Figure 4.
The selective, long-acting opioid KOR-antagonist nor-BNI (nBNI) normalizes rat performance impaired by ethanol in the WMT. Rats were treated for 6 days with water or ethanol followed by the WMT initiated 2 days after the last ethanol administration. The effects of (a–c) systemic (6 mg kg−1; sc) or (d–f) intrahippocampal (CA3 region; 10 nmol per 0.3 μl per site, bilaterally) administration of nor-BNI on ethanol-induced cognitive impairment in rats. Either the nor-BNI or vehicle (saline or aCSF) was administered 2 h after the last ethanol treatment (that is, 2 days before the first WMT training block). Acquisition trials: (a, d) mean values (s) of escape latency for the four daily trials; ANOVA: (a) ethanol-nor-BNI group, treatment × time: F (4, 328)=2.66, P<0.05; (d) ethanol-nor-BNI group, treatment × time: F(4, 162)=4.52, P<0.05). Swim speed: (b, e) the mean values in cm s−1. Quadrant selectivity: (c, f) the percentage of the total swimming time; ANOVA: (c) ethanol-nor-BNI group, treatment × time: F(4, 328)=2.34, P<0.05; (f) ethanol-nor-BNI group, treatment × time: F(4, 162)=2.15, P<0.05). The data for the retention trials are shown as bar graphs associated with and on the same scale as the acquisition curves. In (a–c): n=18 and 16 rats in the saline and nor-BNI-treated groups, respectively. In (d–f), n=8 and 7 in the aCSF- and nor-BNI-treated groups, respectively. The data are shown as means±s.e.m.; *P<0.05; the Newman–Keuls test was used.