Fig. 5: Inhibiting NPY1R leads to a marked decrease in inhibitory currents in pyramidal neurons from adult ELS mice.

a Experimental setup (left) and representative traces (right) from inhibitory postsynaptic currents (mIPSC) from CTR and ELS neurons. To record chloride currents as salient inward currents, in this experiment the composition of the intracellular solution was altered to include high intracellular Cl⁻ concentration, while AMPA and NMDA receptors were blocked (see “Materials and methods” section). Scale bar, 50 pA, 100 ms. Reduced amplitude of mIPSC (b), but no changes to the frequency of events (c). Cumulative distribution plots for individual inhibitory events plotted as amplitude (d) and inter-event interval (e); CTR n = 27/5 cells/mice, ELS n = 19/4 cells/mice. Reduced amplitude of sIPSC (f), but no changes to the frequency of events (g). Cumulative distribution plots for individual inhibitory events plotted as amplitude (h) and inter-event interval (i); CTR n = 28/5 cells, ELS n = 18/4 cells. j Summary data from spontaneous inhibitory currents in ELS mice normalized to CTR, under basal conditions (see Fig. 4) and in the presence of the NPY1R antagonist. k Schematic representation of a potential mechanism where postsynaptic NPY1R leads to increased GABA_A receptor membrane insertion. Statistical comparisons were performed using two-tailed unpaired t-test. Significance was set at, *p < 0.05. Data in bar graphs are presented as means ± SEM.