Experiment shows altered burst activity in hippocampal neurons with potassium load, indicating influence on neural networks.
We studied the effect of changing extracellular potassium concentration ([K+]o) on spontaneous and evoked burst activity of glutamatergic neurons in the mouse hippocampus using whole-cell patch clamp. We show that increasing [K+]o from 3 to 8.5 mM (potassium load) induced spontaneous tonic (1) and pacemaker burst (2) activity of CA1 pyramidal cells (20% and 10% of the total number of cells, respectively). In contrast to CA1, potassium loading did not lead to the appearance of pacemaker granule cells in the dentate gyrus (DG). Similarly, potassium load increased the evoked burst activity of CA1 pyramidal cells and, paradoxically, suppressed the burst activity of DG granule cells over the entire range of current steps from 10 to 200 pA. Potassium load shifted the current-voltage characteristics to the right and substantially increased inward currents in CA1 and DG cells. Inward and outward currents of DG neurons were 4–4.5 times as high as those of CA1 cells. The possible involvement of potassium-activated potassium-conducting channels is discussed in the bimodal effect of potassium load on the excitability of CA1 and DG glutamatergic neurons. Our results suggest that CA1 pyramidal cells may be more sensitive to potassium load than DG granule cells, which may play a role in hyperexcitation of neural networks during epileptogenesis.
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A. S. Galashin (2025) studied this question.
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