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- W2017459569 abstract "The abundance, diversity, and ubiquitous expression of neuronal nicotinic acetylcholine receptors (AChRs) suggest that many are involved in functions other than synaptic transmission. We now report that a major AChR class promotes neuronal survival. The 10-day survival of ciliary ganglion neurons in basal culture medium (MEM) was approximately 35%, but increased to approximately 75% in MEM containing nicotine (MEM/Nic) or carbachol, an effect similar to that achieved by chronic depolarization with KCl. Pharmacological experiments revealed that agonist-enhanced survival requires activation of AChRs sensitive to alpha-bungarotoxin (alphaBgt). alphaBgt-AChRs partly support neuronal survival by limiting apoptosis since fewer apoptotic neurons were observed in MEM/Nic compared to MEM. Moreover, nicotinic survival support was not further enhanced by fibroblast growth factor, as seen for KCl, but increased to 100% by adding PACAP, a trophic neuropeptide present in the ganglion. These results indicate that alphaBgt-AChR activation regulates neuronal survival and suggest a mechanism involving reduced apoptosis and interaction with an endogenous neuropeptide growth factor." @default.
- W2017459569 created "2016-06-24" @default.
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- W2017459569 date "2000-02-01" @default.
- W2017459569 modified "2023-10-06" @default.
- W2017459569 title "Nicotinic Acetylcholine Receptor Agonists Promote Survival and Reduce Apoptosis of Chick Ciliary Ganglion Neurons" @default.
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- W2017459569 doi "https://doi.org/10.1006/mcne.1999.0810" @default.
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