Effects of inositol, 1,4,5-trisphosphate injections into cat spinal motoneurons.
Inositol 1,4,5-trisphosphate (IP3) was injected iontophoretically into cat spinal motoneurons in pentobarbital-anaesthetized cats and nonanaesthetized, decerebrate cats. Injections of IP3 induced a long-lasting, reproducible hyperpolarization without consistent change in input resistance. The peak amplitude of post-spike afterhyperpolarization (AHP) was significantly increased by IP3 when the membrane potential was adjusted to the control level. Intracellular injections of Ca2+ chelators, which depressed the Ca2(+)-activated AHP, prevented the IP3-induced long-lasting hyperpolarization, suggesting that IP3 acts by a Ca2(+)-dependent mechanism. Intracellular injections of myo-inositol did not consistently induce hyperpolarizations. Also intracellular injections of Li+, which blocks IP3 catabolism, did not prevent the IP3-evoked hyperpolarization. These data suggest that IP3 itself, rather than its breakdown product myo-inositol, is mainly responsible for the hyperpolarizing effect. Possible mechanisms for the IP3-induced hyperpolarization are discussed.
Zhang
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Department of Anaesthesia Research, McGill University, Montréal, Qué., Canada.
D000758:Anesthesia; D000818:Animals; D002118:Calcium / Q000502:physiology; D002415:Cats; D002614:Chelating Agents / Q000494:pharmacology; D003655:Decerebrate State; D004558:Electric Stimulation; D007267:Injections; D007294:Inositol / Q000494:pharmacology; D015544:Inositol 1,4,5-Trisphosphate / Q000008:administration & dosage / Q000494:pharmacology*; D007478:Iontophoresis; D008094:Lithium / Q000494:pharmacology; D009046:Motor Neurons / Q000187:drug effects*; D015221:Potassium Channels / Q000187:drug effects; D013116:Spinal Cord / Q000166:cytology* / Q000187:drug effects
D002614:Chelating Agents; D015221:Potassium Channels; D007294:Inositol; D015544:Inositol 1,4,5-Trisphosphate; D008094:Lithium; D002118:Calcium