Characterization of action potential-evoked calcium transients in mouse postganglionic sympathetic axon bundles

• Published in: The Journal of physiology Vol. 537; no. 1; pp. 3 - 16
• Main Authors: Jackson, V. Margaret, Trout, Stephen J., Brain, Keith L., Cunnane, Tom C.
• Format: Journal Article
• Language: English
• Published: Oxford, UK The Physiological Society 15.11.2001; Blackwell Science Ltd; Blackwell Science Inc
• Subjects: Action Potentials - physiology; Animals; Axons - physiology; Calcium - physiology; Calcium Channels - metabolism; Chloride Channels - antagonists & inhibitors; Electric Stimulation - methods; Electrophysiology; Ganglia - physiology; Intracellular Membranes - metabolism; Ion Channel Gating; Ionomycin - pharmacology; Ionophores - pharmacology; Mice; Mice, Inbred BALB C; Original; Potassium Channel Blockers - pharmacology; Potassium Channels - physiology; Sympathetic Nervous System - physiology; Tetrodotoxin - pharmacology; Time Factors
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.2001.0003k.x

Action potential-evoked Ca 2+ transients in postganglionic sympathetic axon bundles in mouse vas deferens have been characterized using confocal microscopy and Ca 2+ imaging. Axonal Ca 2+ transients were tetrodotoxin sensitive. The amplitude depended on both the frequency of stimulation and the number of stimuli in a train. Removal of extracellular Ca 2+ abolished the Ca 2+ transient. Cd 2+ (100 μ m ) inhibited the Ca 2+ transient by 78 ± 10 %. The N-type Ca 2+ channel blocker ω-conotoxin GVIA (0.1 μ m ) reduced the amplitude by −35 ± 4 %, whereas nifedipine (10 μ m ; L-type) and ω-conotoxin MVIIC (0.1 μ m ; P/Q type) were ineffective. Caffeine (10 m m ), ryanodine (10 μ m ), cyclopiazonic acid (30 μ m ) or CCCP (10 μ m ) had no detectable effects. Blockade of large and small conductance Ca 2+ -dependent K + channels with iberiotoxin (0.1 μ m ) and apamin (1 μ m ), respectively, or Ca 2+ -dependent Cl − channels by niflumic acid (100 μ m ) did not alter Ca 2+ transients. In contrast, the non-specific K + channel blockers tetraethylammonium (10 m m ) and 4-aminopyridine (10 m m ) markedly increased the amplitude of the Ca 2+ transient. Blockade of delayed rectifiers and A-like K + channels, by tityustoxin-K (α) (0.1 μ m ) and pandinustoxin-K (α) (10 n m ), respectively, also increased the Ca 2+ transient amplitude. Thus, Ca 2+ transients are evoked by Na + -dependent action potentials in axons. These transients originate mainly from Ca 2+ entry through voltage-dependent Ca 2+ channels (80 % Cd 2+ sensitive of which 40 % was attributable to N-type). Twenty per cent of the Ca 2+ transient was not due to Ca 2+ entry through voltage-gated Ca 2+ channels. Intracellular stores and mitochondria were not involved in the generation of the transient. Ca 2+ transients are modulated by A-like K + channels and delayed rectifiers (possibly K V 1.2) but not by Ca 2+ -activated ion channels.