Within neocortical brain regions, eCB signaling modulates GABA release from a subset of GABAergic interneurons, and modulates cortico-cortico and some thalamocortical glutamatergic inputs to cortical pyramidal neurons (Auclair et al., 2000; Bodor et al., 2005; Hill et al., 2007; Lafourcade et al., 2007). Within the striatum, eCB signaling modulates cortical glutamatergic inputs to medium spiny neurons, as well as recurrent collateral GABAergic transmission onto these cells (Gerdeman and Lovinger, 2001; Uchigashima et al., 2007). Within the globus pallidus, eCB signaling modulates GABA release from striatal neuron terminals onto pallidal neurons (Engler et al., 2006). Based on the anatomical and physiological data on the role of eCB signaling within the amygdala summarized above, a similar pattern can be observed in the amygdaloid complex. The BLA, a cortical-like structure (see introduction), exhibits functional eCB signaling essentially identical to other cortical regions, i.e. eCB modulation of local GABAergic transmission and afferent glutamatergic inputs. Within the CeAL, which exhibits homology to the striatum, eCBs modulate glutamatergic inputs to this region, while eCB signaling modulates GABAergic transmission from the CeAL to the CeAM (which shows
