Química Orgánica Biológica, Departamento de Química, Facultad de Ciencias Exactas Físicas y Naturales, Universidad Nacional de Córdoba. IIByT-CONICET, Av. Vélez Sarsfield 1611, 5016, Córdoba, Argentina.
Pharmacol Biochem Behav. 2013 Feb;103(4):814-20. doi: 10.1016/j.pbb.2012.12.019. Epub 2013 Jan 2.
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 GABA(A) 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 GABA(A) 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 0.50mg/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, 0.25mg/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 GABA(A)R in HL chicks. These results suggest that systemic epinephrine, perhaps by evoking central norepinephrine release, modulated the increase in the forebrain GABA(A) receptor recruitment induced by both insulin and stress in different ways depending on the subpopulation fearfulness.
一日龄小鸡单独评估啄石潜伏期,并根据恐惧程度分为低潜伏期(LL)或高潜伏期(HL)。研究了急性应激和全身胰岛素和肾上腺素对大脑前脑 GABA(A)受体密度的相互作用。在 10 日龄时,LL 和 HL 小鸡分别腹腔注射胰岛素、肾上腺素或生理盐水,然后立即进行 15 分钟的部分水浸应激,并断头处死。取出大脑,通过(3)[H]-氟硝西泮结合测定法在突触体中测量 GABA(A)受体密度。在非应激小鸡中,胰岛素(非低血糖剂量)在 2.50IU/kg 体重增量时,HL 小鸡的 Bmax 增加了 40.53%,而在 LL 亚群个体之间没有观察到显著差异。此外,与 LL 组相比,胰岛素增加了 HL 组的 Bmax(23.48%),表明胰岛素反应根据每个类别的焦虑程度不同。肾上腺素(0.25 和 0.50mg/kg)给药在非应激小鸡中增加了 Bmax,LL 组分别比盐水组增加了约 37%和 33%。在应激小鸡中,0.25mg/kg bw 肾上腺素与盐水相比,HL 组的 Bmax 显著增加了约 24%,表明肾上腺素的作用仅在急性应激条件下的 HL 组中观察到。同样,胰岛素联合给予相同的肾上腺素剂量增加了两个亚群的受体密度,还表明肾上腺素的最高剂量不会进一步增加 HL 小鸡中 GABA(A)R 的最大密度。这些结果表明,全身肾上腺素可能通过引发中枢去甲肾上腺素释放,以不同的方式调节胰岛素和应激诱导的大脑前脑 GABA(A)受体募集的增加,这取决于亚群的恐惧程度。