H CTX only during the absenceNeurosci Lett. Author manuscript; available in PMC 2014 November 27.Tallarida et al.Pageinterval (COC-CTX + COC), cocaine challenge made much less locomotor activity in comparison with CTX-na e mice that had been pretreated only with cocaine (SAL-COC + COC) (P 0.001: ten min post-injection). Similarly, cocaine challenge produced less locomotor activity in mice that had been pretreated concurrently with cocaine and CTX (CTX-COC + COC) than in mice pretreated with only cocaine (SAL-COC + COC) (P 0.001: 10 min post-injection). For clarity, cumulative locomotor activity counts across the very first 20 min following cocaine administration is presented (Fig. 1 box). One-way ANOVA revealed a significant most important impact [F (three, 23) = four.068, P 0.05]. Equivalent to time-course results, cocaine challenge made higher locomotor activity in mice previously exposed to cocaine [SAL-COC + COC] than in previously cocaine-na e mice [SAL-SAL + COC], thus indicating sensitization (P 0.05) (Fig. 1, box). Additional, in mice previously treated with cocaine, cocaine challenge developed much less locomotor activity in those mice that had been also exposed to CTX, either concurrently with repeated cocaine treatment [CTX-COC + COC] or following repeated cocaine treatment [COC-CTX + COC], than in previously CTX-na e mice [SALCOC + COC] (P 0.05) (Fig. 1, box). For cumulative locomotor counts more than the entire 60 min (as opposed to 20 min) following cocaine challenge, one-way ANOVA did not reveal a important key effect [F (three, 23) = 1.2,2′-Dibromo-1,1′-biphenyl Order 761, P 0.05] (data not shown). CTX attenuates acute locomotor stimulant effect of 30 mg/kg cocaine Fig. two presents the effects of CTX against locomotor activity induced by acute exposure to 15 mg/kg (2A) or 30 mg/kg (2B) of cocaine. For experiments with 15 mg/kg of cocaine, two-way ANOVA carried out on the time-course data revealed substantial therapy [F (3, 28) = 25.72, P 0.0001] and time [F (six, 196) = 2.806, P 0.05] effects and identified a considerable interaction [F (18, 196) = 2.861, P = 0.0002] (Fig. 2A). Post-hoc analysis revealed differences in locomotor activity amongst the SAL-SAL and SAL-COC groups (P 0.001 at 30, 40, and 50 min post-injection and P 0.05 at 60 min post injection). Important differences in locomotor activity had been not detected between the SAL-COC and CTX-COC groups at any from the time points (P 0.2,4-Dichloro-6-ethylpyrimidine Order 05). Even so, cocaine’s locomotor impact was somewhat stronger in CTX-na e mice than in CTX-pretreated mice, as significant variations in activity counts amongst the the latter group of animals (CTX-COC) and manage mice (SAL-SAL) have been detected at only two time points (P 0.05 at 40 and 60 min post-injection). For cumulative locomotor activity over the whole 60 min following cocaine injection (Fig.PMID:23805407 2A, box), a considerable principal effect [F (3, 28) = four.801, P 0.01] was detected. Locomotor activity in mice treated with cocaine (SAL-COC) was enhanced in comparison to cocaine-na e mice (SAL-SAL) (P 0.05) but was not considerably different from mice treated with CTX and cocaine (CTX-COC) (P 0.05). CTX effects against locomotor activity developed by 30 mg/kg of cocaine are shown in Fig. 2B. Two-way ANOVA conducted on the temporal data revealed considerable treatment [F (1, 14) = 70.12, P 0.0001] and time [F (six, 98) = two.835, P 0.05] effects and identified a substantial interaction [F (six, 98) = 2.919, P 0.05] (Fig. 2B). Post-hoc analysis revealed that 30 mg/kg of cocaine made substantially less locomotor activity in CTX-tr.