Melatonin increases dendritogenesis in the hilus of hippocampal organotypic cultures
Melatonin increases dendritogenesis in the hilus of hippocampal organotypic cultures
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DOI：
10.1111/j.1600-079x.2011.00957.x
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发表时间：
2012-05-01
影响因子：
10.3
通讯作者：
Benitez-King, Gloria
中科院分区：
文献类型：
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作者：
Dominguez-Alonso, Aline;Ramirez-Rodriguez, Gerardo;Benitez-King, Gloria
神经精神障碍的特征是海马体积减少和下托和前额叶皮层中树突分支的丢失。这些结构变化与记忆力下降有关。海马体的门神经元整合空间记忆，并在痴呆症中丢失。它们通过树突接收来自齿状回神经元的信息，同时将轴突束发送到CA 3区域。树突是神经元的复杂结构，从突触前和突触后末梢接收化学信息。褪黑激素是松果体的主要产物，通过其自由基清除特性具有神经保护作用，并减少神经元凋亡。最近，我们发现褪黑激素增加小鼠齿状回中形成的新神经元的树突成熟和复杂性。此外，在N1 E-115培养的细胞中，吲哚刺激神经突形成的早期阶段，这是已知的先于树突形成和成熟的过程。因此，在这项研究中，我们探讨了褪黑激素是否刺激树突的形成和复杂性在成年大鼠海马的器官型切片文化，这是一个模型，保留海马电路和他们的三维组织的连接。褪黑激素的影响进行了研究，在非病理条件下，在没有有害物质。结果表明，吲哚在夜间浓度达到脑脊液刺激树突形成，生长和成熟阶段。此外，数据表明，树突形成成为主管形成突触前专业化。有证据强烈表明，褪黑激素可用于治疗神经精神疾病，以修复树突的损失并重建失去的突触连接。
Neuropsychiatric disorders are characterized by hippocampus decreased volume and loss of dendrite arborizations in the subiculum and prefrontal cortex. These structural changes are associated with diminished memory performance. Hilar neurons of the hippocampus integrate spatial memory and are lost in dementia. They receive information from dentate gyrus neurons through dendrites, while they send axonal tracts to the CA3 region. Dendrites are complex structures of neurons that receive chemical information from presynaptic and postsynaptic terminals. Melatonin, the main product of the pineal gland, has neuroprotective actions through its free radical-scavenging properties and decreases neuronal apoptosis. Recently, we found that melatonin increases dendrite maturation and complexity in new neurons formed in the dentate gyrus of mice. In addition, in N1E-115 cultured cells, the indole stimulates early stages of neurite formation, a process that is known to antecede dendrite formation and maturation. Thus, in this study, we explored whether melatonin stimulates dendrite formation and complexity in the adult rat hippocampus in organotypic slice cultures, which is a model that preserves the hippocampal circuitry and their tridimensional organizations of connectivity. The effects of melatonin were studied in nonpathological conditions and in the absence of harmful agents. The results showed that the indole at nocturnal concentrations reached in the cerebrospinal fluid stimulates dendritogenesis at formation, growth, and maturation stages. Also, data showed that dendrites formed became competent to form presynaptic specializations. Evidence strongly suggests that melatonin may be useful in the treatment of neuropsychiatric diseases to repair the loss of dendrites and re-establish lost synaptic connections.