ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

A null mutation for the alpha3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner.

Siamak Rassadi et al.PubMed ↗Full text ↗Publisher ↗

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