Acetylcholine elongates neuronal growth cone filopodia via activation of nicotinic acetylcholine receptors.

摘要: In addition to acting as a classical neurotransmitter in synaptic transmission, acetylcholine (ACh) has been shown play role axonal growth and cone guidance. What is not well understood how ACh acts on cones affect filopodia, structures known be important for neuronal pathfinding. We addressed this question using an identified neuron (B5) from the buccal ganglion of pond snail Helisoma trivolvis cell culture. treatment caused pronounced filopodial elongation within minutes, effect that required calcium influx resulted elevation intracellular concentration ([Ca]i). Whole-cell patch clamp recordings showed reduction input resistance, depolarization membrane potential, increase firing frequency B5 neurons. These effects were mediated via activation nicotinic receptors (nAChRs), nAChR agonist dimethylphenylpiperazinium (DMPP) mimicked elongation, [Ca]i elevation, changes electrical activity. Moreover, antagonist tubucurarine blocked all DMPP-induced effects. Lastly, acted locally at cone, because physically isolated their parent responded by with similar time course remained connected neuron. Our data revealed critical modulator dynamics. signaling was nAChRs Ca influx, which, turn, elongation. © 2013 Wiley Periodicals, Inc. Develop Neurobiol 73: 487–501,