Figure 3. Blockade of voltage-activated Ca²⁺ channels decreases the slow excitatory postsynaptic potential (EPSP) in Kiss1^ARH neurons.

(A–D) Representative traces showing that the slow EPSPs induced by high-frequency photostimulation were abolished by perfusing the blocker of the L-type calcium channel, nifedipine (A) or N- and P/Q-type calcium channels, ω-conotoxin MVIIC (B), or the R-type calcium channel, SNX 482 (C), or the T-type calcium channel, TTA-P2 (D), respectively. The arrows indicate the measurements of slow EPSP amplitude, denoted as R1 and R2, after low-pass filtering (shown in C). (E) Bar graphs summarizing the effects of drugs on the R2/R1 ratios. The slow EPSP was generated in OVX Kiss1-Cre::Ai32 mice. Comparisons between different treatments were performed using a one-way ANOVA (F _{(3, 51)} = 14.36, p<0.0001) with the Bonferroni’s post hoc test. *, **, **** indicate p<0.05, 0.01, 0.001, respectively versus control. (F, G) Representative traces show that in voltage clamp senktide induced a significant inward current in Kiss1^ARH neurons (F) in the presence of TTX. This current was inhibited by the calcium channel blocker CdCl₂ (200 μM) in another cell (G). (H) Bar graphs summarize the effect of the calcium channel blocker CdCl₂ on the senktide-induced inward currents. Unpaired t-test for (F) versus (G): t₍₂₀₎ = 2.575, p=0.0181; *p<0.05. Data are expressed as mean ± SEM, with data points representing individual cells.