Electrical coupling between sympathetic preganglionic neurones (SPN) (1) may be an important contributor to the sympathetic rhythms observed in spinal animals (2). The Connexin36 (Cx36) subunit is expressed in SPN (3) and is a likely candidate for forming gap junctions that mediate this electrically coupled activity. In AII amacrine cells of the retina, dopamine receptor 1 (D1R) activation leads to dephosphorylation of the Cx36 subunit at Ser293 which uncouples the channel (4). We investigated the effect of D1R activation on the endogenous and 5-HT-enhanced electrical coupling of SPN in the intermediolateral cell column (IML). Spinal cord slices (300 µm) were prepared using neonatal Wistar rats (9 day old) in slight modification to previously published methods (5). Animals were anaesthetised by i.p. injection of urethane (2g/kg) and transcardially perfused with ice-chilled, oxygenated sucrose aCSF prior to decapitation. Whole-cell recordings from SPN were performed in “bridge-mode” with the cells held at around -50 mV by injection of positive or negative current. The sodium channel blocker, QX-314 bromide (2 mM), was included intracellularly to prevent electrically-coupled activity being obscured by spontaneous action potentials in the recorded cell. Statistical analysis was performed with Prism Graphpad 5 software using a one-way ANOVA with Tukey post-test. The D1R-selective agonist, dihydrexidine (DHX, 200 nM) had no significant effect on the mean interspikelet interval (ISI) or spikelet amplitude (P>0.05 for both, n=4). In the presence of a D2 receptor antagonist, haloperidol (1 µM) and when coadministered with 200 nM DHX no significant effect on mean ISI and spikelet amplitude was observed (n=4). Addition of 5-HT (10 µM) significantly reduced the mean ISI and increased spikelet amplitude (P<0.01 and P<0.05 respectively, n=4). Administration of 5-HT + haloperidol + DHX reduced spikelet amplitude sufficiently that it was not significantly different to either control or 5-HT values. Mean ISI remained significantly reduced but the P value was increased from <0.01 to <0.05 (n=4) with regard to the control. Increasing the concentration of DHX (10 µM) did not affect the mean ISI but spikelets were abolished in the presence of 10 µM DHX and 1 µM haloperidol (n=1). On washing, mean ISI recovered before spikelet amplitude. An increase in the mean ISI during 5-HT exposure was also observed during application of 5-HT + haloperidol + 10 µM DHX (n=1). We present here preliminary data that D1R activation negatively modulates electrical coupling of SPN in the IML.