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Acute gut microbiome changes after traumatic brain injury are associated with chronic deficits in decision-making and impulsivity in male rats.
Behavioral Neuroscience ( IF 1.9 ) Pub Date : 2022-07-28 , DOI: 10.1037/bne0000532
Michelle A Frankot 1 , Christopher M O'Hearn 1 , Alyssa M Blancke 1 , Bryan Rodriguez 1 , Kristen M Pechacek 1 , Jasleen Gandhi 2 , Gangqing Hu 2 , Kris M Martens 1 , Cole Vonder Haar 1
Affiliation  

The mechanisms underlying chronic psychiatric-like impairments after traumatic brain injury (TBI) are currently unknown. The goal of the present study was to assess the role of diet and the gut microbiome in psychiatric symptoms after TBI. Rats were randomly assigned to receive a high-fat diet (HFD) or calorie-matched low-fat diet (LFD). After 2 weeks of free access, rats began training on the rodent gambling task (RGT), a measure of risky decision-making and motor impulsivity. After training, rats received a bilateral frontal TBI or a sham procedure and continued postinjury testing for 10 weeks. Fecal samples were collected before injury and 3-, 30-, and 60 days postinjury to evaluate the gut microbiome. HFD altered the microbiome, but ultimately had low-magnitude effects on behavior and did not modify functional outcomes after TBI. Injury-induced functional deficits were far more robust; TBI substantially decreased optimal choice and increased suboptimal choice and motor impulsivity on the RGT. TBI also affected the microbiome, and a model comparison approach revealed that bacterial diversity measured 3 days postinjury was predictive of chronic psychiatric-like deficits on the RGT. A functional metagenomic analysis identified changes to dopamine and serotonin synthesis pathways as a potential candidate mechanism. Thus, the gut may be a potential acute treatment target for psychiatric symptoms after TBI, as well as a biomarker for injury and deficit severity. However, further research will be needed to confirm and extend these findings. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

中文翻译:

创伤性脑损伤后肠道微生物组的急性变化与雄性大鼠决策和冲动的慢性缺陷有关。

创伤性脑损伤(TBI)后慢性精神类损伤的机制目前尚不清楚。本研究的目的是评估饮食和肠道微生物组在 TBI 后精神症状中的作用。大鼠被随机分配接受高脂肪饮食(HFD)或热量匹配的低脂肪饮食(LFD)。自由活动两周后,老鼠开始接受啮齿动物赌博任务(RGT)的训练,这是一项衡量风险决策和运动冲动的指标。训练后,大鼠接受双侧额叶 TBI 或假手术,并继续进行 10 周的损伤后测试。在受伤前以及受伤后 3 天、30 天和 60 天收集粪便样本以评估肠道微生物群。HFD 改变了微生物群,但最终对行为产生了低程度的影响,并且没有改变 TBI 后的功能结果。损伤引起的功能缺陷要严重得多。TBI 显着降低了 RGT 的最佳选择并增加了次优选择和运动冲动。TBI 也会影响微生物群,模型比较方法显示,受伤后 3 天测量的细菌多样性可以预测 RGT 的慢性精神病样缺陷。功能宏基因组分析将多巴胺和血清素合成途径的变化确定为潜在的候选机制。因此,肠道可能是 TBI 后精神症状的潜在急性治疗靶点,也是损伤和缺陷严重程度的生物标志物。然而,需要进一步的研究来证实和扩展这些发现。(PsycInfo 数据库记录 (c) 2022 APA,保留所有权利)。
更新日期:2022-07-28
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