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IP(s)3, a metabolically stable analog of 1,4,5-inositol trisphosphate (IP3), inhibited action potential firing when injected into hippocampal pyramidal cells. This effect was associated with decreased input resistance, a more negative resting potential, outward rectification at depolarized potentials, and an afterhyperpolarization. The response to IP(s)3 was unaffected by antagonists of Na+, Ca2+, and Cl- conductances, but was sensitive to changes in extracellular K+ concentration. The IP(s)3-induced conductance was voltage-dependent, was activated in 10 ms with depolarization, and was blocked by extracellular Ba2+ or intracellular Ca2+ chelation. It was not suppressed by other K+ conductance antagonists. Thus, IP(s)3 may activate a novel K+ conductance in CA1 pyramidal cells. IP3 itself did not elicit this conductance, suggesting it may be rapidly metabolized in these cells.


Journal article



Publication Date





461 - 471


Action Potentials, Animals, Barium, Calcium, Egtazic Acid, Electric Conductivity, Electrophysiology, Hippocampus, In Vitro Techniques, Inositol, Inositol 1,4,5-Trisphosphate, Male, Organothiophosphorus Compounds, Potassium, Rats, Reaction Time