首页> 美国卫生研究院文献>Frontiers in Behavioral Neuroscience >Stress-Induced Locomotor Sensitization to Amphetamine in Adult but not in Adolescent Rats Is Associated with Increased Expression of ΔFosB in the Nucleus Accumbens
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Stress-Induced Locomotor Sensitization to Amphetamine in Adult but not in Adolescent Rats Is Associated with Increased Expression of ΔFosB in the Nucleus Accumbens

机译:成年但未在青春期大鼠中对苯丙胺的应激诱导的运动敏化与伏隔核中ΔFosB表达的增加有关。

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摘要

While clinical and pre-clinical evidence suggests that adolescence is a risk period for the development of addiction, the underlying neural mechanisms are largely unknown. Stress during adolescence has a huge influence on drug addiction. However, little is known about the mechanisms related to the interaction among stress, adolescence and addiction. Studies point to ΔFosB as a possible target for this phenomenon. In the present study, adolescent and adult rats (postnatal day 28 and 60, respectively) were restrained for 2 h once a day for 7 days. Three days after their last exposure to stress, the animals were challenged with saline or amphetamine (1.0 mg/kg i.p.) and amphetamine-induced locomotion was recorded. Immediately after the behavioral tests, rats were decapitated and the nucleus accumbens was dissected to measure ΔFosB protein levels. We found that repeated restraint stress increased amphetamine-induced locomotion in both the adult and adolescent rats. Furthermore, in adult rats, stress-induced locomotor sensitization was associated with increased expression of ΔFosB in the nucleus accumbens. Our data suggest that ΔFosB may be involved in some of the neuronal plasticity changes associated with stress induced-cross sensitization with amphetamine in adult rats.
机译:尽管临床和临床前证据表明青春期是成瘾发展的危险时期,但其潜在的神经机制在很大程度上尚不清楚。青春期的压力对吸毒成瘾有很大的影响。然而,关于压力,青春期和成瘾之间相互作用的机制知之甚少。研究表明,ΔFosB是此现象的可能目标。在本研究中,青春期和成年大鼠(分别在出生后第28天和第60天)每天约束2小时,共7天。在它们最后一次暴露于应激后三天,用盐水或苯丙胺(1.0mg / kg i.p.)攻击动物,并记录苯丙胺诱导的运动。行为测试后,立即将大鼠断头并解剖伏隔核以测量ΔFosB蛋白水平。我们发现反复的束缚压力在成年和青春期大鼠中均增加了苯丙胺诱导的运动。此外,在成年大鼠中,应激诱导的运动敏化与伏伏核中ΔFosB表达的增加有关。我们的数据表明,ΔFosB可能参与了成年大鼠应激诱导的与苯丙胺的交叉致敏相关的一些神经元可塑性变化。

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