Glial and neuronal alterations in the nucleus tractus solitarii of sudden infant death syndrome victims
Glial and neuronal alterations in the nucleus tractus solitarii of sudden infant death syndrome victims
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DOI：
10.1007/s00401-004-0895-2
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发表时间：
2004-10-01
影响因子：
12.7
通讯作者：
Matturri, L
中科院分区：
文献类型：
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作者：
Biondo, B;Magagnin, S;Matturri, L
婴儿猝死综合征(SID)的发病因素尚不清楚，但近年来，心肺中枢控制系统已引起人们的广泛关注。本文分析了23例SIDS患者和17例年龄匹配的对照组的孤束核(NTS)。我们研究了神经元和神经胶质细胞的功能和形态变化，以评估可能导致猝死的缺氧缺血损伤的结果。对骨髓切片进行形态计量学和免疫组织化学分析。在小儿麻痹症患者的NTS中，我们观察到神经细胞和胶质细胞的改变。脑损伤触发星形胶质细胞和小胶质细胞的激活，星形胶质细胞和小胶质细胞通过特征性变化对神经元损伤做出反应，这可以解释我们在小岛屿发展中国家患者NTS中的观察结果。在对SIDS患者NTS的研究中，我们发现反应性星形胶质细胞密度显著增加，坏死率显著增加，反应性小胶质细胞密度增加，P物质表达显著增加，NMDA受体免疫反应性存在。我们的结果支持小儿麻痹症患者NTS神经元存在损伤的假设，尽管这种损伤的原因尚不清楚。这种神经元损伤可能解释了为什么在缺氧期间经常不能保持足够的通风。这样的组织学发现从来都不足以解释SID，但组织学发现可能是几种病理生理机制受损的迹象，这些机制可能是脑干功能障碍的基础，影响心肺控制。
The factors underlying the sudden infant death syndrome (SIDS) are still unknown, but in recent years much attention has been focused on the central cardiorespiratory control system. In the present work we analyzed the nucleus tractus solitarii (nTS) of 23 SIDS victims and 17 age-matched control cases. We studied the functional and morphological alterations of neurons and glial cells to evaluate the results of possible hypoxic-ischemic injury that could have led to sudden death. Morphometric and immunohistochemical analyses were performed on medullary sections. In the nTS of SIDS victims we observed modifications of both neuronal and glial cells. Brain injury triggers the activation of both astrocytes and microglia, which respond to neuronal damage by characteristic changes that could explain our observations in the nTS of SIDS victims. In our investigation of the nTS of SIDS victims we found a significant increase of reactive astrocytes density, a significantly higher percentage of necrotic cells, an increase of reactive microglial cells density, a significantly higher expression of substance P and the presence of NMDA receptors immunoreactivity. Our results support the hypothesis that there is injury of the nTS neurons in SIDS victims, even if the causes of this damage are still unknown. This neuronal damage may explain why adequate ventilation is often not maintained during hypoxia. Such histological findings have never been thought sufficient to explain SIDS, but the tissue findings could be an indication of the impairment of several pathophysiological mechanisms which may underlie brainstem dysfunction, affecting cardiorespiratory control.