Network behaviour within the 6-13 Hz frequency range is manifest within spinal dorsal horn (DH) in vivo (Sandkuhler & Eblen-Zajjur, 1994). Previous data demonstrated rhythmic network behaviour in rat DH in vitro with a dominant frequency of 7-12 Hz (Asghar et al, 2002), which could be maintained through gap junction (GJ) interconnectivity, and may have a role to play in somatosensory processing of nociceptive signals. The potassium channel blocker 4-aminopyridine (4-AP) triggers widespread oscillatory activity in spinal DH (Ruscheweyh & Sandkuhler, 2003) in vitro but it is not known if GJs contribute to this behaviour. Here, we determined whether GJs localised to glia or neurons may be involved in 4-AP-induced enhanced excitation in DH in vitro. Spinal cords were removed from Wistar rats (aged 12-14 days) terminally anaesthetised with urethane (2g/kg I.P.). Transverse lumbar slices (300μm) were cut and placed in an interface recording chamber perfused with artificial cerebrospinal fluid (aCSF) at 32^oC. Extracellular field recordings were then made from substantia gelatinosa (SG) using aCSF-filled glass microelectrodes (1-2MΩ) and oscillations were induced with bath-perfusion of 50μM 4-AP. Data values for peak amplitude and area of power spectra were quantified before and after application of the non-specific GJ uncouplers, Carbenoxolone (100µM, n=6) and Octanol (1mM, n=7), and the selective neuronal GJ uncouplers, Quinine (250µM, n=10) and Mefloquine (500nM, n=6). Carbenoxolone and Octanol significantly reduced the peak amplitude (64% and 58% respectively, P<0.05) and area (60% and 57% respectively, P<0.05) with no effect on frequency. Quinine had a small but significant effect only on peak amplitude which was reduced by 33% (P<0.05), whilst Mefloquine significantly reduced both peak amplitude (34%, P<0.05) and area (34%, P<0.05). These data suggest that both glial, and more specifically, neuronal gap junctions may contribute to 4-AP-induced oscillations in SG. Further studies are now required to reveal the significance of GJ-mediated activation of large populations of DH neurons in the context of spinal nociceptive signalling. All procedures were carried out in accordance with UK Animals (Scientific Procedures) Act 1986. Supported by The Wellcome Trust.