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Nicotinic Acetylcholine Receptors in Mouse and Rat Optic Nerves

¹Department of Physiology, University of Wisconsin School of Medicine, Madison, Wisconsin 53706; and ²Ottawa Health Research Institute, Ottawa Hospital-Civic Campus, University of Ottawa, Ottawa K1Y 4E9, Canada

Submitted 7 August 2003; accepted in final form 14 October 2003

Receptor-mediated calcium signaling in axons of mouse and rat optic nerves was examined by selectively staining the axonal population with a calcium indicator. Nicotine (1-50 µM) induced an axonal calcium elevation that was eliminated when calcium was removed from the bath, suggesting that nicotine induces calcium influx into axons. The nicotine response was blocked by d-tubocurarine and mecamylamine but not -bungarotoxin, indicating the presence of calcium permeable, non-7 nicotinic acetylcholine receptor (nAChR) subtype. Agonist efficacy order for eliciting the axonal nAChR calcium response was cytisine nicotine >> acetylcholine. The nicotine-mediated calcium response was attenuated during the process of normal myelination, decreasing by approximately 10-fold from P1 (premyelinated) to P30 (myelinated). Nicotine also caused a rapid reduction in the compound action potential in neonatal optic nerves, consistent with a shunting of the membrane after opening of the nonspecific cationic nicotinic channels. Voltagegated calcium channels contributed little to the axonal calcium elevation during nAChR activation. During repetitive stimulations, the compound action potential in neonatal mouse optic nerves underwent a gradual reduction in amplitude that could be partially prevented by d-tubocurarine, suggesting an activity-dependent release of acetylcholine that activates axonal AChRs. We conclude that mammalian optic nerve axons express nAChRs and suggest that these receptors are activated in an activity-dependent fashion during optic nerve development to modulate axon excitability and biology.

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				C.-L. Zhang, J. A. Wilson, J. Williams, and S. Y. Chiu Action Potentials Induce Uniform Calcium Influx in Mammalian Myelinated Optic Nerves J Neurophysiol, August 1, 2006; 96(2): 695 - 709. [Abstract] [Full Text] [PDF]