Jacobian Mapping Reveals Converging Brain Substrates of Disruption and Repair in Response to Ethanol Exposure and Abstinence in 2 Strains of Rats.

Jacobian Mapping Reveals Converging Brain Substrates of Disruption and Repair in Response to Ethanol Exposure and Abstinence in 2 Strains of Rats.
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DOI:
10.1111/acer.14496
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发表时间:
2021-01
期刊:
Alcoholism, clinical and experimental research
影响因子:
--
通讯作者:
Zahr NM
Zahr NM
中科院分区:
其他
文献类型:
--
作者:
Zhao Q;Pohl KM;Sullivan EV;Pfefferbaum A;Zahr NM

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在先前的一项研究中,使用雅可比映射来评估对野生型Wistar大鼠的狂饮(4天)胃内乙醇(EtOH)对大脑的形态学影响,我们报告了可逆的丘脑收缩和侧脑室扩大,但持续的上级和下丘收缩响应于狂饮EtOH治疗。在此,我们使用了类似的基于体素的比较,收集在乙醇暴露相对于对照动物的磁共振图像,以测试假设,无论中毒协议或大鼠品系,丘脑,丘脑和丘将受到影响。两项实验[Fisher 344大鼠中的过量(4天)胃内EtOH和Wistar大鼠中的慢性(1个月)蒸发EtOH]显示了类似的受影响脑区,包括压后和扣带回皮质、背侧丘脑、中央和腹后丘脑、上级和下丘、导水管周围灰质和胼胝体。虽然大多数这些地区表现出显着的恢复,体积的colliculi和导水管周围灰质继续显示响应每个近端酒精暴露,但在减少的水平与重复曝光。考虑到这些严重受影响区域的高代谢率,目前的研究结果表明EtOH本身可能影响细胞呼吸,导致脑容量不足。此外,反应性大大降低,可能反映了神经适应反复酒精暴露。总之,这种无偏见的,在体内的方法表明收敛的大脑系统响应两个乙醇暴露协议在两个大鼠品系突出的地区,值得进一步调查的酒精中毒的动物模型和人类酒精使用障碍。
In a previous study using Jacobian mapping to evaluate the morphological effects on the brain of binge (4-day) intragastric ethanol (EtOH) on wild-type Wistar rats, we reported reversible thalamic shrinkage and lateral ventricular enlargement, but persistent superior and inferior colliculi shrinkage in response to binge EtOH treatment. Herein, we used similar voxel-based comparisons of Magnetic Resonance Images collected in EtOH-exposed relative to control animals to test the hypothesis that regardless of the intoxication protocol or the rat strain, the hippocampi, thalami, and colliculi would be affected. Two experiments [binge (4-day) intragastric EtOH in Fisher 344 rats and chronic (1-month) vaporized EtOH in Wistar rats] showed similarly affected brain regions including retrosplenial and cingulate cortices, dorsal hippocampi, central and ventroposterior thalami, superior and inferior colliculi, periaqueductal gray, and corpus callosum. While most of these regions showed significant recovery, volumes of the colliculi and periaqueductal gray continued to show response to each proximal alcohol exposure but at diminished levels with repeated exposures. Given the high metabolic rate of these enduringly affected regions, the current findings suggest that EtOH per se may affect cellular respiration leading to brain volume deficits. Further, responsivity greatly diminished likely reflecting neuroadaptation to repeated alcohol exposure. In summary, this unbiased, in vivo based approach demonstrating convergent brain systems responsive to two EtOH exposure protocols in two rat strains highlights regions that warrant further investigation in both animal models of alcoholism and in humans with Alcohol Use Disorder.
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