There is convincing evidence that the CB1 receptor is present on both GABAergic and glutamatergic axons in the BLA. Immunohistochemical studies demonstrated that CB1 receptors are present on GABAergic synapses and function to inhibit GABAergic transmission (Katona et al., 2001; McDonald and Mascagni, 2001). Although it has been difficult to demonstrate the presence of CB1 receptors on glutamatergic terminals using immunohistochemistry (Katona et al., 2001; McDonald and Mascagni, 2001), electrophysiological studies have established that activation of CB1 receptors within the BLA inhibits excitatory synaptic transmission and the firing rate of BLA projection neurons (Pistis et al., 2004; Perra et al., 2008; Domenici et al., 2006; Azad et al., 2003). Furthermore, the ability of cannabinoids to reduce glutamatergic signaling overrides the suppression of GABAergic transmission, resulting in a net reduction in the excitability of BLA projection neurons (Azad et al., 2003). In line with this, immediate early-gene studies have found that systemic administration of a CB1 receptor antagonist increases the neuronal activation of the BLA in unstressed animals (Singh et al., 2004; Patel et al., 2005b), supporting the hypothesis that endocannabinoid
