出生前暴露于尼古丁和酒精是婴儿猝死综合征(SIDS)的已知危险因素。新生儿后死亡的主要原因。这里,我们提供了烟碱受体结合的数据,通过125I-epebatidine受体放射自显影术测定,从安全通道研究中收集到的死于SIDS的婴儿的脑干和其他已知的死亡原因,一个潜在的,在开普敦的临床站点进行多中心研究,南非和5个美国网站,包括2个美洲印第安人保留区。我们检查了死于SIDS的婴儿(n=12)和死于已知原因的婴儿(n=20,10从出生时出院前,10放电后)。总的来说,随着5个髓质位点[的受孕后年龄的增加,125I-epebatidine结合的发育性下降,巨大的脂肪细胞,甲状旁腺细胞,centralis,和背侧附件橄榄(p=0.0002-0.03)],其中三个是含有血清素细胞的细胞核。将SIDS与出院后已知死亡原因(KCOD后)对照进行比较,我们发现骨桥中SIDS的结合显着降低(p=0.02),延髓脑桥胆碱能上升唤醒系统的关键组成部分(后KCOD,12.1±0.9fmol/mg和SIDS,9.1±0.78fmol/mg)。此外,我们发现SIDS(n=11)的母亲吸烟与KCOD后对照(n=8)对中缝暗迹的影响(p=0.01),巨细胞(p=0.02),和甲状旁腺(p=0.002),在这项研究中发现的三个髓质位点随着年龄的增长而减少,并且在以前的研究中发现SIDS婴儿的5-羟色胺神经传递指数异常。在这些地点,125I-epibatidine结合随着每周香烟的增加而增加。我们发现孕妇饮酒对任何测量部位的125I-epibatiine结合均无影响。一起来看,这些数据支持与发育有关的烟碱受体结合的变化,死因,和接触孕妇吸烟。这些数据在一项支持发育因素作用的前瞻性研究中提供了新的证据,以及对烟碱受体的不利暴露,在延髓的5-羟色胺能核中-这一发现强调了乙酰胆碱(通过烟碱受体)与延髓中5-羟色胺能神经传递之间的交织和复杂关系。
Pre-natal exposures to nicotine and alcohol are known risk factors for sudden infant death syndrome (SIDS), the leading cause of post-neonatal infant mortality. Here, we present data on nicotinic receptor binding, as determined by 125I-epibatidine receptor autoradiography, in the brainstems of infants dying of SIDS and of other known causes of death collected from the Safe Passage
Study, a prospective, multicenter
study with clinical sites in Cape Town, South Africa and 5 United States sites, including 2 American Indian Reservations. We examined 15 pons and medulla regions related to cardiovascular control and arousal in infants dying of SIDS (n = 12) and infants dying from known causes (n = 20, 10 pre-discharge from time of birth, 10 post-discharge). Overall, there was a developmental decrease in 125I-epibatidine binding with increasing postconceptional age in 5 medullary sites [raphe obscurus, gigantocellularis, paragigantocellularis, centralis, and dorsal accessory olive (p = 0.0002-0.03)], three of which are nuclei containing serotonin cells. Comparing SIDS with post-discharge known cause of death (post-KCOD) controls, we found significant decreased binding in SIDS in the nucleus pontis oralis (p = 0.02), a critical component of the cholinergic ascending arousal system of the rostral pons (post-KCOD, 12.1 ± 0.9 fmol/mg and SIDS, 9.1 ± 0.78 fmol/mg). In addition, we found an effect of maternal smoking in SIDS (n = 11) combined with post-KCOD controls (n = 8) on the raphe obscurus (p = 0.01), gigantocellularis (p = 0.02), and the paragigantocellularis (p = 0.002), three medullary sites found in this
study to have decreased binding with age and found in previous studies to have abnormal indices of serotonin neurotransmission in SIDS infants. At these sites, 125I-epibatidine binding increased with increasing cigarettes per week. We found no effect of maternal drinking on 125I-epibatidine binding at any site measured. Taken together, these data support changes in nicotinic receptor binding related to development, cause of death, and exposure to maternal cigarette smoking. These data present new evidence in a prospective
study supporting the roles of developmental factors, as well as adverse exposure on nicotinic receptors, in serotonergic nuclei of the rostral medulla-a finding that highlights the interwoven and complex relationship between acetylcholine (via nicotinic receptors) and serotonergic neurotransmission in the medulla.