Cx30.2 and Cx36 are neuronal gap junction proteins, contributing to electrical coupling between neurones. Such coupling is important for generation of network activity in the nervous system. To understand the mechanisms and results of this coupling knowledge of the expression of gap junction proteins in central neurones is of prime importance. Our aim here is to examine the expression pattern of Cx30.2 and Cx36 in neurones of spinal cord and medulla oblongata with particular reference to neurones associated with autonomic function. The study employed transgenic mice that expressed LacZ or cyan fluorescent protein (CFP) reporter genes under control of the Cx30.2 (Kreuzberg et al., 2008) or Cx36 (Wellershaus et al., 2008) gene promoters, respectively. Homozygous Cx30.2Lac/LacZ (n=5) and Cx36CFP/CFP (n=5) mice were anaesthetised with sodium pentobarbital (60mg/kg IP) and perfused transcardially with 4% paraformaldehyde. Brainstems and spinal cords were sectioned on a vibratome and sections analysed by standard immunohistochemical and immunofluorescence protocols. Three mice in each group were injected intraperitoneally with 0.1ml of 1% hydroxystilbamidine (Sigma) 3 days prior to perfusion, to label preganglionic and motor neurones. Cx30.2/LacZ-IR was detected with rabbit anti-b-galactosidase (Sigma), Cx36/CFP-IR – with rabbit anti-green fluorescent protein (Abcam). Sections treated for Cx30.2 or Cx36 were double immunostained with mouse antibodies against tyrosine hydroxylase (TH, ABCAM) and/or goat antibodies against choline acetyl transferase (ChAT, CHemicon). Cx30.2 expression, represented by B-galactosidase, was detected throughout the spinal cord and brainstem. Numerous labelled cells were present throughout the NTS, some of which were confirmed as TH positive. No motor or preganglionic neurones contained BGal (identified by the presence of hydroxystilbamidine and/or ChAT) but rather it was detected in cells surrounding these nuclei. TH positive neurones in the A1/C1 regions were also B-Gal positive. Cx36 expression was not detected in cranial nerve nuclei, but was present in sympathetic preganglionic neurones. In the medulla oblongata CFP was detected in the NTS and in TH neurones in the NTS and ventrolateral medulla. Current analysis is quantifying the extent of co-localisation. These experiments show that both Cx30.2 and Cx36 are expressed in neurones that could influence autonomic control. Of the autonomic output neurones only sympathetic preganglionic neurones express one of these gap junctions, Cx36. However, other neurones in a position to influence autonomic function express these proteins, including neurones in the NTS and ventrolateral medulla. Future experiments will characterise the neurochemistry of these neurones and investigate functional properties.