Department of Oral Pathology, Kanagawa Dental College Postgraduate School, Japan.
Acta Histochem Cytochem. 2010 Dec 29;43(6):139-47. doi: 10.1267/ahc.10027. Epub 2010 Dec 3.
We reported that plasma brain-derived neurotrophic factor (BDNF) was maximally elevated following a 60-min period of acute immobilization stress and that salivary glands were the main source of plasma BDNF under this stress condition. However, the expression pattern of the BDNF receptor, Tyrosine receptor kinase B (TrkB), under this condition has yet to be determined. We therefore investigated the effect of this stress on the expression level of TrkB in various rat organs using real-time PCR. No significant differences were found between controls and 60 min-stressed rats with respect to TrkB level in various organs. Only adrenal glands showed significantly increased TrkB mRNA levels after 60 min of stress. TrkB mRNA and protein were observed to localize in chromaffin cells. In addition, we investigated whether BDNF-TrkB interaction influences the release of stress hormones from PC12 cells, derived from chromaffin cells. Truncated receptor, TrkB-T1, was identified in PC12 cells using RT-PCR. Exposure of PC12 cells to BDNF induced the release of catecholamine. This BDNF-evoked release was totally blocked by administration of the K252a in which an inhibitor of Trk receptors. Thus, BDNF-TrkB interactions may modulate catecholamine release from adrenal chromaffin cells under acute stress conditions.
我们曾报道，在 60 分钟的急性束缚应激后，血浆脑源性神经营养因子（BDNF）达到最高水平，而在这种应激条件下，唾液腺是血浆 BDNF 的主要来源。然而，BDNF 受体酪氨酸受体激酶 B（TrkB）在这种条件下的表达模式尚未确定。因此，我们使用实时 PCR 研究了这种应激对各种大鼠器官中 TrkB 表达水平的影响。在各种器官中，与对照组相比，60 分钟应激组的 TrkB 水平没有显著差异。只有肾上腺在应激 60 分钟后显示 TrkB mRNA 水平显著增加。TrkB mRNA 和蛋白被观察到定位于嗜铬细胞中。此外，我们研究了 BDNF-TrkB 相互作用是否会影响源自嗜铬细胞的 PC12 细胞中应激激素的释放。使用 RT-PCR 在 PC12 细胞中鉴定出截断受体 TrkB-T1。BDNF 暴露于 PC12 细胞诱导儿茶酚胺的释放。该 BDNF 诱导的释放被 K252a 完全阻断，K252a 是 Trk 受体的抑制剂。因此，BDNF-TrkB 相互作用可能在急性应激条件下调节肾上腺嗜铬细胞中儿茶酚胺的释放。
