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Recruitment of GABAA receptors and fearfulness in chicks: Modulation by systemic insulin and/or epinephrine

机译:患有Gabaa受体的招募和小鸡的恐惧:通过全身胰岛素和/或肾上腺素调节

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One-day-old chicks were individually assessed on their latency to peck pebbles, and categorized as low latency (LL) or high latency (HL) according to fear. Interactions between acute stress and systemic insulin and epinephrine on GABAA receptor density in the forebrain were studied. At 10 days of life, LL and HL chicks were intraperitoneally injected with insulin, epinephrine or saline, and immediately after stressed by partial water immersion for 15 min and killed by decapitation. Forebrains were dissected and the GABAA receptor density was measured ex vivo by the 3[H]-flunitrazepam binding assay in synaptosomes. In non-stressed chicks, insulin (non-hypoglycemic dose) at 2.50 IU/kg of body weight incremented the Bmax by 40.53% in the HL chicks compared to saline group whereas no significant differences were observed between individuals in the LL subpopulation. Additionally, insulin increased the Bmax (23.48%) in the HL group with respect to the LL ones, indicating that the insulin responses were different according to the anxiety of each category. Epinephrine administration (0.25 and 0.50 mg/kg) incremented the Bmax in non-stressed chicks, in the LL group by about 37% and 33%, respectively, compared to ones injected with saline. In the stressed chicks, 0.25 mg/kg bw epinephrine increased the Bmax significantly in the HL group by about 24% compared to saline, suggesting that the effect of epinephrine was only observed in the HL group under acute stress conditions. Similarly, the same epinephrine doses co-administered with insulin increased the receptor density in both subpopulations and also showed that the highest dose of epinephrine did not further increase the maximum density of GABAAR in HL chicks. These results suggest that systemic epinephrine, perhaps by evoking central norepinephrine release, modulated the increase in the forebrain GABAA receptor recruitment induced by both insulin and stress in different ways depending on the subpopulation fearfulness. ? 2013 Elsevier Inc.
机译:一天大的小鸡被单独评估它们的延迟,以啄鹅卵石,并根据恐惧分类为低延迟(LL)或高延迟(HL)。研究了急性应激与全身胰岛素与肾上腺素对前脑中GABAA受体密度的相互作用。在寿命期间,LL和HL CHICKS腹膜内注射胰岛素,肾上腺素或盐水,并在部分水浸渍15分钟后立即延长15分钟并通过斩波杀死。解剖前脑并在突触体中通过3 [H] -Flunitrazepam结合测定法测量GABAA受体密度。在非压力的雏鸡中,与盐碱相比,在2.50 IU / kg体重下的胰岛素(非降血性剂量)在2.50 IU / kg体重中将BMAX递增40.53%,而LL亚ppopulation中的个体之间没有观察到显着差异。另外,胰岛素相对于L1胰岛增加了HL组中的Bmax(23.48%),表明胰岛素反应根据每个类别的焦虑而不同。与注入盐水的注射相比,肾上腺素施用(0.25和0.50mg / kg)将非应激雏鸡中的非应性雏鸡中的Bmax递增约37%和33%。在压力的雏鸡中,与盐水相比,在HL组中,0.25mg / kg BW肾上腺素显着增加了约24%的BMAX,这表明在急性胁迫条件下仅在HL组中观察到肾上腺素的效果。类似地,与胰岛素共同施用的相同的肾上腺剂量增加了两种群体中的受体密度,并且还表明,最高剂量的肾上腺素未进一步提高HL雏鸡中GABAAR的最大密度。这些结果表明,全身肾上腺素,也许是通过唤起中央比甲坡释放,根据亚贫困恐惧的不同方式调节由胰岛素和应力诱导的前脑GABAA受体募集的增加。还2013年elsevier公司

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