Group II metabotropic glutamate receptors (mGluRs) are G-protein coupled receptors, which are negatively linked to adenylyl cyclase. There are two subtypes of group II mGluRs; mGluR2 and mGluR3, which are located perisynaptically in many brain regions and are thought to act as autoreceptors of glutamatergic synaptic transmission. The activation of group II metabotropic glutamate receptors has been shown to cause a lasting depression of synaptic transmission both within the basolateral amygdala complex and in thalamic afferents to the lateral amygdala (Heinbockel and Pape, 2000; Lin et al., 2000). It has been suggested that low frequency stimulation (LFS) induced long-term depression (LTD) within the basolateral amygdala complex may involve group II mGluRs (Wang & Gean, 1999; Kaschel et al., 2004). However the role of group II mGluRs in modulating transmission and in particular plasticity within the cortical input to the lateral amygdala is not clear. We have therefore investigated the role of group II mGluRs in this cortical input to the lateral amygdala. Experiments were performed on acute coronal amygdala slices from adult male CD-1 mice. Whole-cell patch-clamp recordings were made from pyramidal-type cells in the lateral amygdala while stimulating the external capsule, which contains the cortical input to the lateral amygdala. We show that the pharmacological activation of group II mGluRs with the selective agonist, DCG-IV, induces a dose-dependent long-term depression of synaptic transmission; 1 µM DCG-IV results in a persisting depression of 46 ± 10 % (± S.E.) at 60 min post application (n=8). The DCG-IV induced depression is associated with a transient increase in paired pulse facilitation (68 ± 15 %, n=6), suggesting that the initial depression may involve a presynaptic mechanism, while the long-term depression may involve a postsynaptic mechanism. In the cortical input to the lateral amygdala a low frequency stimulation protocol (900 pulses at 1 Hz, holding cells at -70mV) is found to induce LTD (39 ± 6 % at 40 min post LFS, n=10). This LFS-LTD is dependent upon the activation of group II mGluRs, as it can be blocked by LY341495, a group II mGluR selective antagonist at 300 nM. The NMDA antagonist, D-AP-5 (50 µM) also blocks this LTD, suggesting that NMDA receptor activation is also involved in mediating this LFS-LTD.