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首页> 外文期刊>Acta Neuropathologica >Glial and neuronal alterations in the nucleus tractus solitarii of sudden infant death syndrome victims
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Glial and neuronal alterations in the nucleus tractus solitarii of sudden infant death syndrome victims

机译:婴儿猝死综合征受害者的孤束核神经胶质和神经元改变

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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.
机译:婴儿猝死综合症(SIDS)的潜在因素仍然未知,但是近年来,人们将许多注意力集中在中央心肺控制系统上。在目前的工作中,我们分析了23名小岛屿发展中国家受害者和17名年龄匹配的对照病例的孤束核(nTS)。我们研究了神经元和神经胶质细胞的功能和形态改变,以评估可能导致缺氧缺血性脑损伤的结果。在髓样切片上进行形态计量学和免疫组化分析。在SIDS受害者的nTS中,我们观察到了神经元和神经胶质细胞的改变。脑损伤会触发星形胶质细胞和小胶质细胞的激活,这些星形胶质细胞和小胶质细胞通过特征变化来响应神经元损伤,这可能解释了我们在SIDS受害者nTS中的观察结果。在我们对SIDS受害者nTS的研究中,我们发现反应性星形胶质细胞密度显着增加,坏死细胞百分比显着增加,反应性小胶质细胞密度增加,P物质的表达明显更高以及NMDA受体存在免疫反应性。我们的结果支持以下假设:即使尚不清楚这种损伤的原因,SIDS受害者中的nTS神经元也会受到伤害。这种神经元损伤可以解释为什么在缺氧期间通常不能保持足够的通气。从未认为这样的组织学发现足以解释SIDS,但组织发现可能表明可能是脑干功能障碍基础上的几种病理生理机制受损,从而影响心肺控制。

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