1 本文实验设计构思介绍
In order to explore CSD-induced changes in gene expression in the spinal trigeminal nucleus, we first established a rat model of migraine with aura by high potassium stimulation and then conducted gene expression microarray analysis of the trigeminal vascular system.
2 国内外同类研究水平的介绍
Several studies have examined the impact of CSD on gene expression. Following CSD, the mRNA and protein levels of nitric oxide synthase (NOS) are increased in cortical astrocytes (9). The resulting increase in the level of nitric oxide (NO), a vasodilator, is believed to contribute to the pathogenesis of migraine (10). In addition, CSD quickly activates several key members of the activating protein 1 family, including c-Fos, c-Jun, heat shock protein 27 (hsp27), Hsp32, and cyclooxygenase-2 (COX-2) (11-15). Furthermore, CSD also stimulates glial cells by activating glial fibrillary acidic protein, basic fibroblast growth factor, and brain-derived neurotrophic factor (16-19).
3 本文与其他同类研究的比较
Most studies have focused on a single pathway; thus, a genome-wide picture is not available. Our study casts further insight into this topic by using medulla oblongata and upper cervical tissues, rather than the whole brain tissue, as the study material. The spinal trigeminal nucleus plays an important role in migraine headache as the primary headache center and can be activated by CSD (20). In order to reveal the molecular mechanism, we used microarray gene chip (Affymetrix Rat Genome 230 2.0 Arrays) analysis of CSD in the spinal trigeminal nucleus of rats.
