Figure 1.

NPY significantly blunted binge-like 20% ethanol consumption. (a) Central infusion (i.c.v.) of NPY dose-dependently reduced binge-like ethanol consumption (g/kg per 4 h) and (b) associated BECs (mg/dl; n=32–38 per group). NPY modulates binge-like consumption of 20% ethanol via NPY Y1R activation and Y2R inactivation. (c) The i.c.v. infusion of the Y1R agonist [D-His²⁶]-NPY significantly reduced binge-like ethanol consumption (g/kg per 4 h; n=9 per group). (d) The i.c.v. infusion of the Y1R antagonist BIBP-3226 significantly enhanced binge-like ethanol consumption (n=24–28 per group). (e) The i.c.v. infusion of the Y2R agonist NPY₁₃₋₃₆ did not alter binge-like ethanol consumption (n=7–10 per group), (f) but i.c.v. infusion of the Y2R antagonist BIIE-0246 significantly reduced binge-like ethanol consumption (n=8–10 per group). For each compound, i.c.v. infusions were given on day 4 of the 4-day binge-like drinking cycle. The NPY and BIBP-3226 infusion studies involved Latin Square designs in which mice experienced the various doses of compound over multiple binge-like drinking cycles. All data are shown as mean±SEM, and significance was accepted at the p<0.05 level (two tailed). ^*Significant differences from vehicle.