Guirado R, Varea E, Castillo-Gómez E, Gómez-Climent M A, Rovira-Esteban L, Blasco-Ibáñez J M, Crespo C, Martínez-Guijarro F J, Nàcher J
Cell Biology Department, Neurobiology Unit and Program in Basic and Applied Neurosciences, Universitat de València., Spain.
Neurosci Lett. 2009 Jun 19;457(1):12-5. doi: 10.1016/j.neulet.2009.03.104. Epub 2009 Apr 5.
Recent hypotheses support the idea that disruption of normal neuronal plasticity mechanisms underlies depression and other psychiatric disorders, and that antidepressant treatment may counteract these changes. In a previous report we found that chronic fluoxetine treatment increases the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a molecule involved in neuronal structural plasticity, in the somatosensory cortex. In the present study we intended to find whether, in fact, cell activation and neuronal structural remodeling occur in parallel to changes in the expression of this molecule. Using immunohistochemistry, we found that chronic fluoxetine treatment caused an increase in the expression of the early expression gene c-fos. Golgi staining revealed that this treatment also increased spine density in the principal apical dendrite of pyramidal neurons. These results indicate that, apart from the medial prefrontal cortex or the hippocampus, other cortical regions can respond to chronic antidepressant treatment undergoing neuronal structural plasticity.
近期的假说支持这样的观点，即正常神经元可塑性机制的破坏是抑郁症和其他精神疾病的基础，而抗抑郁治疗可能会抵消这些变化。在之前的一份报告中，我们发现慢性氟西汀治疗会增加躯体感觉皮层中神经细胞黏附分子多唾液酸化形式（PSA-NCAM）的表达，该分子参与神经元结构可塑性。在本研究中，我们旨在探究事实上细胞激活和神经元结构重塑是否与该分子表达的变化同时发生。通过免疫组织化学，我们发现慢性氟西汀治疗导致早期表达基因c-fos的表达增加。高尔基染色显示，这种治疗还增加了锥体神经元主要顶端树突的棘密度。这些结果表明，除了内侧前额叶皮层或海马体之外，其他皮质区域也可以对经历神经元结构可塑性的慢性抗抑郁治疗产生反应。
