Figure 4. Substance P, but not blockade of inhibitory synaptic transmission, relieves DAMGO-mediated depression.

(A) Representative traces of ∫preBötC and ∫XII population activity in 3/1 ACSF control and 500 nM SP and 30 nM DAMGO. SP mitigated the effects of DAMGO, and preBötC activity, consisting of both burstlets (•) and bursts, resembled that in control conditions. Scale bar, 10 s. (B) Average normalized burstlet fraction and preBötC f when 30 nM DAMGO was added alone (9/1.5, 3/1) or following application of either 100 µM picrotoxin/1 µM strychnine or 500 nM SP. For each experiment, values were normalized to burstlet fraction or preBötC f during baseline 9/1.5 or 3/1 ACSF in that experiment. The normalized preBötC f when SP was added with DAMGO was significantly higher than all other conditions. *, p<0.05, one-way ANOVA, post-hoc Tukey test, n = 6 for 9/1.5, n = 7 for 3/1, n = 13 for picrotoxin/strychnine, n = 6 for SP. (C) Representative traces of ∫preBötC and ∫XII population activity in 3/1 ACSF control and 500 nM SP. In 3/1 ACSF, rhythmic activity consisted of both burstlets (•) and bursts. After SP, f was unchanged, but more preBötC bursts were observed. Scale bar, 10 s. (D) Average burstlet fraction and f in 3/1 ACSF control condition and 500 nM SP. SP significantly decreased the burstlet fraction, but did not change preBötC f. *, p<0.05, Student’s t-test, n = 13. (E) Representative traces of ∫preBötC and ∫XII population activity in 3/1 ACSF control and 100 µM picrotoxin/1 µM strychnine. In 3/1 ACSF, rhythmic activity consisted of both burstlets (•) and bursts. After picrotoxin/strychnine, f was unchanged; however, more preBötC bursts were observed, and XII bursts were larger. Scale bar, 10 s. (F) Average burstlet fraction and f in 3/1 ACSF control condition and 100 µM picrotoxin/1 µM strychnine. Picrotoxin/strychnine significantly decreased the burstlet fraction, but did not change preBötC f. *, p<0.05, Student’s t-test, n = 13.