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The ability of P2X7 receptors to potentiate rhythmically evoked acetylcholine (ACh) release through Ca 2+ entry via P2X7 receptors and via L-type voltage-dependent Ca 2+ channels (VDCCs) was compared by loading Ca 2+ chelators into motor nerve terminals. Neuromuscular preparations of the diaphragms of wild-type (WT) mice and pannexin-1 knockout (Panx1 -/- ) mice, in which ACh release is potentiated by the disinhibition of the L-type VDCCs upon the activation of P2X7 receptors, were used. Miniature end-plate potentials (MEPPs) and evoked end-plate potentials (EPPs) were recorded when the motor terminals were loaded with slow or fast Ca 2+ chelators (EGTA-AM or BAPTA-AM, respectively, 50 μM). In WT and Panx1 -/- mice, EGTA-AM did not change either spontaneous or evoked ACh release, while BAPTA-AM inhibited synaptic transmission by suppressing the quantal content of EPPs throughout the course of the short rhythmic train (50 Hz, 1 s). In the motor synapses of either WT or Panx1 -/- mice in the presence of BAPTA-AM, the activation of P2X7 receptors by BzATP (30 μM) returned the EPP quantal content to the control level. In the neuromuscular junctions (NMJs) of Panx1 -/- mice, EGTA-AM completely prevented the BzATP-induced increase in EPP quantal content. After Panx1 -/- NMJs were treated with BAPTA-AM, BzATP lost its ability to enhance the EPP quantal content to above the control level. Nitrendipine (1 μM), an inhibitor of L-type VDCCs, was unable to prevent this BzATP-induced enhancement of EPP quantal content to the control level. We propose that the activation of P2X7 receptors may provide additional Ca 2+ entry into motor nerve terminals, which, independent of the modulation of L-type VDCC activity, can partially reduce the buffering capacity of Ca 2+ chelators, thereby providing sufficient Ca 2+ signals for ACh secretion at the control level. However, the activity of both Ca 2+ chelators was sufficient to eliminate Ca 2+ entry via L-type VDCCs activated by P2X7 receptors and increase the EPP quantal content in the NMJs of Panx1 -/- mice to above the control level.

Interaction between Calcium Chelators and the Activity of P2X7 Receptors in Mouse Motor Synapses