1. Sympathetic and somatic motor outflow results from the summation of excitatory and inhibitory inputs arising from intra- and supra-spinal origins. Here we determined the contribution of intra- and supra-spinal GABAergic inputs, utilizing GABA-A receptors, in producing sympathetic and somatic motor outflow. 2. Spinal GABA-A receptor blockade, with bicuculline or picrotoxin injected intrathecally at T9, increased the level and lability of arterial pressure, sympathetic (splanchnic and cervical sympathetic) and motor (phrenic) nerve activity. Bursts of activity occurring irregularly, at low frequency were seen in all nerves. 3. C1 spinal transection abolished phrenic nerve activity and reduced sympathetic nerve activities and arterial pressure. Intrathecal bicuculline-induced bursting in sympathetic and motor (phrenic, sciatic and brachial) nerves was similar to that seen prior to C1 transection. Thus supraspinal control of sympathetic and somatomotor outflow is not dependent on GABA-A receptors. 4. Bicuculline-induced effects on phrenic nerve activity were eliminated after C8 spinal cord transection and regular phrenic rhythm resumed indicating that bicuculline was not acting directly on phrenic motoneurons. 5. Bicuculline evoked similar bursting characteristics in both sympathetic and motor nerves attributable to increased excitability of spinal cor d neurons. The bursting patterns evoked were often coincident in sympathetic and motor nerves suggesting a common site of origin. 6. These data suggest there is intraspinal coupling between multiple sympathetic and motor outflows in the adult rat spinal cord in vivo. Cervicothoracic spinal cord generator/s perhaps in the form of interneuronal networks, utilizing GABA-A and glutamate receptors, can simultaneously drive functionally independent nerves.