Hwang I K, Yoo K-Y, Park J-K, Nam Y S, Lee I S, Kang J H, Choi S Y, Lee J-Y, Kang T-C, Won M H
Department of Anatomy, College of Medicine, Hallym University, Chunchon 200-702, South Korea.
Neuroscience. 2004;126(4):871-7. doi: 10.1016/j.neuroscience.2004.03.061.
In the present study, the temporal and spatial alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the gerbil hippocampus after 5 min transient forebrain ischemia were investigated as followed up 7 days after ischemic insult, and the effects of ACTH after ischemic insult were also investigated 4 days after ischemic insult. The ectopic expression of ACTH (1-24 fragments) immunoreactive neurons in the cornus ammonis 1 (CA1) region of hippocampus and hilar region of the dentate gyrus 1 day after the ischemic insult was observed. Judging from the double immunofluorescence study, these neurons contain GABA. Four days after ischemic insult, the ACTH immunoreactivity was localized in CA1 pyramidal cells and glia near the stratum pyramidale, which normally do not express ACTH. In addition, in the saline-treated groups, the percentage of the detected Cresyl Violet positive neurons was 11.2% compared with the sham-operated group 4 and 7 days after ischemic insult. In these groups, the OX-42 immunoreactive microglia were detected in the strata pyramidale, oriens and radiatum. However, in the Org2766 (analog of ACTH)-treated group, 57.8% neurons compared with the sham-operated group were stained with Cresyl Violet 4 and 7 days after ischemic insult. In these groups, the OX-42 immunoreactive microglia were significantly reduced in the stratum pyramidale. These results suggest that transient forebrain ischemia may provoke selective ectopic and enhanced expression of ACTH in the hippocampus, and further suggest that ACTH plays an important role in reducing the ischemic damage.
在本研究中，对沙土鼠前脑短暂缺血5分钟后海马中促肾上腺皮质激素（ACTH）免疫反应性的时空变化进行了研究，缺血损伤7天后进行随访，并在缺血损伤4天后研究了ACTH在缺血损伤后的作用。观察到缺血损伤1天后海马齿状回角回1（CA1）区和齿状回门区ACTH（1 - 24片段）免疫反应性神经元的异位表达。从双重免疫荧光研究判断，这些神经元含有γ-氨基丁酸（GABA）。缺血损伤4天后，ACTH免疫反应性定位于CA1锥体细胞和靠近锥体层的胶质细胞，这些细胞通常不表达ACTH。此外，在生理盐水处理组中，缺血损伤4天和7天后，检测到的甲酚紫阳性神经元百分比与假手术组相比为11.2%。在这些组中，在锥体层、 Oriens层和辐射层检测到OX - 42免疫反应性小胶质细胞。然而，在Org2766（ACTH类似物）处理组中，缺血损伤4天和7天后，与假手术组相比，57.8%的神经元被甲酚紫染色。在这些组中，锥体层中OX - 42免疫反应性小胶质细胞显著减少。这些结果表明，前脑短暂缺血可能引发海马中ACTH的选择性异位和增强表达，并进一步表明ACTH在减轻缺血损伤中起重要作用。
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