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首页> 外文期刊>The European Journal of Neuroscience >Detecting neuroinflammation in the brain following chronic alcohol exposure in rats: A comparison between in vivo and in vitro TSPO radioligand binding
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Detecting neuroinflammation in the brain following chronic alcohol exposure in rats: A comparison between in vivo and in vitro TSPO radioligand binding

机译：在大鼠慢性酒精暴露之后检测脑中的神经炎炎症：体内和体外Tspo放射性配体结合的比较

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Excessive alcohol consumption is associated with neuroinflammation, which likely contributes to alcohol-related pathology. However, positron emission tomography (PET) studies using radioligands for the 18-kDa translocator protein (TSPO), which is considered a biomarker of neuroinflammation, reported decreased binding in alcohol use disorder (AUD) participants compared to controls. In contrast, autoradiographic findings in alcohol exposed rats reported increases in TSPO radioligand binding. To assess if these discrepancies reflected differences between in vitro and in vivo methodologies, we compared in vitro autoradiography (using [H-3]PBR28 and [H-3]PK11195) with in vivo PET (using [C-11]PBR28) in male, Wistar rats exposed to chronic alcohol-vapor (dependent n = 10) and in rats exposed to air-vapor (nondependent n = 10). PET scans were obtained with [C-11]PBR28, after which rats were euthanized and the brains were harvested for autoradiography with [H-3]PBR28 and [H-3]PK11195 (n = 7 dependent and n = 7 nondependent), and binding quantified in hippocampus, thalamus, and parietal cortex. Autoradiography revealed significantly higher binding in alcohol-dependent rats for both radioligands in thalamus and hippocampus (trend level for [H-3]PBR28) compared to nondependent rats, and these group differences were stronger for [H-3]PK11195 than [H-3]PBR28. In contrast, PET measures obtained in the same rats showed no group difference in [C-11]PBR28 binding. Our in vitro data are consistent with neuroinflammation associated with chronic alcohol exposure. Failure to observe similar increases in [C-11]PBR28 binding in vivo suggests the possibility that a mechanism mediated by chronic alcohol exposure interferes with [C-11]PBR28 binding to TSPO in vivo. These data question the sensitivity of PBR28 PET as a methodology to assess neuroinflammation in AUD.
机译：过量的醇消耗与神经炎症有关，可能有助于与酒精有关的病理学。然而，使用用于18-kDa易位蛋白（Tspo）的辐射配体的正电子发射断层扫描（PET）研究被认为是神经炎性炎症的生物标志物，报告与对照相比，酒精使用障碍（AUD）参与者的结合降低。相比之下，酒精暴露大鼠的放射显影结果报告了Tspo放射性配体的增加。评估这些差异是否反映了体外和体内方法之间的差异，我们在体外放射造影（使用[H-3] PBR28和[H-3] PK11195）与体内PET（使用[C-11] PBR28）进行比较雄性，暴露于慢性醇 - 蒸气（依赖性N = 10）和暴露于空气 - 蒸气（N = 10）的大鼠中的雄性。用[C-11] PBR28获得PET扫描，之后将大鼠制止大鼠，并将大脑与[H-3] PBR28和[H-3] PK11195进行放射缩影（n = 7依赖性，n = 7 n = 7），在海马，丘脑，丘脑和顶叶皮质中量化和结合。与非依赖性大鼠相比，Autoradopraphy在丘脑和海马的放射性配体（趋势水平）中的醇依赖性大鼠含有显着更高的结合，并且这些基团PK11195比[H-]较强3] PBR28。相反，在同一大鼠中获得的宠物措施在[C-11] PBR28结合中没有群体差异。我们的体外数据与与慢性酒精暴露相关的神经炎症一致。未观察到类似的增加[C-11] PBR28在体内结合表明，慢性酒精暴露的机制干扰在体内与TSPO结合的[C-11] PBR28结合。这些数据质疑PBR28 PET作为评估AUD中神经炎症的方法的敏感性。

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