All sympathetic control of end organs in the body relies on the activity of the sympathetic preganglionic neurones (SPNs) within the spinal cord that form the final pathway from the central nervous system. These SPNs exhibit heterogeneity with respect to their neurochemistry, location, descending inputs and patterns of activity. Part of this heterogeneity is bestowed by the local spinal cord circuitry, comprising interneurones located in a number of regions of the spinal cord. Our understanding of the role of these local circuits and indeed the significance of connections between the SPNs themselves, through specialised gap junctions, is patchy, but it is clear that the spinal cord itself is capable of generating activity that is physiologically relevant.Transneuronal tracing studies first identified presympathetic interneurones that were located in laminae V, VII, X and the intermediolateral cell column (IML) and these IML presympathetic interneurones are fast firing due to the presence of the Kv3.1b channel subunit (1) while those in lamina X are GABAergic and directly inhibit SPNs (2;3). Some of the interneurones in lamina X may play a more integrative role than just the control of sympathetic outflow since axons of single filled interneurones directly synapse onto both SPNs and motoneurones in a 500 μm spinal cord slice. There may be a further subset of these interneurones that colocalise acetylcholine and GABA but their role is yet to be fully investigated. GABAergic inputs onto SPNs exert their effects via a number of mechanisms, through activation of GABAA and GABAB receptors (4) and also through extrasynaptic receptors which serve to stabilise the membrane at more negative potentials (5). These GABAergic interneurones contribute to the rhythmic patterns of activity that can be generated in the spinal cord either spontaneously or through activation of 5-HT2 receptors since bicuculline reduces the network oscillatory activity (6).Gap junctions also play a significant role in sympathetic control; they are located on SPNS in the IML where they enable rapid communication between these neurones. Blockade of these gap junctions reduces local rhythmic activity in the spinal cord slice (6) and also disrupts autonomic control in the working heart brainstem preparation (7). In mice lacking the connexin 36 subunits (Cx36 -/-) that are the main component of SPN gap junctions, spikelet occurrence is almost abolished in single SPNs and is severely diminished even after 5-HT application, while in Cx 36 +/- mice, there is a significant reduction in ongoing and evoked spikelet frequency compared to the wild-type. In the working heart brainstem preparation of Cx36 -/- mice, respiratory-related sympathetic activity is diminished and responses to chemoreceptor activation are also reduced. Using telemetry recordings in the awake Cx36 -/- mouse, the variance in blood pressure and heart rate is much greater than the wild type animals indicating that these gap junctions are critical to enable the rapid changes in sympathetic activity that underlie homeostasis.These studies together indicate that local spinal cord circuitry is critical in enabling appropriate levels and patterning of activity in sympathetic outflow. It is of interest to understand how these circuits may be harnessed in the situation of spinal cord injury. Another avenue of exploration into recovery of functionality after spinal cord injury is to elucidate whether there is neurogenic capacity within the spinal cord, similar to that observed in other CNS regions such as the subventricular zone. Our very recent research suggests that it is possible to manipulate this plasticity, which may in future facilitate restoration normal sympathetic function after injury.