Rho-kinase 抑制对可卡因和 BDNF 诱导的行为可塑性的发育差异效应。
Developmentally divergent effects of Rho-kinase inhibition on cocaine- and BDNF-induced behavioral plasticity.
机构信息
Department of Pediatrics, Emory School of Medicine, Atlanta, GA, United States.
出版信息
Behav Brain Res. 2013 Apr 15;243:171-5. doi: 10.1016/j.bbr.2013.01.004. Epub 2013 Jan 14.
Abstract
Prefrontal cortical dendritic spine remodeling during adolescence may open a window of vulnerability to pathological stimuli that impact long-term behavioral outcomes, but causal mechanisms remain unclear. We administered the Rho-kinase inhibitor HA-1077 during three adolescent periods in mice to destabilize dendritic spines. In adulthood, cocaine-induced locomotor activity was exaggerated. By contrast, when administered in adulthood, HA-1077 had no psychomotor consequences and normalized food-reinforced instrumental responding after orbitofrontal-selective knockdown of Brain-derived neurotrophic factor, a potential factor in addiction. Thus, early-life Rho-kinase inhibition confers cocaine vulnerability, but may actually protect against pathological reward-seeking - particularly in cases of diminished neurotrophic support - in adulthood.
摘要
青少年前额皮质树突棘重塑可能为病理性刺激打开一个窗口，从而影响长期的行为结果，但因果机制尚不清楚。我们在小鼠的三个青春期期间给予 Rho 激酶抑制剂 HA-1077，以破坏树突棘的稳定性。在成年期，可卡因引起的运动活性增强。相比之下，当在成年期给予 HA-1077 时，它没有精神运动后果，并在眶额选择性敲低脑源性神经营养因子（成瘾的潜在因素）后使食物强化的工具性反应正常化。因此，早期生活中的 Rho 激酶抑制赋予可卡因易感性，但实际上可能在成年期预防病理性的寻求奖励的行为——尤其是在神经营养支持减弱的情况下。
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