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首页> 外文期刊>The European Journal of Neuroscience >5,7-Dihydroxytryptamine lesions enhance and serotonergic grafts normalize the evoked overflow of acetylcholine in rat hippocampal slices.
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5,7-Dihydroxytryptamine lesions enhance and serotonergic grafts normalize the evoked overflow of acetylcholine in rat hippocampal slices.

机译：5,7-二羟基色胺的损害增强，血清素能移植物使大鼠海马切片中诱发的乙酰胆碱溢出正常化。

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摘要

Adult rats were subjected to intracerebroventricular injections of 5,7-dihydroxytryptamine (5,7-DHT; 150 micro g) and, 15 days later, to intrahippocampal grafts of fetal raphe cell suspensions. About 11 months later, we assessed baseline and electrically evoked release of tritium ([3H]) in hippocampal slices, preloaded with tritiated ([3H])choline or [3H]serotonin (5-HT), in the presence or absence of the 5-HT1B receptor agonist CP-93,129 and the 5-HT receptor antagonist methiothepine. HPLC determinations of monoamine concentrations were also performed. The lesions reduced the concentration of 5-HT (-90%) and the accumulation (-80%) as well as the evoked release (-90%) of [3H]5-HT. They also decreased the inhibitory effects of CP-93,129 on the evoked release of [3H]5-HT. Most interestingly, they facilitated the evoked release of [3H]acetylcholine (+20%). In slices from rats subjected to lesions and grafts, the responsiveness of the serotonergic autoreceptors (presumably located on the terminals of the grafted neurons) and the release of acetylcholine were close to normal. These results confirm that grafts rich in serotonergic neurons may partially compensate for the dramatic effects of 5,7-DHT lesions on serotonergic hippocampal functions. The lesion-induced reduction of the 5-HT1B autoreceptor-mediated inhibition of evoked 5-HT release may be an adaptation enhancing serotonergic transmission in the (few) remaining terminals. The facilitated release of acetylcholine is probably caused by a reduced serotonergic tone on the inhibitory 5-HT1B heteroreceptors of the cholinergic terminals. When related to data in the literature, this facilitation may be of particular interest in terms of transmitter-based strategies developed to tackle cognitive symptoms related to neurodegenerative diseases.
机译：成年大鼠脑室内注射5,7-二羟基色胺（5,7-DHT; 150微克），并在15天后海马内注射胎儿拉菲细胞悬液。大约11个月后，我们评估了存在或不存在the化（[3H]）胆碱或[3H] 5-羟色胺（5-HT）的海马片中基线和电诱发release的释放[3H]。 5-HT1B受体激动剂CP-93,129和5-HT受体拮抗剂Methiothepine。还进行了单胺浓度的HPLC测定。病变减少了[3H] 5-HT的5-HT浓度（-90％）和积累（-80％）以及诱发的释放（-90％）。他们还降低了CP-93,129对[3H] 5-HT诱发释放的抑制作用。最有趣的是，它们促进了[3H]乙酰胆碱（+ 20％）的诱发释放。在来自遭受损伤和移植的大鼠的切片中，血清素能自受体的反应性（可能位于移植神经元的末端）和乙酰胆碱的释放接近正常。这些结果证实，富含5-羟色胺能神经元的移植物可以部分补偿5,7-DHT病变对5-羟色胺能海马功能的巨大影响。病变引起的5-HT1B受体介导的5-HT释放抑制的减少可能是一种适应性增强，在剩余的（少数）末端发生了血清素能传递。乙酰胆碱的促进释放可能是由于胆碱能末端的抑制性5-HT1B异型受体上的血清素能降低而引起的。当与文献中的数据相关时，就为解决与神经退行性疾病相关的认知症状而开发的基于发射器的策略而言，这种便利可能特别令人感兴趣。

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