Ventricular administration of urocortin (UCN) inhibits feeding, but specifi
c site(s) of UCN action are unknown. In the current studies we examined the
effect of UCN in the hypothalamic paraventricular nucleus (PVN) on feeding
. We tested UCN administered into the PVN in several paradigms: deprivation
-induced, nocturnal, and neuropeptide Y (NPY)-induced feeding. We compared
the effect of equimolar doses of UCN and corticotrophin releasing hormone (
CRH) on NPY-induced and nocturnal feeding, determined whether UCN in the PV
N produced a conditioned taste aversion (CTA) and induced changes in c-Fos
immunoreactivity (c-Fos-ir) after UCN and NPY administration in the PVN. UC
N in the PVN significantly decreased NPY and nocturnal and deprivation-indu
ced feeding at doses of 1, 10, and 100 pmol, respectively. UCN anorectic ef
fects lasted longer than those attributed to CRH. Ten and thirty picomoles
UCN did not induce a CTA, whereas 100 pmol UCN produced a CTA. UCN (100 pmo
l) in the PVN neither increased c-Fos-ir in any brain region assayed nor al
tered c-Fos-ir patterns resulting from PVN NPY administration. These data s
uggest the hypothalamic PVN as a site of UCN action.