We have recently discovered that the stimulus selectivity for amygdala synaptic potentiation is altered as a result of fear memory formation. A novel form of long-term potentiation that is low-frequency stimulation dependent is revealed, while potentiation that is high-frequency stimulation dependent is attenuated. Other forms of low-frequency stimulation dependent plasticity require activation of group II metabotropic glutamate receptors and antagonists of these receptors within the amygdala block fear conditioning. Here we will test the hypothesis that low frequency induced potentiation is a unique form of plasticity with features that diverge from those previously described in the amygdala by addressing the following specific aims: 1. Analyze the signaling mechanisms underlying the low frequency stimulation-induced long-term potentiation of the cortico-lateral amygdala synapse following fear conditioning and 2. Characterize the role of group II mGluRs in synaptic transmission and on low frequency dependent synaptic plasticity within the cortico-lateral amygdala pathway in control and fear-conditioned animals. These experiments will enhance our understanding of neuronal mechanisms underlying the formation and expression of anxiety and fear and provide valuable insight into potential avenues of treatment for human anxiety disorders.