Increased sodium ion conductance through nicotinic acetylcholine receptor channels in PC12 cells exposed to nerve growth factors

This is the authors' abstract. We don't add key points for this paper.

22Na+ uptake in response to cholinergic stimulation was measured in PC12 cells grown in media containing either beta-nerve growth factor (NGF) from mouse submaxillary gland or a component of Bungarus multicinctus venom (fraction 9B) which has nerve growth factor activity. Our results showed that each of these nerve growth factors increased the Na+ conductance capacity of ACh receptor-linked ion channels in PC12 cells. Compared to untreated cells, Na+ uptake was enhanced by about 40% in cells exposed for 24 to 30 hr to either 50 ng/ml of beta-NGF or to 5 micrograms/ml of fraction 9B. This cholinergically stimulated Na+ flux increased with time and reached a level 2- to 3-fold higher than that of untreated cells after 4 to 6 days' exposure to NGFs. The generation of neurites in response to NGFs from either source occurred with the same time course as the increase in Na+ channel conductance. Growth factor-enhanced Na+ uptake remained for several days after NGFs were removed from cells and neurites were lost. Na+ flux into untreated and into 9B- or beta-NGF-treated cells was inhibited to a greater extent by a nicotinic than by a muscarinic antagonist. Dibutyryl cyclic AMP did not cause an increase in Na+ uptake in response to cholinergic agonists at concentrations which stimulated neurite-like process formation, and dibutyryl cyclic AMP did not potentiate the effects of NGFs.