Medullary serotonergic network deficiency in the sudden infant death syndrome: Review of a 15-year study of a single dataset
Medullary serotonergic network deficiency in the sudden infant death syndrome: Review of a 15-year study of a single dataset
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DOI：
10.1093/jnen/60.3.228
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发表时间：
2001-03-01
影响因子：
3.2
通讯作者：
White, WF
中科院分区：
文献类型：
--
作者：
Kinney, HC;Filiano, JJ;White, WF
婴儿猝死综合征(SIDS)是当今美国新生儿后死亡的主要原因，尽管由于倡导仰卧位睡眠的全国性降低风险运动，发病率大幅下降了38%。我们对小岛屿发展中国家脑组织的研究始于1985年，涉及一个单一的大型数据集，越来越多地专注于特定的神经递质(5-羟色胺)和特定的区域(延髓腹侧和延髓网状结构中包含5-羟色胺能神经元的区域)。基于这项研究，我们认为，小岛屿发展中国家或小岛屿发展中国家的一个子集，是由于延髓网络的发育异常，该延髓网络由(至少部分)菱形唇源性5-羟色胺能神经元组成，包括在中缝尾侧和弓状核(推测人类与猫呼吸化学敏感区同源)；这种异常导致婴儿在睡眠中对危及生命的应激源(如窒息、缺氧、高碳酸血症)的保护性反应失败，因为婴儿正在经历一个关键的动态平衡控制时期。我们称之为延髓5-羟色胺能网络缺陷假说。我们回顾了小岛屿发展中国家的三重风险模型，使用组织放射自显影技术分析神经递质受体结合的数据集的发展；早期人类脑干中与年龄相关的基线神经化学发现；至少在一些小岛屿发展中国家患者中存在5-羟色胺能、菱形嘴唇和腹侧延髓缺陷的证据；与这些缺陷相关的婴儿猝死的可能机制；以及小岛屿发展中国家患者延髓5-羟色胺能网络缺陷的潜在原因。最后，我们总结了小岛屿发展中国家脑干研究的未来方向。
The sudden infant death syndrome (SIDS) is the leading cause of postneonatal infant mortality in the United States today, despite a dramatic 38% decrease in incidence due to a national risk reduction campaign advocating the supine sleep position. Our research in SIDS brainstems, beginning in 1985 and involving a single, large dataset, has become increasingly focused upon a specific neurotransmitter (serotonin) and specific territories (ventral medulla and regions of the medullary reticular formation that contain serotonergic neurons). Based on this research, we propose that SIDS, or a subset of SIDS, is due to a developmental abnormality in a medullary network composed of (at least in part) rhombic lip-derived, serotonergic neurons, including in the caudal raphe and arcuate nucleus (putative human homologue of the cat respiratory chemosensitive fields); and this abnormality results in a failure of protective responses to life-threatening stressors (e.g. asphyxia, hypoxia, hypercapnia) during sleep as the infant passes through a critical period in homeostatic control. We call this the medullary serotonergic network deficiency hypothesis. We review the triple-risk model for SIDS, the development of the dataset using tissue autoradiography for analyzing neurotransmitter receptor binding; age-dependent baseline neurochemical findings in the human brainstem during early life; the evidence for serotonergic, rhombic lip, and ventral medullary deficits in at least some SIDS victims; possible mechanisms of sudden infant death related to these deficits; and potential causes of the deficits in the medullary serotonergic network in SIDS victims. We conclude with a summary of future directions in SIDS brainstem research.