Extracellular potassium concentration in chronic alumina cream foci of cats.
Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.
D000536:Aluminum Hydroxide / Q000633:toxicity*; D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D004827:Epilepsy / Q000139:chemically induced* / Q000378:metabolism; D005071:Evoked Potentials / Q000187:drug effects; D005110:Extracellular Space / Q000187:drug effects* / Q000378:metabolism; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D009044:Motor Cortex / Q000187:drug effects; D009434:Neural Pathways / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D013003:Somatosensory Cortex / Q000187:drug effects* / Q000378:metabolism; D013787:Thalamic Nuclei / Q000187:drug effects
D007473:Ion Channels; D000536:Aluminum Hydroxide; D011188:Potassium