An EP2 Agonist Facilitates NMDA-Induced Outward Currents and Inhibits Dendritic Beading through Activation of BK Channels in Mouse Cortical Neurons

Figure 4

The facilitatory effects of butaprost, an EP2 receptor agonist, on the recovery phase of NMDA-induced dendritic beading through the activation of BK channels in the primary cultured mouse cortical neurons. (a) Immunofluorescent CLMS images for MAP2 in the primary cultured cortical neurons of pretreatment (left panel) or posttreatment (right panel) of NMDA (30 μM) for 10 min. Arrowheads indicate beads-structure in the dendrite. Scale bar = 20 μm. (b) Cortical neurons were fixed 10 min after the stimulation with NMDA (i) or 60 min after the elimination of NMDA (ii). Experimental schedules of (i) and (ii) were corresponding to (c, d) and (e, f), respectively. Data are represented as the mean ± SEM ( = 180–235 cells). (c, e) Immunofluorescent CLMS images for MAP2 in the primary cultured cortical neurons at 10 min after stimulation of NMDA (c) or 60 min after the elimination of NMDA (e). Butaprost (1 μM), TG6-10-1 (10 μM), an EP2 receptor antagonist, and paxilline (2 μM) were treated 30 min before the application of NMDA. (d, f) The formation of dendritic beading of 10 min after the stimulation with NMDA (d) or 60 min after the elimination of NMDA (f). The columns and bars represent the mean ± SEM ( = 142–173 cells). Asterisks indicate a significant difference between the values (, one-way ANOVA post hoc Tukey’ test).

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