Fig. 8
SST14-induced LTP of EPSPs is blocked by GABAAR antagonism. a–c EPSPs (top) and time plots of EPSP amplitude from representative SOM-INs receiving 5 µM SST14 in a normal slice (a), SST14 in a slice with a CA3-CA1 cut (b), or SST14 in a slice with a CA3-CA1 cut and the GABAA receptor antagonist gabazine (5 µM) (c). d Summary time plots of EPSPs (normalized to baseline) for all cells, showing LTP of EPSPs after SST14 application in normal slices (filled green circle) and in slices with a CA3-CA1 cut (open green circle), but not after SST14 application in the presence of gabazine in slices with a CA3-CA1 cut (black). For SST14 in normal slices; n = 10 cells and 7 mice; rmANOVA with Dunnett’s multiple comparisons (0–5 min p = 0.008, 5–10 min p = 0.023, 10–15 min p = 0.033, 15–20 min p = 0.033, 20–25 min p = 0.009, 25–30 min p = 0.007, 30–35 min p = 0.009). For SST14 in slices with CA3 cut; n = 11 cells and 6 mice; rmANOVA with Dunnett’s multiples comparisons (10–15 min p = 0.023, 15–20 min p = 0.046, 20–25 min p = 0.027, 25–35 min p = 0.003, 30–35 min p = 0.004). For SST14 in gabazine; n = 11 cells and 6 mice; rmANOVA p = 0.974. e Summary bar graph of EPSP amplitude at 30–35 min, showing absence of long-term changes in EPSP amplitude induced by SST14 in the presence of gabazine. SST14 vs SST14 in gabazine comparison, two-way mixed ANOVA, univariate analysis at 30–35 min p = 0.001. SST14 with CA3 cut vs SST14 with CA3 cut and gabazine comparison, two-way mixed ANOVA, univariate analysis at 30–35 min p = 0.001. f Model of the mechanism of SST actions in LTP of excitatory synapses onto SOM-INs (details in text). *p < 0.05; **p < 0.01