Apoptosis is increased in the hippocampus of infants who died of sudden infant death syndrome (SIDS), yet it is not known via which mechanism this has occurred. Following existing support for a role of the α7 and β2 nicotinic acetylcholine receptor (nAChR) subunits in apoptotic regulation, we aimed to determine whether these subunits are altered in the SIDS hippocampus and if they are correlated with cell death markers of active caspase-3 (Casp-3) and TUNEL. Further analyses were run according to the presence of major SIDS risk factors related to hypoxia (bed-sharing and prone sleeping), infection (presence of an upper respiratory tract infection (URTI)), cigarette smoke exposure and gender. Immunohistochemical expression of the markers was studied in 4 regions of the hippocampus (Cornu Ammonis (CA)1, CA2, CA3, CA4) and subiculum amongst 52 infants (aged 1–7 months) who died suddenly and unexpectedly (SUDI) and for whom the cause of death was explained (eSUDI; n = 9), or not and characterised as SIDS I (n = 8) and SIDS II (n = 35) according to the San Diego diagnostic criteria. Results showed that SIDS II infants had widespread increases in TUNEL compared with eSUDI and SIDS I infants, as well as increased α7 and Casp-3 in CA2 compared to eSUDI infants, although these changes were predominant amongst infants who did not bed-share. Cigarette smoke exposure had minimal effects on the markers, while an URTI was associated with changes in all markers (after accounting for bed-sharing). Our findings support the role of nAChRs in regulating apoptosis in the SIDS hippocampus, and highlight the need for separate analysis according to risk factors.

因婴儿猝死综合症（SIDS）死亡的婴儿海马中的细胞凋亡增加，但尚不清楚其发生的机制。继现有对α7和β2烟碱乙酰胆碱受体（nAChR）亚基在凋亡调控中的作用的支持后，我们旨在确定这些亚基在SIDS海马体中是否发生改变，以及它们是否与活性caspase-3的细胞死亡标记相关（ Casp-3）和TUNEL。根据与低氧（床共享和俯卧睡眠），感染（上呼吸道感染（URTI）的存在），香烟烟雾暴露和性别相关的主要SIDS危险因素的存在，进行了进一步分析。在海马4个区域（Cornu Ammonis（CA）1，CA2，CA3，突然死亡（SUDI）的52例婴儿（1-7个月）中有CA4）和亚细小管，其死亡原因得到了解释（eSUDI； n = 9），或者没有，被归类为SIDS I（n = 8 ）和SIDS II（n = 35），根据圣地亚哥的诊断标准。结果显示，与eSUDI婴儿相比，SIDS II婴儿的TUNEL广泛升高，与eSUDI婴儿相比，CA2的α7和Casp-3升高，尽管这些变化在没有卧床的婴儿中尤为明显。香烟烟雾暴露对标记物的影响最小，而URTI与所有标记物的变化相关（在计及床共享后）。我们的发现支持nAChRs在调节SIDS海马细胞凋亡中的作用，并强调需要根据危险因素进行单独分析。