Spinal trauma may result in severe disruption of sensory, motor and autonomic function. Unfortunately repair of affected neuronal circuits is minimal. Nevertheless, there is some evidence that spinal related trauma can trigger proliferation and migration of progenitor cell sources in the spinal cord (Vessal et al. 2007; Ke et al. 2006). An endogenous source of neural progenitor cells is the ependymal region of the central canal, (Adrian & Walker, 1962; Horner et al. 2000). Here we investigate a peri-ependymally located group of cells which have an unusual morphology: they extend a single process ending in a terminal bulb into the lumen of the central canal and are known as cerebrospinal fluid contacting neurones (CSFcNs). Our hypothesis is that CSFcNs are immature neurones that may have the ability to provide an early response to injury. Neurochemistry of CSFcNs was investigated using fluorescence immunohistochemistry on both transgenic reporter mice expressing GFP under control of the promoter for GAD67 (Tamamaki et al. 2003), and Wistar rats. Briefly, animals were deeply anaesthetised with Sagatal (60mg/kg) and perfused transcardially with phosphate buffered saline followed by 4% paraformaldehyde in 0.1M phosphate buffer. Spinal cord was dissected and 50µm sections cut using a vibrating microtome. CSFcNs were identified in rats using anti-P2X₂ (Sigma) and anti-GAD67 (Chemicon) antibodies, and in mice using anti-GFP (Abcam/Invitrogen). Preliminary immunohistochemical data supports the concept that the CSFcNs are immature neurones, since they express neuronal markers Tuj1 (Neuromics) and HuC/D (Abcam) that are switched on early during development, and express little or no NeuN (Chemicon), a marker of mature neurones (n=3 rats, 3 mice). The terminal bulb is potentially able to release transmitter substances into the CSF, since it contains some of the necessary synaptic machinery for release, such as synaptic vesicle proteins SV2 (DHSB) and synaptophysin (Sigma), and the vesicular GABA transporter. Further to these findings, potential responses of these cells to injury were investigated in rats using a mild dorsal root ganglion injury caused by injection of neuronal tracer CTb. In this case, preliminary data indicates a redistribution of the CSFcNs around the central canal and in some circumstances what appears to be migration of the cells in response to injury. Investigation into potential changes in neurochemistry in response to injury is currently underway. Given the immature status of CSFcNs, and their potential response to injury, this is an interesting avenue to explore in the context of aiding endogenous repair in spinal trauma.