A critical period of transcription required for differentiation of the action potential of spinal neurons.
The early development of excitability of amphibian spinal neurons is characterized by a change from a long Ca2(+)-dependent action potential to a brief Na(+)-dependent impulse. The delayed rectifier K+ current plays a major role in this cell autonomous differentiation. Here we show that the maturation of the delayed rectifier current, and hence the action potential, involves a critical period of mRNA synthesis. It is blocked by inhibition of transcription during an early period of development in culture and fails to develop following removal of the inhibitor and resumption of RNA synthesis. However, the development of an inactivating K+ A-current recovers in these neurons, indicating that some programs of neuronal development are affected during this critical period, while others are spared.
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Department of Biology, University of California, San Diego, La Jolla 92093.
Spitzer
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D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002478:Cells, Cultured; D004004:Dichlororibofuranosylbenzimidazole / Q000494:pharmacology*; D004625:Embryo, Nonmammalian; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D012313:RNA / Q000096:biosynthesis; D012263:Ribonucleosides / Q000494:pharmacology*; D013116:Spinal Cord / Q000502:physiology*; D014158:Transcription, Genetic / Q000187:drug effects; D014529:Uridine / Q000378:metabolism; D014981:Xenopus
D015221:Potassium Channels; D012263:Ribonucleosides; D004004:Dichlororibofuranosylbenzimidazole; D012313:RNA; D014529:Uridine