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Because systemic application of \u03b17-nicotinic acetylcholine receptor (nAChR) antagonists prevents this cell loss, we examined differences in receptor densities and responses of intracellular calcium to nicotine using the calcium-sensitive dye fura-2. In addition, we determined whether cell-autonomous inhibition of \u03b17 activation in neurons prevented cell death. E8 neurons are heterogeneous with respect to \u03b17-nAChR density, which leads to large increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in some neurons; E8 neurons also exhibit a slower rate of Ca<jats:sup>2+<\/jats:sup>decay after nicotinic stimulation than E13 neurons. Expressing \u03b1-bungarotoxin that is tethered to the membrane by a glycosylphosphatidylinositol linkage (GPI\u03b1btx) in ciliary ganglion neurons with the retroviral vector RCASBP(A) blocks increases in intracellular calcium induced by nicotine through \u03b17-nAChRs and prevents neurons from dying. Expression of GPI\u03b1btx in surrounding non-neural tissues, but not in neurons, does not prevent cell loss. Furthermore, the GPI\u03b1btx is not efficiently expressed in the accessory oculomotor neurons, eliminating preganglionic inputs as another site for action of the antagonist. These results support the hypothesis that cholinergic inputs facilitate cell death in the developing autonomic nervous system by activating \u03b17-nAChRs, possibly by leading to increases in intracellular calcium that exceed the threshold for cell survival.<\/jats:p>","DOI":"10.1523\/jneurosci.3057-07.2007","type":"journal-article","created":{"date-parts":[[2007,10,24]],"date-time":"2007-10-24T14:56:17Z","timestamp":1193237777000},"page":"11501-11509","source":"Crossref","is-referenced-by-count":23,"title":["Cell-Autonomous Inhibition of \u03b17-Containing Nicotinic Acetylcholine Receptors Prevents Death of Parasympathetic Neurons during 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