多巴胺D1样受体激活可诱导脑源性神经营养因子蛋白表达。
Dopamine D1-like receptor activation induces brain-derived neurotrophic factor protein expression.
作者信息
Williams Stacey N, Undieh Ashiwel S
机构信息
Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, Maryland, USA.
出版信息
Neuroreport. 2009 Apr 22;20(6):606-10. doi: 10.1097/WNR.0b013e32832a0a98.
Abstract
Recent studies showed that dopamine or D1 receptor-selective agonists increased brain-derived neurotrophic factor (BDNF) mRNA and protein expression in neuronal cultures, and this action was blocked by SCH23390. Moreover, SKF38393 activated Trk receptors and downstream signaling in striatal neurons. This study examined whether dopamine agonists induce the expression of BDNF protein in rat brain tissue. Acute slice preparations were incubated with dopamine agonists in Hibernate A medium and BDNF protein was measured by a sensitive enzyme-linked immunosorbent assay. Results showed that dopamine increased BDNF in tissue slices after 24 h of incubation. Furthermore, SKF38393 produced a significant increase in BDNF protein in striatal and hippocampal tissue slices. These findings suggest that the induction of BDNF expression may constitute a downstream response to D1-like dopamine receptor activation.
摘要
近期研究表明，多巴胺或D1受体选择性激动剂可增加神经元培养物中脑源性神经营养因子（BDNF）的mRNA和蛋白质表达，且该作用可被SCH23390阻断。此外，SKF38393可激活纹状体神经元中的Trk受体及下游信号传导。本研究检测了多巴胺激动剂是否能诱导大鼠脑组织中BDNF蛋白的表达。将急性脑片标本置于Hibernate A培养基中，与多巴胺激动剂共同孵育，并用灵敏的酶联免疫吸附测定法检测BDNF蛋白。结果显示，孵育24小时后，多巴胺可增加组织切片中的BDNF含量。此外，SKF38393可使纹状体和海马组织切片中的BDNF蛋白显著增加。这些发现提示，BDNF表达的诱导可能是对D1样多巴胺受体激活的一种下游反应。
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