Varea E, Castillo-Gómez E, Gómez-Climent M A, Blasco-Ibáñez J M, Crespo C, Martínez-Guijarro F J, Nàcher J
Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Department, Universitat de València, Spain.
Eur Neuropsychopharmacol. 2007 Jul;17(8):546-57. doi: 10.1016/j.euroneuro.2007.01.001. Epub 2007 Feb 20.
Structural modifications occur in the brain of severely depressed patients and they can be reversed by antidepressant treatment. Some of these changes do not occur in the same direction in different regions, such as the medial prefrontal cortex, the hippocampus or the amygdala. Differential structural plasticity also occurs in animal models of depression and it is also prevented by antidepressants. In order to know whether chronic fluoxetine treatment induces differential neuronal structural plasticity in rats, we have analyzed the expression of synaptophysin, a protein considered a marker of synaptic density, and the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a molecule involved in neurite and synaptic remodeling. Chronic fluoxetine treatment increases synaptophysin and PSA-NCAM expression in the medial prefrontal cortex and decreases them in the amygdala. The expression of these molecules is also affected in the entorhinal, the visual and the somatosensory cortices.
严重抑郁症患者的大脑会发生结构改变，而抗抑郁治疗可使其逆转。其中一些变化在不同区域并非朝着相同方向发生，比如内侧前额叶皮质、海马体或杏仁核。在抑郁症动物模型中也会出现差异性结构可塑性，抗抑郁药同样可对其产生抑制作用。为了解慢性氟西汀治疗是否会在大鼠中诱导差异性神经元结构可塑性，我们分析了突触素（一种被视为突触密度标志物的蛋白质）的表达，以及神经细胞黏附分子多唾液酸化形式（PSA-NCAM，一种参与神经突和突触重塑的分子）的表达。慢性氟西汀治疗会增加内侧前额叶皮质中突触素和PSA-NCAM的表达，而在杏仁核中则使其降低。这些分子的表达在内嗅皮质、视觉皮质和躯体感觉皮质中也会受到影响。
