Nishiguchi Naoki, Shirakawa Osamu, Ono Hisae, Nishimura Akiyoshi, Nushida Hideyuki, Ueno Yasuhiro, Maeda Kiyoshi
Division of Psychiatry and Neurology, Department of Environmental Health and Safety Faculty of Medical Sciences, Kobe University Graduate School of Medicine, Kobe, Japan.
Am J Med Genet. 2002 May 8;114(4):423-5. doi: 10.1002/ajmg.10414.
A serotonergic dysfunction in the brain has been reported to be involved in suicidal behavior independently of the presence of a specific psychiatric disorder. Serotonin 1A (5-HT1A) receptors are known to be located on serotonergic nerve terminals and to be involved in the presynaptic regulation of serotonin release. Genetic factors partly explain the risks for suicide, and a suicide completion group is thought to be more uniform than a suicide attempt group. To explore the hypothesis that the 5-HT1A receptor-induced serotonergic dysfunction is implicated genetically in suicide, we focused on the structural polymorphisms, Pro16Leu and Gly272Asp, of the 5-HT1A receptor gene, and examined the association between suicide victims who completed suicide and these two polymorphisms. In both polymorphisms, we found no significant difference in genotype distribution or allele frequencies between suicide victims and controls. These findings suggest that neither of these two polymorphisms is associated with suicide victims and it is unlikely that the 5-HT1A receptor gene is implicated in the susceptibility to suicide.
据报道，大脑中的血清素功能障碍与自杀行为有关，且与特定精神疾病的存在无关。已知血清素1A（5-HT1A）受体位于血清素能神经末梢，并参与血清素释放的突触前调节。遗传因素部分解释了自杀风险，而且自杀身亡组被认为比自杀未遂组更为同质。为了探究5-HT1A受体诱导的血清素功能障碍在基因层面与自杀有关这一假说，我们聚焦于5-HT1A受体基因的结构多态性Pro16Leu和Gly272Asp，并研究了自杀身亡者与这两种多态性之间的关联。在这两种多态性中，我们发现自杀身亡者与对照组在基因型分布或等位基因频率上均无显著差异。这些发现表明，这两种多态性均与自杀身亡者无关，而且5-HT1A受体基因不太可能与自杀易感性有关。
