Glial and neuronal Na+-K+ pump in epilepsy.
Because high extracellular K+ concentrations (18-20 mM) increased glial Na+- and K+ -dependent adenosine triphosphatase [(Na+ + K+)-ATPase] activities, while this increase was not observed in neuronal preparations, it is hypothesized that K+ released in the extracellular space during neuronal firing is actively taken up by glial cells. In acute and chronic epileptogenic lesions of cats, glial (Na+ + K+)-ATPase dramatically decreased when compared to both control animals and the perifocal area, while its activation by extracellular K+ in concentrations between 3 and 18 mM was absent 3, 6, and up to 45 days after production of freezing lesions. Similar results were observed in 13 specimens of anterolateral temporal neocortex obtained during temporal lobectomies in patients with intractable temporal lobe epilepsy, compared with postmortem human specimen or control brain tissues. Hence, a glial (Na+ + K+)-ATPase abnormality exists in epileptogenic tissue. Further experimental data are presented supporting the notion that this glial abnormality may favor the transition from interictal episodes to ictal phenomena.
D000818:Animals; D002415:Cats; D004569:Electroencephalography; D004827:Epilepsy / Q000201:enzymology*; D004833:Epilepsy, Temporal Lobe / Q000201:enzymology; D006801:Humans; D007473:Ion Channels / Q000201:enzymology; D009457:Neuroglia / Q000201:enzymology*; D009474:Neurons / Q000201:enzymology; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D009435:Synaptic Transmission; D013702:Temporal Lobe / Q000201:enzymology
D007473:Ion Channels; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium