Recently, it has been shown that NPY and CRF have opposing effects on stress and anxiety as well as on synaptic activity in BNST (Heilig et al. 1994; Kash and Winder 2006). Kash and Winder found that NPY and CRF inhibit and enhance GABAergic transmission, respectively: NPY depresses GABAergic transmission through activation of the Y2 receptors, whereas CRF and urocortin enhance GABAergic transmission through activation of CRF1 receptors. Further, NPY appears to reduce GABA release, whereas CRF enhances postsynaptic responses to GABA, suggesting potential anatomic and cellular substrates for the robust behavioral interactions between NPY and CRF in the extended amygdala.
