Abstract:
The failure of chemoreflexes, arousal, and/or autoresuscitation to asphyxia may underlie some sudden infant death syndrome (SIDS) cases. In Part I, we showed that some SIDS infants had altered 5-hydroxytryptamine (5-HT)2A/C receptor binding in medullary nuclei supporting chemoreflexes, arousal, and autoresuscitation. Here, using the same dataset, we tested the hypotheses that the prevalence of low 5-HT1A and/or 5-HT2A/C receptor binding (defined as levels below the 95% confidence interval of controls-a new approach), and the percentages of nuclei affected are greater in SIDS versus controls, and that the distribution of low binding varied with age of death. The prevalence and percentage of nuclei with low 5-HT1A and 5-HT2A/C binding in SIDS were twice that of controls. The percentage of nuclei with low 5-HT2A/C binding was greater in older SIDS infants. In >80% of older SIDS infants, low 5-HT2A/C binding characterized the hypoglossal nucleus, vagal dorsal nucleus, nucleus of solitary tract, and nuclei of the olivocerebellar subnetwork (important for blood pressure regulation). Together, our findings from SIDS infants and from animal models of serotonergic dysfunction suggest that some SIDS cases represent a serotonopathy. We present new hypotheses, yet to be tested, about how defects within serotonergic subnetworks may lead to SIDS.
摘要:
化疗的失败,唤醒,和/或窒息自动复苏可能是一些婴儿猝死综合征(SIDS)病例的基础。在第一部分,我们发现一些SIDS婴儿在支持化疗的髓核中改变了5-羟色胺(5-HT)2A/C受体结合,唤醒,和自动复苏。这里,使用相同的数据集,我们测试了低5-HT1A和/或5-HT2A/C受体结合的患病率的假设(定义为低于对照的95%置信区间的水平-一种新方法),SIDS中受影响的细胞核百分比高于对照组,低结合的分布随死亡年龄而变化。SIDS中具有低5-HT1A和5-HT2A/C结合的细胞核的患病率和百分比是对照的两倍。在年龄较大的SIDS婴儿中,具有低5-HT2A/C结合的细胞核百分比更高。在>80%的年龄较大的SIDS婴儿中,低5-HT2A/C结合表征舌下神经核,迷走神经背核,孤束核,和小脑子网的核(对血压调节很重要)。一起,我们从SIDS婴儿和5-羟色胺能功能障碍动物模型的发现表明,一些SIDS病例代表5-羟色胺病。我们提出了新的假设,还有待测试,关于血清素能子网内的缺陷如何导致SIDS。