukyanovh, 1967;Bures and FifkovA, 1968). Finally a marked increase of the extracellular potassium concentration was demonstrated with K + sensitive microelectrodes during SD (Vyskokil, Ki.ii, and BureS, 1972).…”

“…This concept was supported by the demonstration of a release of K + from cerebral cortex invaded by SD (Brinley, Kandel, and Marshall, 1960;Ki-ivhek and Bureg, 1960). Concomitants of SD discovered subsequently, such as the impendance increase, the transport of extracellular chloride and water into cellular elements, and the contraction of the extracellular space, could be explained by an increase in Na + permeability of the plasma membrane of cellular elements (for references see Van Harreveld, 1966, 1972.…”

Activation of Meningeal Nociceptors by Cortical Spreading Depression: Implications for Migraine with Aura

“…Human studies have shown that the aura phase of migraine is associated with biphasic changes in cortical blood flow (initial hyperemia followed by sustained oligemia) that propagate throughout the surface of the visual cortex (Lauritzen and Olesen, 1984; Cao et al, 1999; Hadjikhani et al, 2001). The going theory is that ATP as well as glutamate, potassium, and hydrogen ions are released locally during the hyperemic phase of the CSD by neurons, glia (Brinley et al, 1960; Rapoport and Marshall, 1964; Csiba et al, 1985; Marrannes et al, 1988; D’Andrea et al, 1991; Lauritzen and Hansen, 1992; Fabricius et al, 1993; Mayevsky et al, 1996; James et al, 2001; Schock et al, 2007; Charles and Brennan, 2009) or vascular cells (Brennan et al, 2007). Regardless of the origin of their release, these mediators diffuse outward into the leptomeninges overlaying the affected cortical region, resulting in activation of pial nociceptors, local neurogenic inflammation and the persistent activation of dural nociceptors which triggers the migraine headache (Moskowitz, 1993).…”

Disturbances of Consciousness and the Application of Anticholinergic Compounds

“…T his m ig h t a p p ly to all th o se co n d itio n s w hich -in n eu ro physiological e x p e rim e n ts -are know n causes of sp read in g depression (M arshall [49]). On th e a ssu m p tio n th a t in all these cases, th e findings of B rin ley et al [8] are a p arallel to ch anges in acety lch o lin e (still to be in v e stig a te d , as m en tio n e d p rev io u sly ), it m ight be w orthw hile to s tu d y th e possible use o f an tich o lin erg ics in th e follow ing in sta n c e s: all in sta n c e s o f in ju ry (tra u m a , o p e ra tio n s, in sertio n o f electrodes), o f m etab o lically depressiv e a g e n ts (an o x ia, v ario u s poisons, ions [ K ! ], hypo g ly cem ia) or electrical (depolarizing) stim u li (seizures, E -shock, electro n arco sis ?…”