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Neuropeptide Y (NPY) is abundant in the nervous system. It acts through Y1, Y2, Y4 and Y5 receptors and is involved in a variety of brain functions. When applied locally into the amygdala, NPY exerts an anxiolytic action, presumably mediated by Y1 receptors. Depletion of Y2 receptors induces an anxiolytic phenotype, possibly by abolishing the release-inhibiting action of presynaptic Y2 receptors. In the present study we aimed to find the exact site of the presumed anxiogenic action mediated by Y2 receptors. We conducted site-specific deletions of Y2 receptors in Y2 mice by local injection of an AAV-Cre vector into the hippocampus and the amygdala. As controls, an AAV-GFP vector was injected in Y2 littermates at the same sites. Expression of Cre and GFP was verified by in situ hybridization and immunohistochemistry. Deletion of Y2 receptors was visualized by receptor autoradiography and in situ hybridization. After bilateral injection of an AAV-Cre vector into the basolateral amygdala, mice revealed a tendency towards an anxiolytic phenotype in the light-dark test (LDT). When deletion of Y2 receptors was confined to the central nucleus of the amygdala, an anxiolytic phenotype was observed in the elevated plus maze and the LDT. Moreover, a better stress coping ability was demonstrated in the tail suspension test. In contrast, no anxiolytic effect was detected after intrahippocampal injections. The experiments indicate that the anxiolytic and antidepressant-like effects of Y2 receptor deletion may be generated in certain subnuclei of the amygdala.

Experiments to localize the site for the anxiogenic action of NPY mediated by Y2 receptors in the mouse brain