Kinney Hannah C, Randall Leslie L, Sleeper Lynn A, Willinger Marian, Belliveau Richard A, Zec Natasa, Rava Luciana A, Dominici Laura, Iyasu Solomon, Randall Bradley, Habbe Donald, Wilson Harry, Mandell Frederick, McClain Mary, Welty Thomas K
Department of Pathology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
J Neuropathol Exp Neurol. 2003 Nov;62(11):1178-91. doi: 10.1093/jnen/62.11.1178.
The rate of the sudden infant death syndrome (SIDS) among American Indian infants in the Northern Plains is almost 6 times higher than in U.S. white infants. In a study of infant mortality among Northern Plains Indians, we tested the hypothesis that receptor binding abnormalities to the neurotransmitter serotonin (5-HT) in SIDS cases, compared with autopsied controls, occur in regions of the medulla oblongata that contain 5-HT neurons and that are critical for the regulation of cardiorespiration and central chemosensitivity during sleep, i.e. the medullary 5-HT system. Tritiated-lysergic acid diethylamide binding to 5-HT(1A-D) and 5-HT2 receptors was measured in 19 brainstem nuclei in 23 SIDS and 6 control infants using tissue receptor autoradiography. Binding in the arcuate nucleus, a part of the medullary 5-HT system along the ventral surface, in the SIDS infants (mean age-adjusted binding 7.1 +/- 0.8 fmol/mg tissue, n = 23) was significantly lower than in controls (mean age-adjusted binding 13.1 +/- 1.6 fmol/mg tissue, n = 5) (p = 0.003). Binding also demonstrated significant diagnosis x age interactions (p < 0.04) in 4 other nuclei that are components of the 5-HT system. These data suggest that medullary 5-HT dysfunction can lead to sleep-related, sudden death in affected SIDS infants, and confirm the same binding abnormalities reported by us in a larger dataset of non-American Indian SIDS and control infants. This study also links 5-HT abnormalities in the arcuate nucleus with exposure to adverse prenatal exposures, i.e. cigarette smoking (p = 0.011) and alcohol (p = 0.075), during the periconceptional period or throughout pregnancy. Prenatal exposure to cigarette smoke and/or alcohol may contribute to abnormal fetal medullary 5-HT development in SIDS infants.
美国北部平原印第安婴儿的婴儿猝死综合征(SIDS)发生率几乎是美国白人婴儿的6倍。在一项关于北部平原印第安人婴儿死亡率的研究中,我们检验了这样一个假设:与经尸检的对照婴儿相比,SIDS病例中延髓中含有5-羟色胺(5-HT)神经元且对睡眠期间心肺呼吸调节和中枢化学敏感性至关重要的区域(即延髓5-HT系统)存在神经递质5-羟色胺(5-HT)受体结合异常。使用组织受体放射自显影术,在23例SIDS婴儿和6例对照婴儿的19个脑干核中测量了氚标记的麦角酰二乙胺与5-HT(1A-D)和5-HT2受体的结合。位于延髓5-HT系统腹侧表面的一部分的弓状核中的结合,SIDS婴儿(平均年龄校正结合量为7.1±0.8 fmol/mg组织,n = 23)显著低于对照婴儿(平均年龄校正结合量为13.1±1.6 fmol/mg组织,n = 5)(p = 0.003)。在5-HT系统的其他4个核中,结合也显示出显著的诊断×年龄相互作用(p < 0.04)。这些数据表明,延髓5-HT功能障碍可导致受影响的SIDS婴儿发生与睡眠相关的猝死,并证实了我们在一个更大的非美国印第安SIDS和对照婴儿数据集中报告的相同结合异常。这项研究还将弓状核中的5-HT异常与孕期暴露于不良因素联系起来,即在受孕期间或整个孕期接触香烟(p = 0.011)和酒精(p = 0.075)。孕期接触香烟烟雾和/或酒精可能导致SIDS婴儿胎儿延髓5-HT发育异常。