Disinhibited bursting is accelerated by oxytocin, an effect prevented by its selective antagonist.

<p>A, regular disinhibited rhythm induced by 1 μM strychnine and 20 μM bicuculline (top trace in A) is stably sped up (with burst length reduction) by the cumulative addition of oxytocin (5, 100 nM and 1 μM), without any further modifications in the characteristics of single bursts. The cumulative dose response curve in B indicates significant reduction in the average period (expressed as a percentage of the mean variation), starting at concentration of 5 nM (*; one way ANOVA followed by multiple comparison vs strychnine + bicuculline only with Dunnett's method; P = <0.001; the number of preparations used to calculate the mean is shown in parentheses; the error bars indicate SD). C, on a different preparation, a stable disinhibited rhythm (top) remains unchanged by the addition of the OTRs antagonist, atosiban (5 μM, middle), which prevents any acceleration during the following addition of oxytocin (100 nM). The histograms in D, which report the average value of period of disinhibited rhythm in correspondence to the different treatments, show significant rhythm acceleration in the presence of oxytocin (100 nM), an effect reverted to control values after washout (30 min), and prevented by the addition of atosiban (5 nM), which does not <i>per se</i> vary rhythm periodicity (*; Kruskal-Wallis one way ANOVA on ranks followed by multiple comparison vs strychnine + bicuculline only with Dunn's method; P = 0,038; the number of preparations used to calculate the mean is shown in parentheses; the error bars indicate SD).