2,3,7,8-Tetrachlorodibenzo-p-dioxin alters hippocampal astroglia-neuronal gap junctional communication.
2,3,7,8-Tetrachlorodibenzo-p-dioxin alters hippocampal astroglia-neuronal gap junctional communication.
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发表时间：
2000-12
期刊：
影响因子：
3.4
通讯作者：
Marie E. Legare;W. Hanneman;R. Barhoumi;Robert C. Burghardt;E. Tiffany‐Castiglioni
中科院分区：
文献类型：
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作者：
Marie E. Legare;W. Hanneman;R. Barhoumi;Robert C. Burghardt;E. Tiffany‐Castiglioni
卤代芳烃（HAH），如二苯并二恶英，已知会改变认知功能。然而，这种破坏的细胞基础还不清楚。暴露于HAH的一个可能的有害影响可能是对脑中神经元和星形胶质细胞之间的间隙连接细胞间通讯（GJIC）的影响。因此，本研究探讨了高毒性原型HAH，2，3，7，8-四氯二苯并-p-二恶英（TCDD）对大鼠海马原代细胞培养GJIC的影响。光漂白（缺口FRAP）后的荧光恢复的初步测量显示，星形胶质细胞和神经元之间的染料转移。正辛醇是一种亲脂性醇，已知通过降低缝隙连接通道的开放概率来解除细胞偶联，从而阻断星形胶质细胞-神经元（A-N）通讯以及星形胶质细胞-星形胶质细胞（A-A）通讯。TCDD最初下调神经元和星形胶质细胞之间的GJIC，但对星形胶质细胞对没有影响。这些结果表明，在培养的神经元和星形胶质细胞之间的GJIC的存在下，并表现出不同的敏感性，同源和异源细胞对TCDD的间隙连接反应。2，3，7，8-TCDD通过A-N而不是A-A通道破坏GJIC的发现可能对发育暴露于TCDD导致的脑功能受损具有重要意义。
Halogenated aromatic hydrocarbons (HAHs) such as dibenzo-p-dioxins are known to alter cognitive function. However, the cellular basis of this disruption is not well understood. One possible deleterious effect of exposure to HAHs could be on gap junctional intercellular communication (GJIC) between neurons and astroglia in the brain. As such, this study examined the effects of the highly toxic prototypic HAH, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on GJIC in rat hippocampal primary cell culture. Initial measurements of fluorescence recovery after photobleaching (gap-FRAP) showed dye transfer between astroglia and neurons. N-octanol, a lipophilic alcohol known to uncouple cells by decreasing the open probability of gap junctional channels blocked astroglial-neuronal (A-N) communication as well as astroglial-astroglial (A-A) communication. TCDD initially downregulated GJIC between neurons and astroglia of treatment, but had no effect on astroglial cell pairs. These results indicate the presence of GJIC between neurons and astroglia in culture and demonstrate different sensitivities of gap junction responses to TCDD in homologous and heterologous cell pairs. The finding that 2,3,7,8-TCDD disrupts GJIC through A-N but not A-A channels may have important implications for impaired brain function resulting from developmental exposure to TCDD.