The effects of innervation on the developmental expression of Ca(2+)-activated K+ currents in embryonic parasympathetic neurons are not activity-dependent.
Chronic blockade of synaptic transmission in ovo using mecamylamine, a neuronal nicotinic receptor antagonist, caused a large increase in naturally occurring cell death in the embryonic chick ciliary ganglion. However, the Ca(2+)-activated K+ currents in embryonic day 13 mecamylamine-treated ciliary ganglion neurons were indistinguishable from those of saline-treated controls. Therefore, the trophic effect of preganglionic innervation on the developmental expression of Ca(2+)-activated K+ current is not dependent upon intact nicotinic cholinergic synaptic transmission and may instead be mediated by a nerve terminal-derived differentiation factor.
Subramony
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Department of Biological Science, Florida State University, Tallahassee 32306-4075, USA.
Dryer
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D000818:Animals; D001339:Autonomic Fibers, Preganglionic / Q000502:physiology; D002118:Calcium / Q000502:physiology*; D016923:Cell Death / Q000187:drug effects; D002642:Chick Embryo; D005726:Ganglia, Parasympathetic / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D005730:Ganglionic Blockers / Q000494:pharmacology; D008464:Mecamylamine / Q000494:pharmacology; D009411:Nerve Endings / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010275:Parasympathetic Nervous System / Q000166:cytology / Q000196:embryology* / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects
D005730:Ganglionic Blockers; D015221:Potassium Channels; D008464:Mecamylamine; D002118:Calcium