Many CNS regions and neuronal types shape the level of sympathetic activity by ultimately influencing spinal sympathetic preganglionic neurones (SPNs), the sole sympathetic output from the CNS. The spinal cord itself provides a high degree of complexity and co-ordination of sympathetic control through the many interneurones that are crucial components of CNS circuits. Surprisingly, there is little information regarding the characteristics of these interneurones involved in sympathetic control, partly due to problems associated with their identification. We have identified novel groups of local sympathetic interneurones and here we discuss how these interneurones may fit into circuits involved in sympathetic control and how activation of specific receptors, both on these interneurones and on SPNs may contribute to control of SPN activity. These data are obtained using recording and filling of neurones in thoracic spinal cord slices of rats (11-14 days) that were terminally anaesthetised with urethane (2g/kg, i.p.) and transcardially perfused with ice cold 215 mM sucrose aCSF (Deuchars et al. 2005). One group of interneurones in particular will be considered here, within the central autonomic area (CAA). We have shown that GABAergic neurones in the CAA form direct monosynaptic, inhibitory connections with SPNs (Deuchars et al., 2005). Recording and filling interneurones within the CAA has revealed a complex degree of local axonal projection. The local axon ramifies extensively in the intermediolateral cell column and intercalated nucleus where it forms direct synaptic contacts (verified at the electron microscope level) onto immunohistochemically identified cholinergic SPN dendrites. Furthermore, axons also extend to the ventral horn where they also directly synapse onto cholinergic motoneurones. This exciting finding has implications for a possible spinal cord site of co-ordination of sympathetic and motor outflow, as suggested by (Chizh et al., 1998). Since serotonin is known to profoundly influence sympathetic outflow at the spinal level (Madden & Morrison, 2006;Marina et al., 2006) and also shapes the rhythmic activity of motor outflow (e.g. (Schmidt & Jordan, 2000), the effects of serotonin on CAA interneurones and on rhythmic oscillations recorded from populations of neurones in the IML has been investigated. Depolarisations and hyperpolarisations of CAA neurones were elicited with both 5-HT and, somewhat surprisingly, the 5-HT 2 receptor agonist α-methyl5-HT. The unusual pharmacological profile of the hyperpolarisations is currently under investigation. 5-HT also induced or increased the power of ongoing oscillations recorded in the IML, using “field” recording techniques. We have shown that this 5-HT driven oscillatory activity relies on the presence of gap junctions in the network and on ongoing GABAergic activity. Since these GABAergic interneurones provide the first evidence of a local GABAergic inhibitory influence on SPNs, we have also re-examined how GABA may affect SPN activity and have uncovered a novel tonic inhibitory GABAergic role, mediated by receptors containing α5, rather than delta subunits. This tonic GABAergic inhibition is maintained in low Ca2+/high Mg2+ and also in tetrodotoxin and acts to reduce the excitability of SPNs by holding them at a more hyperpolarised potential and reducing the numbers of action potentials elicited during a depolarising pulse. Elevation of such a tonic inhibitory influence may be a potential target for treatment of conditions where there is a chronic elevation in sympathetic activity. To summarise, these data provide evidence for a complex level of control of sympathetic outflow within the spinal cord. As we unravel the circuits involved in influencing sympathetic activity, we gain insight into ways in which precise control of specific pathways may be achieved.