Article Figures & Data
Figures
- Figure 1.
GABAergic sPSC frequency is highest on proestrous PM. A, Representative sPSC recording from a neuron in each group. B, Individual values and mean ± SEM of spontaneous GABAergic PSC frequency for cells recorded on diestrous (di) PM, proestrous (pro) AM and pro PM (Kruskal–Wallis, KW = 14.4, *p < 0.05 Dunn’s). C, Mean by-cell cumulative probability distribution of interevent interval (IEI) for each group (Kruskal–Wallis, KW = 191, *p < 0.0001, Dunn’s). D, By-cell average of all sPSC from all cells in each group. E, Individual values and mean ± SEM of sPSC amplitude (ANOVA F(2,33) = 6.69, *p < 0.05, **p < 0.005 Tukey). F, Histogram of mean by-cell sPSC amplitude distribution (Kruskal–Wallis, KW = 23.9, proestrous AM vs both diestrous PM and proestrous PM, *p < 0.001, Dunn’s). G, Individual values and mean ± SEM of sPSC time decay time between 90% and 10% of the maximum event amplitude (ANOVA F(2,33) = 1.34).
- Figure 2.
Blocking action potentials does not affect GABAergic PSC frequency or amplitude in diestrous or proestrous mice. A, Representative recordings from a representative neuron in each group before (control or con, top) and during (bottom) TTX treatment (from n = 6 cells diestrous PM, n = 5 cells proestrous PM). B, Individual values and mean ± SEM of GABAergic PSC frequency. C, Average of all PSC traces for control or ttx periods from all cells in each group. D, E, Individual values and mean ± SEM for: (D) PSC amplitude, (E) decay time between 90% and 10% of the maximum current amplitude. No statistical differences were detected using two-way repeated-measures ANOVA/Bonferroni test (B, cycle stage: F(1,9) = 1.3; TTX: F(1,9) = 1.6; cycle stage × TTX: F(1,9) = 0.0; D, cycle stage: F(1,9) = 0.3; TTX: F(1,9) = 0.6; cycle stage × TTX: F(1,9) = 0.5; E, cycle stage: F(1,9) = 0.5; TTX: F(1,9) = 6.4 (p = 0.01); cycle stage × TTX: F(1,9) = 0.9).
- Figure 3.
GnRH neuron excitability is increased on proestrus versus diestrus. A, Representative traces from a neuron in each group during 500-ms current injections of 12 and 24 pA (current injection protocol below). B, Mean ± SEM spikes elicited for each current injection step (two-way repeated-measures ANOVA cycle stage: F(2,22) = 10.2, current: F(15,330) = 93.03, interaction: F(30,330) = 9.503, *p < 0.05 diestrous PM vs proestrous PM and p < 0.05 proestrous AM vs proestrous PM; *p < 0.05 among all three groups, Fisher’s LSD). C–H, Individual values and mean ± SEM for: (C) rheobase current (ANOVA F(2,22) = 12.8, *p < 0.05, **p < 0.0001), (D) latency to first spike (ANOVA F(2,22) = 2.85, p = 0.0792), (E) action potential threshold (ANOVA F(2,22) = 6.18, *p < 0.01 Tukey), (F) action potential amplitude (ANOVA, F(2,22) = 0.676), (G) FWHM (ANOVA F(2,22) = 26.2, **p < 0.0001 Tukey), (H) action potential rate of rise (Kruskal–Wallis, KW = 6.69, *p < 0.05 Dunn’s), (I) AHP amplitude (ANOVA F(2,22) = 0.252), and (J) AHP time (Kruskal–Wallis, KW = 7.03, *p < 0.05 Dunn’s).
Tables
Mean ± SEM of GnRH whole-cell passive properties from Figure 1 Diestrous PM Proestrus AM Proestrus PM Rin (MΩ) 929 ± 42 1336 ± 160* 1034 ± 63 Capacitance (pF) 14.7 ± 0.7 13.0 ± 0.8 14.5 ± 0.7 Rs (MΩ) 13.2 ± 0.6 13.5 ± 1.0 14.6 ± 0.7 Ihold (pA) -13.6 ± 4.2 -0.15 ± 4.7# -17.4 ± 2.8 *p < 0.05 vs diestrous PM; #p < 0.01 vs proestrous PM, Tukey’s ANOVA parameters for comparison of GnRH passive properties (Fig. 1) Rin (MΩ) F(2,33) = 4.84 Capacitance (pF) F(2,33) = 1.32 Rs (MΩ) F(2,33) = 0.951 Ihold (pA) F(2,33) = 5.38 Mean ± SEM of GnRH whole-cell passive properties from Figure 2 Diestrous PM Proestrus PM Rin (MΩ)
Before TTX
During TTX
1053 ± 88
846 ± 83
1113 ± 145
775 ± 91Capacitance (pF)
Before TTX
During TTX
15.8 ± 0.8
15.0 ± 0.8
13.2 ± 0.9
13.8 ± 1.0Rs (MΩ)
Before TTX
During TTX
12.1 ± 0.9
13.3 ± 1.5
12.3 ± 0.6
14.7 ± 0.8Ihold (pA)
Before TTX
During TTX
-16.4 ± 3.5
-25.1 ± 6.3
-19.4 ± 2.6
-28.5 ± 3.8Two-way repeated measures ANOVA for comparison of GnRH passive properties among groups (Fig. 2) Group TTX Group × TTX Rin (MΩ) F(1,9) = 0.001 F(1,9) = 36.0*** F(1,9) = 2.1 Capacitance (pF) F(1,9) = 2.5 F(1,9) = 0.1 F(1,9) = 6.9* Rs (MΩ) F(1,9) = 0.4 F(1,9) = 6.0* F(1,9) = 0.7 Ihold (pA) F(1,9) = 0.3 F(1,9) = 14.1** F(1,9) = 0.01 Mean ± SEM of GnRH whole-cell passive properties from Figure 3 Diestrous PM Proestrous AM Proestrous PM Rin (MΩ) 1125 ± 150 667 ± 43* 1361 ± 144 Capacitance (pF) 13.7 ± 0.7 13.8 ± 0.7 12.5 ± 0.8 Rs (MΩ) 13.5 ± 0.9 11.9 ± 0.9 13.5 ± 1.4 Ihold (pA) -0.7 ± 5.2 -2.8 ± 6.3 -10.1 ± 4.4 *p < 0.05 vs diestrous PM, Tukey’s ANOVA parameters for comparison of GnRH passive properties (Fig. 3) Rin (MΩ) F(2,22) = 6.65 Capacitance (pF) F(2,22) = 1.02 Rs (MΩ) F(2,22) = 0.62 Ihold (pA) KW = 3.36
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