Sympathetic preganglionic neurones (SPNs) receive synaptic inputs from both spinal and supraspina(l) regions. Activation of metabotropic glutamate receptors reduces excitatory postsynaptic potentials in SPNs1. However, its influence on GABAergic transmission is still unknown. In this study, we focused on two monosynaptic GABAergic pathways from local interneurones in the central autonomic area (CAA)(2) and fibres descending in the lateral funiculus (Lf) from higher autonomic centres. Wistar rats of either sex (10-15 day) were anaesthetised with urethane (2g/kg, ip) followed by a cardiac perfusion of 215mM sucrose aCSF. Transverse thoracic spinal cord slices (300μm) were prepared for whole-cell patch clamp recording, made in aCSF containing the non-selective ionotropic Glutamate receptor antagonist, kynurenic acid (2mM). Paired pulse stimuli were used to evoke inhibitory postsynaptic potentials from Lf (Lf-IPSPs) and CAA (CAA-IPSPs) sequentially. The group III metabotropic glutamate receptor (mGluR III) agonist L-AP4 (10 µM) and its antagonist MPPG (10 µM) were bath applied. Amplitudes of IPSPs were measured by averaging 10 consecutive sweeps. The difference between the two IPSPs from each pathway was calculated (2nd/1st) as paired pulse ratio (PPR). All results are shown in mean ± S.E.M. Statistic significance was considered when p<0.05, using Student t-test. In agreement with an earlier study(3), L-AP4 did not alter cell membrane potential or input resistance during postsynaptic recordings. Bath application of L-AP4 decreased the peak amplitudes of both Lf- and CAA-IPSPs (Lf 1st 10.3 ± 1.6 to 4.7 ± 0.8 mV, Lf 2nd 10.0 ± 1.5 to 5.5 ± 1.0, n=10, p<0.001; CAA 1st 6.9 ± 1.1 to 2.9 + 0.7 mV, CAA 2nd 7.2 ± 0.9 to 3.6 ± 0.8 mV, n=11, p<0.001) associated with an increase in PPR (Lf 0.98 ± 0.04 to 1.14 ± 0.05, p<0.001; CAA 1.07 ± 0.06 to 1.34 ± 0.10, p<0.001). Pre-incubating slices with MPPG for 5 minutes did not cause significant changes in the amplitude of IPSPs or PPR (p>0.05). However further addition of L-AP4 failed to induce the reduction in peak amplitudes of IPSPs from either pathway (Lf n=4, p>0.05; CAA n=5, p>0.05). These data show that GABAergic transmission on SPNs is modulated by presynaptic mGluR III receptors. This synaptic depression is due to a decrease in neurotransmitter release, possibly by affecting Ca influx. All experiments accord with current UK legislation.