Purpose: Comparison of extracellular K+ regulation in sclerotic and nonscle
rotic epileptic hippocampus.
Methods: Measurements of K+ signals with double-barreled K+-selective refer
ence microelectrodes in area CA1 of slices from human and rat hippocampus,
induction of increases in extracellular potassium concentration by repetiti
ve alvear stimulation or iontophoresis, and block of inward-rectifying and
background K+ channels in astrocytes by barium.
Results: In the CAI pyramidal layer from normal rat hippocampus, barium aug
mented extracellular K+ accumulation induced by iontophoresis or antidromic
stimulation in a dose-dependent manner. Similarly, barium augmented stimul
us-induced K+ signals from nonsclerotic hippocampi (human mesial temporal l
obe epilepsy), in contrast, barium failed to do so in sclerotic hippocampi
(human mesial temporal lobe epilepsy, rat pilocarpine model).
Conclusions: Our findings suggest that in areas of reduced neuronal density
(hippocampal sclerosis), glial cells adapt to permit rather large increase
s in extracellular potassium accumulation. Such increases might be involved
in the transmission of activity through the sclerotic area.