Fig. 4.

DAMGO suppressed the response of rNST neurons to ST-evoked input. A: effect of DAMGO on the amplitude of a ST-evoked current in a single GAD67− neuron under gabazine-strychnine (GS) blockade in a pup. ST-evoked responses were measured at 3.33-s intervals. B: mean ± SE amplitudes of rNST responses in GAD67+ and GAD67− neurons across the population before (baseline), during (DAMGO), and after (washout) DAMGO application (n = 53; the 1 response facilitated by DAMGO was omitted). ANOVA indicated an overall effect of DAMGO (*P < 0.0005) but no effect of GAD67-EGFP status or DAMGO × GAD67-EGFP interaction; Bonferroni-adjusted post hoc comparisons revealed significant differences between all 3 conditions: baseline, DAMGO, and washout (all P < 0.005). C: dot density plot showing the degree to which individual responses were suppressed by DAMGO (response increment omitted). Responses are grouped by animal age and bath solution: artificial cerebral spinal fluid (ACSF), gabazine and strychnine (GS), and gabazine and strychnine with the μ-opioid receptor (MOR) antagonist CTAP (CTAP). Symbols indicate monosynaptic vs. polysynaptic responses and GAD67-EGFP status. D: effect of DAMGO shown for normalized responses over time for GAD67+ (n = 15) and GAD67− (n = 15) neurons recorded when gabazine and strychnine were included in the bath. Individual measurements are for the moving average of 5 adjacent time points. When inhibitory amino acid receptors were blocked, DAMGO had a significantly larger effect on ST-evoked responses in GAD67+ than in GAD67− neurons, although responses in both cell types were affected.