Papa M, Sagvolden T, Sergeant J A, Sadile A G
Institute of Human Anatomy, Second University of Naples (SUN), Italy.
Neuroreport. 1996 Nov 25;7(18):3017-20. doi: 10.1097/00001756-199611250-00044.
THIS study aimed at investigating putative neural substrates of attention-deficit hyperactivity disorder in children using the spontaneously hypertensive rat (SHR) as animal model and the Ca2+/calmodulin-dependent protein kinase II (CaMKII) as a marker in the nucleus accumbens, an interface between limbic and motor systems. In prehypertensive male SHR and Wistar-Kyoto rats image analysis of CaMKII immunocytochemistry showed more positive elements in the shell than in the core, and in the former a lower level in SHR. The data indicate a reduced number of nucleus accumbens modules available for limbic-motor integration revealing putative substrates of the altered attentional and reinforcement mechanisms demonstrated in the SHR and in children with attention-deficit hyperactivity disorder.
本研究旨在以自发性高血压大鼠（SHR）作为动物模型，以伏隔核（边缘系统和运动系统的接口）中的钙/钙调蛋白依赖性蛋白激酶II（CaMKII）作为标志物，研究儿童注意力缺陷多动障碍的假定神经基质。在高血压前期雄性SHR和Wistar-Kyoto大鼠中，CaMKII免疫细胞化学的图像分析显示，壳部的阳性元素比核心部更多，且在壳部中SHR的水平较低。数据表明，可用于边缘-运动整合的伏隔核模块数量减少，揭示了SHR和注意力缺陷多动障碍儿童中表现出的注意力和强化机制改变的假定基质。
