a(MESH:antalarmin)
Overall, no changes were observed in dopamine D1 receptor binding in the brain regions examined following social isolation and ⁄ or antalarmin treatment under these conditions PubMed:16820021
antalarmin increased dopamine D2 ⁄ 3 binding in the CPu (+7%, P < 0.001; Fig. 3C) and olfactory tubercle (OT; +15%, P 1⁄4 0.006; Fig. 3D) of group-housed rats. PubMed:16820021
Antalar- min treatment reversed this effect and returned dopamine D2 ⁄ 3 receptor density levels back to those of the vehicle-treated GH rats. PubMed:16820021
antalarmin increased dopamine D2 ⁄ 3 binding in the CPu (+7%, P < 0.001; Fig. 3C) and olfactory tubercle (OT; +15%, P 1⁄4 0.006; Fig. 3D) of group-housed rats. PubMed:16820021
Antalar- min treatment reversed this effect and returned dopamine D2 ⁄ 3 receptor density levels back to those of the vehicle-treated GH rats. PubMed:16820021
Furthermore a significant interaction was found between housing and treatment in both the central nucleus of the amygdala (CeA; F1,139 1⁄4 11.560, P < 0.001; Fig. 3F) and basolateral amygdala (BLA; F1,137 1⁄4 7.616, P 1⁄4 0.007; Fig. 3E).Thus, isolation caused an up-regulation in dopamine D2 ⁄ 3 receptors in these regions, an effect that was reversed by antalarmin treatment (but only reached statistical significance in the CeA). PubMed:16820021
Treatment with antalarmin had no impact upon the isolation-induced alterations of BDNF expression. PubMed:16820021
As was the case with BDNF expression, treatment with antalarmin had no impact upon the isolation-induced alterations in TrkB expression. PubMed:16820021
Treatment with antalarmin had no impact upon the isolation-induced alterations of BDNF expression. PubMed:16820021
Interestingly however, antalarmin treatment of GH rats caused a down-regulation of TrkB mRNA in the LC ()15%, P 1⁄4 0.012) and Pir ()26%, P 1⁄4 0.013) whilst increases were observed in the hippocampus (CA1–3; +36%, P 1⁄4 0.042) and RSc (+53%, P < 0.001). PubMed:16820021
Interestingly however, antalarmin treatment of GH rats caused a down-regulation of TrkB mRNA in the LC ()15%, P 1⁄4 0.012) and Pir ()26%, P 1⁄4 0.013) whilst increases were observed in the hippocampus (CA1–3; +36%, P 1⁄4 0.042) and RSc (+53%, P < 0.001). PubMed:16820021
However, embryos that recovered from heat shock in the presence of the CRF-R1 antagonist, antalarmin, experienced a greater increase in caspase-3 activity than embryos not given the antagonist PubMed:29807032
However, embryos that recovered from heat shock in the presence of the CRF-R1 antagonist, antalarmin, experienced a greater increase in caspase-3 activity than embryos not given the antagonist PubMed:29807032
The greatest heat shock-induced mortality occurred during the first 1 h of recovery and plateaued after 5 h recovery (main effect of time P<0.001; n=3; Fig. 3B), but the presence of antalarmin did not influence this response. PubMed:29807032
At all embryo stages, significant differences were noted between the CRH 107 and control groups as well as be- tween the CRH 107 and CRH 107/antalarmin 106 groups, with the rates being lower in the former. PubMed:23211705
With regard to the morula/blastocyst stage, the rates in the CRH 107 group were lower compared with the control (P 0.003) and lower compared with the CRH 107/antalarmin 106 group (P 0.001) (Table 2). PubMed:23211705
With regard to the morula/blastocyst stage, the rates in the CRH 107 group were lower compared with the control (P 0.003) and lower compared with the CRH 107/antalarmin 106 group (P 0.001) (Table 2). PubMed:23211705
Interestingly, the addition of a 10-fold excess of the CRH-R1 antagonist, antalarmin, overcame the negative effect of CRH on estradiol release (d 5, P 0.009; d 7, P 0.010; d 9, P 0.001; and d 11, P 0.002), indicating that the suppressive effect of CRH was receptor mediated (Fig. 1). PubMed:23211705
The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on beta-hCG release (d 11 beta-hCG 185.6 6.087 mIU/ml, P 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705
The addition of a 10-fold excess of the CRH-R1 antagonist antalarmin reversed the negative ef- fect of CRH on progesterone release (d 11 progesterone 0.712 0.004 ng/ml, P 0.001), suggesting that the suppressive effect of CRH was receptor mediated (Fig. 2). PubMed:23211705
The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on -hCG release (d 11 beta-hCG 185.6 6.087 mIU/ml, P 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705
The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on -hCG release (d 11 beta-hCG 185.6 6.087 mIU/ml, P 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705
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