A, example IPSCs recorded from 4 neurons demonstrating the variation in amplitude and duration. B, lack of correlation between decay kinetics and amplitude of 5‐HT1A‐IPSCs in 30 DRN neurons from Fig. 1. C, example IPSCs evoked with different stimulation intensities (low: 10–20 μA; high: 60–80 μA). Inset shows the traces normalized and aligned to their peak, illustrating that responses to lower stimuli had similar rates of decay. Right, quantification of amplitudes and decay times between conditions. D, example IPSCs evoked in 2.5 mm and 1.0 mm extracellular Ca2+. Inset shows the traces normalized and aligned to their peak, illustrating that responses in reduced calcium had similar rates of decay. Right, quantification of amplitudes and decay times between conditions. Scale bar (for D and E): 30 pA, 500 ms. n.s. represents P > 0.05. E, example traces (left) and quantification (right) of IPSCs in the presence of SB216641 (1 μm) + citalopram (200 nm) evoked with low (10–20 μA) and high (60–80 μA) stimulation intensities. Lower trace shows the recordings normalized, illustrating that in the presence of citalopram, larger stimuli prolong the decay time of 5‐HT1A‐IPSCs. F, cartoon schematic of the proposed mechanisms underlying 5‐HT1A receptor‐mediated transmission in the DRN. Reuptake transporters limit the extent of transmitter spillover to prevent synaptic crosstalk. This may result in functionally independent sites of transmission.