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  • Based on the finding described above the present study

    2020-02-14

    Based on the finding described above, the present study was designed to investigate the effects of specific CRF receptors, CRF1 and CRF2, in the BLA and CeA on the duration of TI in guinea pigs (Cavia porcellus). To this end, we evaluated whether administration of the CRF1 BCTC antagonist CP-376395 or the CRF2 receptor antagonist Astressin 2B into the BLA or CeA could alter TI duration. Additionally, we investigated whether previous microinjection of CP-376395 or Astressin 2B into the BLA or CeA could modify the CRF-induced increase in TI behavior.
    Materials and methods
    Results The present results showed that microinjection of CP-376395 (CRF1 receptor antagonist) or Astressin 2B (CRF2 receptor antagonist) into the BLA or CeA (at a dose of 0.8 μg) decreased the duration of TI in guinea pigs (Fig. 1A–D). In addition, treatment with 0.4 μg of CP-376395 or 0.4 μg of Astressin 2B followed by the injection of 0.2 μg of CRF into the BLA or CeA prevented the increase in TI induced by the activation of CRF receptors in these areas (Fig. 2A–D). Regarding the CRF1 receptor antagonist, a repeated-measures ANOVA revealed significant differences between treatment doses (F6,27 = 6.99, P < 0.01) in the group that received CP-376395 microinjection into the BLA (Fig. 1A). A Newman-Keuls post hoc test showed a significant difference between the 0.8 μg dose of the CRF1 receptor antagonist (CP-376395) and the control and sham (P < 0.05); however, there was no difference compared to the 0.4 μg dose. Nevertheless, no differences were observed among the control, sham and the 0.4 μg dose of CP-376395. Similarly, there was a significant difference between the doses of CP-376395 microinjected into the CeA (F6,27 = 8.629, P < 0.001, ANOVA). The 0.8 μg CP-376395 treatment differed significantly from the control, sham and 0.4 μg CP-376395 treatments according to the Newman-Keuls post hoc test (P < 0.05, Fig. 1C). No differences were observed among the control, sham and 0.4 μg CP-376395 treatments. A repeated-measures ANOVA revealed significant differences among the treatments (F3,19 = 10.800, P < 0.05) in the group that received Astressin 2B (ASTR 2B) microinjection into the BLA. A Newman-Keuls test demonstrated a significant difference (P < 0.05) between the 0.8 μg ASTR 2B treatment and the control, sham and 0.4 μg ASTR 2B treatments (Fig. 1B). No differences, however, were found among the control, sham and 0.4 μg ASTR 2B treatments. Likewise, there was a significant difference between the doses of ASTR 2B injected into the CeA (F4,19 = 4.575, P < 0.05). A Newman-Keuls test demonstrated a significant difference (P < 0.05) between the 0.8 μg ASTR 2B treatment and the control and sham treatments (Fig. 1D). No differences, however, were found among the control, sham and 0.4 μg ASTR 2B treatments or between the injections of 0.8 μg ASTR 2B and 0.4 μg ASTR 2B into the CeA (Fig. 1D). As shown in a previous report (Donatti and Leite-Panissi, 2011), microinjection of CRF into the BLA or CeA of the guinea pig increased the duration of TI episodes compared to control episodes (Fig. 2A–D). However, when the microinjection of CRF into the BLA or CeA was preceded by the injection of CP-376395 (0.4 μg) or ASTR 2B (0.4 μg) into these areas, the effect of CRF was blocked. A repeated-measures ANOVA revealed a significant difference between treatments (F6,27 = 6.03, P < 0.05; F5,23 = 8.482, P < 0.005, into the BLA and CeA, respectively) when CRF was preceded by the CRF1 receptor antagonist (CP-376395). A Newman-Keuls post hoc test demonstrated that the treatment with CRF differed (P < 0.05) from the control, sham and CP-376395 + CRF treatments in the BLA (Fig. 2A) and CeA (Fig. 2C). However, there was no difference between the control, sham and CP-376395 + CRF treatments in these areas. Similarly, a repeated-measures ANOVA revealed a significant difference between treatments (F6,27 = 3.630, P < 0.05; F5,23 = 8.430, P < 0.02, into the BLA and CeA, respectively) when CRF was preceded by the CRF2 receptor antagonist (Astressin 2B). A Newman-Keuls post hoc test showed that the treatment with CRF differed (P < 0.05) from the control, sham and ASTR 2B + CRF treatments in the BLA (Fig. 2B) and CeA (Fig. 2D). No differences were observed among the control, sham and ASTR 2B + CRF treatments in both areas.