Figure 5.
Development of AMPH-induced CMS and CPP require hippocampal Trk receptors. A, Timeline of intracerebral and systemic drug treatments and the behavioral paradigms. On AMPH-conditioning days 1, 3, and 5, the tyrosine kinase inhibitor K-252a (25 ng/0.5 μl of 25% DMSO in saline per side) or its vehicle was infused intracerebrally into the DG/CA3 (DG) or cortex immediately before each systemic injection (1.0 mg/kg AMPH or saline), and rats were placed into the activity chambers. B, C, Intracerebral injections listed are those given on days 1, 3, and 5; vehicle was 25% DMSO in saline. Data are presented as mean ± SEM. *p < 0.0125; **p < 0.0025; two-tailed paired t test (α value was Bonferroni adjusted to 0.0125). B, Horizontal activity. AMPH induced CMS in rats pretreated with intra-DG vehicle or intra-cortex K-252a. Rats pretreated with intra-DG K-252a failed to develop AMPH-induced CMS. DG K-252a with intraperitoneal saline, t(7) = 1.089, p = 0.3124; DG vehicle with intraperitoneal AMPH, t(9) = 3.374, p = 0.0082; DG K-252a in the DG with intraperitoneal AMPH, t(13) = 1.118, p = 0.2838; cortex K-252a in the cortex with intraperitoneal AMPH, t(4) = 3.836, p = 0.0105. C, CPP. Rats conditioned with intra-DG K-252a before AMPH intraperitoneally on days 1, 3, and 5 failed to express AMPH-induced CPP on the test day (day 8), whereas CPP remained intact in rats conditioned with intra-DG vehicle or intra-cortex K-252a. DG K-252a with intraperitoneal saline, t(7) = 0.1284, p = 0.9014; DG vehicle with intraperitoneal AMPH, t(9) = 4.425, p = 0.0017; DG K-252a with intraperitoneal AMPH, t(13) = 0.4129, p = 0.6864; cortex K-252a with intraperitoneal AMPH, t(4) = 5.096, p = 0.0070. i.c., Intracerebral; i.p., intraperitoneal; Ctx, cortex.