Astroglial contribution in human temporal lobe epilepsy: K+ activation of Na+,K+-ATPase in bulk isolated glial cells and synaptosomes.
Potassium activation of Na+,K+-ATPase within glial cells and synaptosomes, bulk isolated from temporal neocortices of 15 patients with hippocampal-amygdalar epilepsy were compared to two patients with extratemporal complex partial epilepsies and 8 post-mortem temporal neocortices from patients with no known neurological ailments. Temporal neocortices were obtained from 17 patients who had undergone 'en bloc' anterior temporal lobectomy. In 15 patients with hippocampal amygdalar epilepsy, enzymatic activities of glial fractions were lower than those shown in 2 control lobectomy specimens and post-mortem brains. Glial enzymes had no or poor activation when K+ concentrations increased from 3 to 18 mM. Two patients served as control lobectomy specimens since they had normal neuropathological studies, and electroclinical correlations indicated an extratemporal lobe origin for complex partial seizures. In these two control specimens, glial Na+,K+-ATPase activities were similar to normal animals or post-mortem specimens. Na+,K+-ATPase activities were also slightly decreased in the synaptosomal fractions of patients with hippocampal-amygdalar epilepsy. K+ response of enzyme activities, however, corresponded to what had been described in controls, i.e. hyperbolic curves saturated at 3-6 mM K+. These results indicate that a defect in glial Na+,K+-ATPase exists in temporal neocortices of patients with hippocampal-amygdalar epilepsy.
D000328:Adult; D000679:Amygdala; D004789:Enzyme Activation; D004833:Epilepsy, Temporal Lobe / Q000201:enzymology*; D006624:Hippocampus; D006801:Humans; D009457:Neuroglia / Q000201:enzymology*; D011188:Potassium / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013574:Synaptosomes / Q000201:enzymology; D013702:Temporal Lobe / Q000201:enzymology*
D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium