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首页> 外文期刊>Neuroscience and Biobehavioral Reviews >Remodeling of neural networks in the anterior forebrain of an animal model of hyperactivity and attention deficits as monitored by molecular imaging probes.
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Remodeling of neural networks in the anterior forebrain of an animal model of hyperactivity and attention deficits as monitored by molecular imaging probes.

机译：通过分子成像探针监测的多动症和注意力缺陷动物模型的前脑中神经网络的重塑。

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Remodeling of neural networks in the anterior forebrain of an animal model of hyperactivity and attention deficits as monitored by molecular imaging probes. These studies report on the remodeling of neural networks which are likely to be the consequences of the segmental defect in the anterior forebrain of an animal model of hyperactivity and attention-deficit, the juvenile prehypertensive male spontaneously hypertensive rat (SHR). Molecular biology and microscope imaging techniques were used such as: (i) dopamine (DA) D-1 and D-2 receptors by radioligand binding studies; (ii) the Ca2+/Calmodulin-dependent protein kinase II (CaMKII); (iii) transcription factors (TF) such as c-FOS by Immunocytochemistry; and (iv) the respiratory chain enzyme cytochrome-oxidase (C.O.), as markers of neuronal activity in the anterior forebrain of SHR and Wistar Kyoto normotensive (WKY) controls rats. Microcomputer-assisted high-resolution image analysis using DA receptor binding and C.O., as probes revealed by cross-correlations among different regions within brain an altered cross-talk in the anterior forebrain of the SHR as compared to the controls. In particular, an altered cross-talk was also observed within the amygdala complex in the SHR by CaMKII and c-FOS expression. Therefore, the hypothesized segmental defect in the anterior forebrain of the SHR produces network consequences leading to behavioral alteration in the attentional activity and emotional domains. Subchronic treatment with metilphenidate (MP) that is known to block the reuptake of biogenic amines (mainly DA) produced network remodeling which are known to be paralleled by behavioral modifications in the attentive activity and emotional domains. Imperspective, the results from this model system that features the main aspects of attention-deficit hyperactivity disorder (ADHD), can be useful for the understanding of the neural substrates of hyperactivity and attention deficits and possibly for an early diagnosis and appropriate treatment of ADHD children.
机译：通过分子成像探针监测的多动症和注意力缺陷动物模型的前脑中神经网络的重塑。这些研究报告了神经网络的重塑，这很可能是过度活动和注意力不足的动物模型，即高血压前雄性自发性高血压大鼠（SHR）的前脑前段缺陷的后果。使用了分子生物学和显微镜成像技术，例如：（i）通过放射性配体结合研究的多巴胺（DA）D-1和D-2受体; （ii）Ca2 + /钙调蛋白依赖性蛋白激酶II（CaMKII）; （iii）通过免疫细胞化学的转录因子（TF），例如c-FOS; （iv）呼吸链酶细胞色素氧化酶（C.O.），作为SHR和Wistar Kyoto正常血压（WKY）对照大鼠前脑中神经元活动的标志物。使用DA受体结合和C.O.的微机辅助高分辨率图像分析，作为探针，与对照组相比，大脑不同区域之间的互相关揭示了SHR前脑的相声改变。尤其是，还通过CaMKII和c-FOS表达在SHR的杏仁核复合体内观察到改变的串扰。因此，假设的SHR前脑段节段性缺陷会产生网络后果，从而导致注意力活动和情感领域的行为发生变化。已知用甲苯哌甲酯（MP）进行的亚慢性治疗会阻止生物胺（主要是DA）的再摄取，从而产生网络重塑，而网络重塑与注意力活动和情感领域中的行为修饰平行。该模型系统的结果具有注意缺陷多动障碍（ADHD）的主要方面，在某种意义上是无意的，对于理解多动症和注意缺陷的神经底物可能有用，并且可能有助于ADHD儿童的早期诊断和适当治疗。

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