DTI-identified microstructural changes in the gray matter of mice overexpressing CRF in the forebrain.
DTI-identified microstructural changes in the gray matter of mice overexpressing CRF in the forebrain.
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DOI：
10.1016/j.pscychresns.2020.111137
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发表时间：
2020-10-30
期刊：
影响因子：
--
通讯作者：
Brown GG
中科院分区：
文献类型：
--
作者：
Deslauriers J;Toth M;Scadeng M;McKenna BS;Bussell R;Gresack J;Rissman R;Risbrough VB;Brown GG
促肾上腺皮质激素释放因子（CRF）的增加有助于与应激相关的障碍（包括创伤后应激障碍）相关的脑回路异常。然而，CRF高信号和与应激障碍相关的回路异常之间的因果关系尚不清楚。我们假设CRF暴露增加会引起边缘回路形态和功能的变化。采用可诱导的前脑特异性过表达CRF（CRFOE）转基因小鼠系，纵向研究其对几个脑区行为和微结构完整性的慢性影响。在治疗前、治疗3 - 4周后和治疗结束后3个月再次进行行为和弥散张量成像研究，以评估恢复情况。与对照组相比，CRFOE仅在治疗3周后与持续运动增加相关，以及内侧前额叶皮层3周时各向异性分数降低和腹侧海马3个月时各向异性分数增加。在背侧海马中，CRFOE小鼠在治疗期间和治疗结束后的平均扩散率均较低。我们的数据表明，不同的反应和恢复模式的皮质和海马亚区在响应CRFOE。总的来说，这些发现支持CRF高信号和与应激障碍相关的脑区微结构变化之间的因果关系。
Increased corticotroping releasing factor (CRF) contributes to brain circuit abnormalities associated with stress related disorders including posttraumatic stress disorder. However, the causal relationship between CRF hypersignaling and circuit abnormalities associated with stress disorders is unclear. We hypothesized that increased CRF exposure induces changes in limbic circuit morphology and functions. An inducible, forebrain specific overexpression of CRF (CRFOE) transgenic mouse line was used to longitudinally investigate its chronic effects on behaviors and microstructural integrity of several brain regions. Behavioral and diffusion tensor imaging studies were performed before treatment, after 3–4 wks of treatment, and again 3 mo after treatment ended to assess recovery. CRFOE was associated with increased perseverative movements only after 3 wks of treatment, as well as reduced fractional anisotropy at 3 wks in the medial prefrontal cortex and increased fractional anisotropy in the ventral hippocampus at 3 mo compared to the control group. In the dorsal hippocampus, mean diffusivity was lower in CRFOE mice both during and after treatment ended. Our data suggest differential response and recovery patterns of cortical and hippocampal subregions in response to CRFOE. Overall these findings support a causal relationship between CRF hypersignaling and microstructural changes in brain regions relevant to stress disorders.
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