The central canal region of the mammalian spinal cord displays increases in proliferation after injury and suggests neurogenic potential [1, 2]. Ependymal cells and Cerebrospinal fluid-contacting cells (CSFcCs) are involved in these functions. The specific role of the CSFcCs is not known, nor how they communicate with the ependymal cells. The presence of purinergic P2X2 receptors [3] indicates a role for ATP signalling. The P2X receptors in this region could be a damage recognition system, as in cochlea [4], initiating cell proliferation. This study aims to investigate the response to ATP and analogues in the cell types in this area.Spinal cord slices were obtained from Wistar rats (8 days) anaesthetised with either pentobarbital 120 mg kg-1 or urethane 2 g kg-1 I.P. and transcardially perfused with sucrose ACSF. The whole cell patch clamp method was used to obtain single cell recordings from CSFcCs or ependymal cells. GABA (100 μM) was applied in the bath solution; ATP (300 μM) was applied using a puff electrode and a PicoPump (World Precision Instruments). A fluorescent dye was included in the intracellular solution allowing post-recording visualisation. Data are presented as mean ± standard error of the mean and analysed with T-tests, using a 5 % level of significance. Cells were characterised by their responses to hyperpolarising and depolarising current pulses. Results show significantly different responses between the different cell types to bath application of GABA in terms of the input resistance (IR). Ependymal cells show a small increase in IR (6.00 ± 3.29 MΩ; n=16), whilst CSFcCs show a consistent decrease in IR (-284.29 ± 85.63 MΩ; n=7). No significant difference was found with respect to changes in membrane potential.Local application of ATP elicited fast depolarisations (63.01 ± 13.87 ms from onset of pressure pulse to start of response; n=12) in CSFcC type 1, type 2 and ependymal cells; however the majority of responses were seen in CSFcCs. Bath application of suramin (50 μM) significantly antagonised the responses to ATP, reducing the magnitude from 21.50 ± 5.16 mV to 9.73 ± 3.03 mV (n=7). The time to response was also significantly longer after suramin application (71.50 ± 20.95 ms in control and 154.43 ± 24.30 ms with suramin; n=7). This data shows clear evidence for a role for purinergic signalling via P2X receptors in the central canal area of the spinal cord. The differences in GABA responses between ependymal cells and CSFcFs allowed for differentiation between cell types and verification of cell viability. Suramin is a broad-spectrum antagonist that blocks both P2X and P2Y receptors so could be acting on multiple receptor types and subtypes. The next steps for this study are to repeat the experiments using more specific antagonists for P2X receptors and for specific P2X subtypes.