The role of GABA receptors in synaptic transmission to neonatal rat sympathetic preganglionic neurones (SPNs) was investigated utilising whole-cell patch clamp recording techniques in longitudinal and transverse spinal cord slice preparations. In the presence of glutamate receptor antagonists (NBQX, 5µM and D-APV, 10µM), electrical stimulation of the ipsilateral or contralateral lateral funiculi (iLF and cLF, respectively) revealed monosynaptic inhibitory postsynaptic potentials (IPSPs) in 75% and 65% of SPN, respectively. IPSPs were sensitive to bicuculline (10 µM) in all neurones tested and reversed polarity around -55mV, the latter indicating mediation via chloride conductances. In 3 neurones IPSPs evoked by stimulation of iLF (n=1) or cLF (n=2) were partly sensitive to strychnine (2µM). The expression of postsynaptic GABAA and GABAB receptors were confirmed by the sensitivity of SPN to agonists; GABA (2mM), Muscimol (10-100µM) or Baclofen (10-100µM), in the presence of TTX, each of which produced membrane hyperpolarisation in all SPN tested. Muscimol induced responses were sensitive to bicuculline (1-10µM) and SR95531 (10µM) and baclofen induced responses were sensitive to 2-hydroxy-saclofen (100-200µM) and CGP55845 (200nM). The GABA_C receptor agonist CACA (200µM) was without significant effect on SPN. These results suggest that SPN possess postsynaptic GABA_A and GABA_B receptors and that subsets of SPN receive bilateral GABAergic inputs which activate GABA_A receptors, coupled to a chloride conductance. At resting or holding potentials close to threshold either single or bursts (10-100Hz) of IPSPs gave rise to a rebound excitation and action potential firing at the termination of the burst. This effect was mimicked by injection of small (10-20pA) rectangular-wave current pulses, which revealed a time-dependent, Cs⁺-sensitive inward rectification and rebound excitation at the termination of the response to current injection. Synaptic activation of a rebound excitation mediated by a time-dependent inward rectification expressed intrinsically by SPN may provide a novel mechanism enabling SPN to be entrained to rhythms driven from the brainstem or higher centres.