期刊
NEUROSCIENCE LETTERS
卷 457, 期 1, 页码 12-15出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2009.03.104
关键词
Spine density; Structural plasticity; c-fos; GAD67; Antidepressant; PSA-NCAM
资金
- Spanish Ministry of Education and Science (MEC-FEDER) [BFU2004-00931, BFU2006-07313/BFI, AP2006-01953, AP2005-4672, BES 2007-15757]
- Generalitat Valenciana [ACOMP06/093]
- Foundation Jerome Lejeune
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 (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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