Figure 4.

The competitive OT-receptor antagonist ([d(CH₂)₅¹,Tyr(Me)²,Thr⁴,Orn⁸,des-Gly-NH₂⁹]-vasotocin) attenuates the OT-induced increase in mEPSC frequency. TTX and GZ were present throughout to isolate mEPSCs. A, Representative current traces show that OT (100 nm) increased the mEPSC frequency. The competitive oxytocin receptor antagonist was applied at 100-fold excess and blocked the effect of OT. B, In an OT-sensitive NTS neuron, exposure to the OT-receptor antagonist blocked the OT-induced increase in mEPSC frequency. Frequency data were grouped into 10 s bins and plotted over time. C, Normalized group data across similarly treated OT-sensitive NTS neurons under each condition. OT (100 nm) increased the frequency of isolated mEPSCs (*p > 0.05). The presence of the OT receptor antagonist (10 μm) alone did not significantly change mEPSC frequency; however, coapplication with OT (100 nm) attenuated the OT-induced increase in frequency. These results indicate that OT acts specifically via OT receptors to increase glutamate release onto OT-sensitive second-order NTS neurons.