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首页> 外文期刊>The European Journal of Neuroscience >Stress-induced sensitization to cocaine: Actin cytoskeleton remodeling within mesocorticolimbic nuclei
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Stress-induced sensitization to cocaine: Actin cytoskeleton remodeling within mesocorticolimbic nuclei

机译：应激诱导的对可卡因的致敏作用：中皮层皮质核内的肌动蛋白细胞骨架重塑

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This study investigated the consequence of repeated stress on actin cytoskeleton remodeling in the nucleus accumbens (NAc) and prefrontal cortex (Pfc), and the involvement of this remodeling in the expression of stress-induced motor cross-sensitization with cocaine. Wistar rats were restrained daily (2h) for 7days and, 3weeks later, their NAc and Pfc were dissected 45min after acute saline or cocaine (30mg/kg i.p.). F-actin, actin-binding proteins (ABP) and GluR1 were quantified by Western blotting, and dendritic spines and postsynaptic density (PSD) size measured by electron microscopy. In the NAc from the stress plus cocaine group we observed a decrease in the phosphorylation of two ABPs, cofilin and cortactin, and an increase in the PSD size and the surface expression of GluR1, consistent with a more highly branched actin cytoskeleton. The Pfc also showed evidence of increased actin polymerization after stress as an increase was observed in Arp2, and in the number of spines. Inhibiting actin cycling and polymerization with latrunculin A into the NAc, but not the Pfc, inhibited the expression of cross-sensitization to cocaine (15mg/kg i.p.) and restored the expression of GluR1 to control levels. This study shows that a history of repeated stress alters the ability of a subsequent cocaine injection to modulate dendritic spine morphology, actin dynamics and GluR1 expression in the NAc. Furthermore, by regulating GluR1 expression in the NAc, elevated actin cycling contributes to the expression of cross-sensitization between stress and cocaine, while stress-induced changes in the Pfc were not associated with cross-sensitization.
机译：这项研究调查了反复伏击对伏伏核（NAc）和前额叶皮层（Pfc）中肌动蛋白细胞骨架重塑的结果，以及这种重塑参与应激诱导的可卡因运动交叉敏化的表达。 Wistar大鼠每天（2小时）被束缚7天，并且在3周后，在急性盐水或可卡因（30mg / kg i.p.）后45分钟解剖它们的NAc和Pfc。 F-肌动蛋白，肌动蛋白结合蛋白（ABP）和GluR1通过蛋白质印迹法定量，并通过电子显微镜测量树突棘和突触后密度（PSD）大小。在应激加可卡因组的NAc中，我们观察到了两个ABP（可可蛋白和cortactin）的磷酸化减少，以及PSD大小和GluR1表面表达的增加，这与更高度分支的肌动蛋白细胞骨架一致。 Pfc还显示出应力后肌动蛋白聚合增加的证据，因为观察到Arp2和棘数目增加。抑制肌动蛋白循环和用扁桃体素A进入NAc（而不是Pfc），抑制了对可卡因的交叉敏化的表达（15mg / kg腹腔注射），并使GluR1的表达恢复到控制水平。这项研究表明，反复受压的历史改变了随后可卡因注射调节NAc中树突棘形态，肌动蛋白动力学和GluR1表达的能力。此外，通过调节NAc中GluR1的表达，肌动蛋白循环的增加有助于应激和可卡因之间的交叉敏化表达，而应激诱导的Pfc变化与交叉敏化无关。

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