P2X7 receptors trigger XXXX exocytosis and modify secretory vesicle dynamics in @entity521 cells.

@entity57557 @entity19 @entity377 @entity72711 @entity1360 @entity521 @entity1154 @entity141 @entity35706 @entity6200 @entity855
Previously, we reported that purinergic ionotropic P2X7 receptors negatively regulate neurite formation in Neuro-2a (N2a) @entity19 @entity521 cells through a @entity141 /calmodulin-dependent kinase II-related mechanism. In the present study we used this cell line to investigate a parallel though faster @entity6200 -mediated signaling pathway, namely @entity141 -regulated exocytosis. Selective activation of P2X7 receptors evoked exocytosis as assayed by high resolution membrane capacitance measurements. Using dual-wavelength total internal reflection microscopy, we have observed both the increase in near-membrane @entity141 concentration and the exocytosis of fluorescently labeled vesicles in response to @entity6200 stimulation. Moreover, activation of P2X7 receptors also affects vesicle motion in the vertical and horizontal directions, thus, involving this receptor type in the control of early steps (docking and priming) of the secretory pathway. Immunocytochemical and RT-PCR experiments evidenced that N2a cells express the three neuronal SNAREs as well as vesicular @entity377 and @entity1154 ( @entity72711 and @entity57557 ) transporters. Biochemical measurements indicated that @entity1360 induced a significant release of @entity855 from N2a cells. Finally, @entity6200 stimulation and @entity1360 increased the incidence of small transient inward currents, reminiscent of postsynaptic quantal events observed at synapses. Small transient inward currents were dependent on extracellular @entity141 and were abolished by @entity35706 , suggesting they were mediated by P2X7 receptors. Altogether, these results suggest the existence of a positive feedback mechanism mediated by @entity6200 -stimulated exocytotic release of @entity855 that would act on P2X7 receptors on the same or neighbor cells to further stimulate its own release and negatively control N2a cell differentiation.
