The timing of protein synthesis required for the development of the sodium action potential in embryonic spinal neurons.
Embryonic amphibian neurons grown in dissociated cell culture extend neurites and can produce action potentials. The ionic dependence of the inward current of the action potential gradually changes from primarily calcium to primarily sodium. Early exposure of these neurons to protein synthesis inhibitors (cycloheximide, puromycin) blocked the appearance of neurites; later exposure blocked the normal change in the ionic basis of the action potential. These drugs apparently arrested the development of the sodium component of the action potential and, additionally, may have blocked a reduction in the calcium component. Inhibitor applied at still later times did not prevent the normal development of these traits. The development of voltage-sensitive delayed rectification was unaffected by the addition of inhibitor at any of the times tested.
D000200:Action Potentials; D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D009469:Neuromuscular Junction / Q000378:metabolism / Q000502:physiology*; D009474:Neurons / Q000378:metabolism / Q000502:physiology; D011691:Puromycin / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism* / Q000502:physiology; D013116:Spinal Cord / Q000378:metabolism* / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects; D014981:Xenopus
D009419:Nerve Tissue Proteins; D011691:Puromycin; D003513:Cycloheximide; D012964:Sodium