NPY is generally co-localized with GABA in inhibitory interneurons. NPY mediates its actions by interacting with a family of G protein-coupled receptors (GPCRs), at least five of which have been cloned and designated Y1, Y2, Y4, Y5, and Y6. These receptors are widely distributed throughout the brain. NPY has also been shown to be a regulator of neuronal excitability in hippocampus, where its cellular actions have been most extensively studied (Colmers et al. 1991). In the amygdala, NPY has anxiolytic effects that are mediated via activation of Y1 receptors (Heilig et al. 1993). NPY neurons in the amygdala project to the BNST (Allen et al. 1984), which also contains Y1 receptors and Y1 and Y2 receptor mRNA. Further, the CeA receives NPYergic input from the nucleus of the solitary tract, arcuate nucleus, and the lateral septum (see (Kask et al. 2002) for a review). Y1, Y2, and Y5 receptors, and receptor mRNA are found in the amygdala, and each of these receptor subtypes has been implicated in anxiety (Kask et al. 2002). Y2 receptors are thought to act presynaptically as
