Báez M, Siriczman I, Volosin M
Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
Physiol Behav. 1996 Sep;60(3):795-801. doi: 10.1016/0031-9384(96)00025-x.
Inescapable shock (IS) exposure induces behavioral inactivity, related to behavioral alterations in subsequent tests (i.e., escape failure, and inactivity during shuttle box task). Metyrapone (150 mg/kg, IP), a corticosterone (CS) synthesis inhibitor, administered 3 h prior to IS reduced inactivity during this aversive experience. Forty-eight hours later, when these rats were submitted to a shuttle box task, a reduction in both escape failure and inactivity was observed. These effects were reversed by CS (20 mg/kg, SC) and dose dependent of the synthetic glucocorticoid dexamethasone, both administered 1 h before IS. When metyrapone was administered 3 h before the shuttle box task to IS-exposed animals, escape failures and inactivity were markedly reduced. This effect was subsequently reversed by CS. The dynamics of changes in serum CS concentrations after both IS and shuttle box task paralleled behavioral changes. Animals injected with metyrapone before IS, which displayed active behavior, showed serum CS levels stable at their basal levels after shock, and their secretion pattern was quite attenuated after the shuttle box task, whereas vehicle-, CS alone-, and metyrapone + CS-injected animals showed higher serum CS concentrations post-IS, which slowly decreased to their corresponding basal levels. CS secretion after the shuttle box task was similar for the three groups: it had the same magnitude as after IS, though the decrease was faster. In all groups, animals displayed passive behavior. These results indicate that glucocorticoids are involved in the onset and expression of passive behaviors induced by uncontrollable stressors. Therefore, it is possible to suggest a functional relationship between CS released by exposure to inescapable stressor and the behavioral strategies adopted by rats under this stressful condition.
不可避免电击（IS）暴露会导致行为不活跃，这与后续测试中的行为改变有关（即逃避失败以及穿梭箱任务期间的不活动）。甲吡酮（150毫克/千克，腹腔注射），一种皮质酮（CS）合成抑制剂，在IS暴露前3小时给药，可减少这种厌恶经历期间的不活动。48小时后，当这些大鼠接受穿梭箱任务时，观察到逃避失败和不活动均减少。CS（20毫克/千克，皮下注射）和合成糖皮质激素地塞米松的剂量依赖性可逆转这些效应，两者均在IS暴露前1小时给药。当在穿梭箱任务前3小时对IS暴露动物给予甲吡酮时，逃避失败和不活动明显减少。随后这种效应被CS逆转。IS和穿梭箱任务后血清CS浓度的变化动态与行为变化平行。在IS暴露前注射甲吡酮并表现出活跃行为的动物，在电击后血清CS水平稳定在基础水平，并且在穿梭箱任务后其分泌模式明显减弱，而注射溶剂、单独注射CS以及注射甲吡酮+CS的动物在IS暴露后血清CS浓度更高，随后缓慢降至相应的基础水平。三组在穿梭箱任务后的CS分泌相似：其幅度与IS暴露后相同，尽管下降更快。在所有组中，动物均表现出被动行为。这些结果表明糖皮质激素参与了由不可控应激源诱导的被动行为的发生和表达。因此，可以推测暴露于不可避免应激源释放的CS与大鼠在这种应激条件下采取的行为策略之间存在功能关系。
