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. 2010 Feb 10;30(6):2300–2310. doi: 10.1523/JNEUROSCI.5724-09.2010

Figure 5.

Figure 5.

Hcrtr-1, but not CRF1 receptor, regulates the reinstatement of nicotine-seeking behavior induced by Hcrt-1. Mice that achieved the extinction criterion received an intracerebroventricular saline infusion preceded by SB334867 (5 mg/kg, i.p.) (n = 4), antalarmin (30 mg/kg, s.c.) (n = 4), or vehicle (n = 9) 10 min before the reinstatement session. Next day, the same mice were infused with Hcrt-1 (0.75 nmol/1 μl, i.c.v.) preceded by the same SB334867 (5 mg/kg, i.p.) (n = 4), antalarmin (30 mg/kg, s.c.) (n = 4), or vehicle (n = 9) and tested for reinstatement 10 min later. SB334867 and antalarmin were administered 30 min and 1 h, respectively, before intracerebroventricular Hcrt-1/vehicle infusions. Mean number of nose-pokes in the active (■) and inactive (□) holes during the different experimental phases: acquisition of nicotine self-administration behavior (mean of 3 d acquisition criteria), extinction (mean of 3 d criterion), and reinstatement (intracerebroventricular infusion of vehicle/Hcrt-1). *p < 0.05, **p < 0.01, differences between experimental phases when considering the active hole; +p < 0.05, ++p < 0.01, differences between holes within the same experimental phase (Newman–Keuls test).

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