The release of acetylcholine from post‐ganglionic cell bodies in response to depolarization.

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Abstract
Acetylcholine (ACh) release from parasympathetic ganglia cell somata was investigated in denervated avian ciliary ganglia. Three days after the input to the ganglion (the oculomotor nerve) was sectioned, all presynaptic nerve terminals had degenerated. Denervated ganglia contain endogenous ACh and are capable of synthesizing [3H]ACh from [3H]choline added to the incubation medium. In response to depolarization induced by incubation in 50 mM-[K+]o, denervated ganglia released [3H]ACh into bath effluents in amounts approximately 15% of the non-denervated contralateral control. This release was Ca2+ dependent in both intact and denervated ganglia. Antidromic electrical stimulation of ciliary nerves also elicited [3H]ACh release. Nicotine (1 .mu.g/.mu.l) depolarized denervated ciliary ganglion cells and evoked release of the transmitter and this release was antagonized by curare. The ganglionic cell bodies synthesized ACh and released the transmitter in response to K+ depolarization, antidromic stimulation and cholinergic agonists, despite the lack of morphological specializations usually associated with stimulus-induced release of neurotransmitter. The existence of a mechanism of transmitter release may be Ca2+ dependent, probably from a cytoplasmic pool and distinct from the usual vesicular release at the nerve terminal.