Effects of chronic social defeat on expression of dopamine β-hydroxylase in rat brains.
Effects of chronic social defeat on expression of dopamine β-hydroxylase in rat brains.
复制标题
DOI：
10.1002/syn.21641
复制
发表时间：
2013-06
期刊：
影响因子：
2.3
通讯作者：
Zhu, Meng-Yang
中科院分区：
文献类型：
--
作者：
Fan, Yan;Chen, Ping;Li, Ying;Zhu, Meng-Yang
据记载，压力激活蓝斑-去甲肾上腺素系统。然而，关于应激对去甲肾上腺素能神经元的标志性酶多巴胺β-羟化酶表达的影响的报道很少。在本研究中，成年Fischer 344大鼠进行了为期4周的慢性社会失败。用原位杂交和Western印迹法检测蓝斑及其末端多巴胺β羟化酶的表达水平。结果表明，与对照组相比，慢性社交失败后即刻蓝斑多巴胺β-羟化酶mRNA和蛋白水平显著升高，海马、额叶皮质和杏仁核多巴胺β-羟化酶蛋白水平显著升高。肾上腺切除术和/或皮质类固醇受体拮抗剂米非司酮和螺内酯单独或联合治疗可完全消除这种慢性社交失败诱导的多巴胺β-羟化酶上调。此外，地昔帕明（一种对去甲肾上腺素转运具有特异性抑制作用的抗抑郁药）治疗可防止蓝斑及其主要终末区域（如海马、额叶皮质和杏仁核）中慢性社交失败导致的多巴胺β-羟化酶表达增加。然而，氟西汀（一种特异性抑制5-羟色胺转运的抗抑郁药）治疗仅选择性阻断CSD引起的海马多巴胺β-羟化酶蛋白水平升高。目前的研究结果表明，慢性社交失败激活蓝斑-去甲肾上腺素系统通过上调多巴胺β-羟化酶的表达，这可能会增加去甲肾上腺素的合成。这种慢性社会失败诱导的DBH表达上调是通过皮质酮和皮质类固醇受体介导的，可能有抗抑郁药的干扰。
It is documented that stress activates the locus coeruleus-norepinephrine system. However, there are far few reports regarding effects of stress on the expression of dopamine β-hydroxylase, a hallmark enzyme of the noradrenergic neuron. In the present study, adult Fischer 344 rats were subjected to chronic social defeat for 4 weeks. Dopamine β-hydroxylase expressional levels in the locus coeruleus and its terminal regions were measured by in situ hybridization and western blotting. The results showed that immediately following chronic social defeat there are significantly increased mRNA and protein levels of dopamine β-hydroxylase in the locus coeruleus, and dopamine β-hydroxylase protein levels in the hippocampus, frontal cortex and amygdala, compared with those in the control. This chronic social defeat-induced upregulation of dopamine β-hydroxylase was completely abolished by adrenalectomy, and/or by treatment with corticosteroid receptor antagonists, mifepristone and spironolactone, either alone or in combination. Furthermore, treatment with desipramine, an antidepressant with specific inhibitory effects on norepinephrine transport, prevented an increased dopamine β-hydroxylase expression by chronic social defeat in the locus coeruleus and its main terminal regions such as the hippocampus, frontal cortex and amygdala. However, treatment with fluoxetine, an antidepressant with specific inhibition for serotonin transport, only selectively blocked increased dopamine β-hydroxylase protein levels in the hippocampus caused by CSD. The present findings indicate that chronic social defeat activates the locus coeruleus-norepinephrine system by upregulating the expression of dopamine β-hydroxylase, which may increase norepinephrine synthesis. This chronic social defeat induced upregulation of DBH expression was mediated through corticosterone and corticosteroid receptors, with possible interference from antidepressants.
登录
查看更多内容
影响因子：
10.6
作者：
Biederman, J;Spencer, T
通讯作者：
Spencer, T
影响因子：
2.3
作者：
JORDAN, S;KRAMER, GL;PETTY, F
通讯作者：
PETTY, F
影响因子：
3
作者：
Armario, Antonio
通讯作者：
Armario, Antonio
影响因子：
3.6
作者：
GLAVIN, GB;TANAKA, M;NAGASAKI, N
通讯作者：
NAGASAKI, N
影响因子：
4.7
作者：
BARUCHIN, A;WEISBERG, EP;KAPLAN, BB
通讯作者：
KAPLAN, BB