Wong Peiyan, Sze Ying, Gray Laura Jane, Chang Cecilia Chin Roei, Cai Shiwei, Zhang Xiaodong
Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore Singapore, Singapore ; Department of Pharmacology, Neuroscience Phenotyping Core, National University of Singapore Singapore, Singapore.
Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore Singapore, Singapore.
Front Behav Neurosci. 2015 Apr 27;9:94. doi: 10.3389/fnbeh.2015.00094. eCollection 2015.
Dysregulations in the brain serotonergic system and exposure to environmental stressors have been implicated in the development of major depressive disorder. Here, we investigate the interactions between the stress and serotonergic systems by characterizing the behavioral and biochemical effects of chronic stress applied during early-life or adulthood in wild type (WT) mice and mice with deficient tryptophan hydroxylase 2 (TPH2) function. We showed that chronic mild stress applied in adulthood did not affect the behaviors and serotonin levels of WT and TPH2 knock-in (KI) mice. Whereas, maternal separation (MS) stress increased anxiety- and depressive-like behaviors of WT mice, with no detectable behavioral changes in TPH2 KI mice. Biochemically, we found that MS WT mice had reduced brain serotonin levels, which was attributed to increased expression of monoamine oxidase A (MAO A). The increased MAO A expression was detected in MS WT mice at 4 weeks old and adulthood. No change in TPH2 expression was detected. To determine whether a pharmacological stressor, dexamethasone (Dex), will result in similar biochemical results obtained from MS, we used an in vitro system, SH-SY5Y cells, and found that Dex treatment resulted in increased MAO A expression levels. We then treated WT mice with Dex for 5 days, either during postnatal days 7-11 or adulthood. Both groups of Dex treated WT mice had reduced basal corticosterone and glucocorticoid receptors expression levels. However, only Dex treatment during PND7-11 resulted in reduced serotonin levels and increased MAO A expression. Just as with MS WT mice, TPH2 expression in PND7-11 Dex-treated WT mice was unaffected. Taken together, our findings suggest that both environmental and pharmacological stressors affect the expression of MAO A, and not TPH2, when applied during the critical postnatal period. This leads to long-lasting perturbations in the serotonergic system, and results in anxiety- and depressive-like behaviors.
大脑血清素能系统失调和暴露于环境应激源与重度抑郁症的发生有关。在此,我们通过表征在野生型(WT)小鼠和色氨酸羟化酶2(TPH2)功能缺陷小鼠的生命早期或成年期施加慢性应激的行为和生化效应,来研究应激系统和血清素能系统之间的相互作用。我们发现成年期施加的慢性轻度应激不影响WT和TPH2基因敲入(KI)小鼠的行为和血清素水平。然而,母婴分离(MS)应激增加了WT小鼠的焦虑样和抑郁样行为,而TPH2 KI小鼠未检测到行为变化。生化方面,我们发现MS WT小鼠脑血清素水平降低,这归因于单胺氧化酶A(MAO A)表达增加。在4周龄和成年期的MS WT小鼠中检测到MAO A表达增加。未检测到TPH2表达变化。为了确定药理应激源地塞米松(Dex)是否会产生与MS相似的生化结果,我们使用体外系统SH-SY5Y细胞,发现Dex处理导致MAO A表达水平增加。然后我们在出生后第7 - 11天或成年期用Dex处理WT小鼠5天。两组接受Dex处理的WT小鼠基础皮质酮和糖皮质激素受体表达水平均降低。然而,只有在出生后第7 - 11天接受Dex处理才导致血清素水平降低和MAO A表达增加。与MS WT小鼠一样,出生后第7 - 11天接受Dex处理的WT小鼠中TPH2表达未受影响。综上所述,我们的研究结果表明,在关键的出生后时期施加环境和药理应激源都会影响MAO A的表达,而不是TPH2的表达。这会导致血清素能系统的长期紊乱,并导致焦虑样和抑郁样行为。