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首页> 外文期刊>International Journal of Environmental Research and Public Health >Proposed Toxic and Hypoxic Impairment of a Brainstem Locus in Autism
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Proposed Toxic and Hypoxic Impairment of a Brainstem Locus in Autism

机译：孤独症中脑干基因座的拟议毒性和低氧性损伤

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Electrophysiological findings implicate site-specific impairment of the nucleus tractus solitarius (NTS) in autism. This invites hypothetical consideration of a large role for this small brainstem structure as the basis for seemingly disjointed behavioral and somatic features of autism. The NTS is the brain’s point of entry for visceral afference, its relay for vagal reflexes, and its integration center for autonomic control of circulatory, immunological, gastrointestinal, and laryngeal function. The NTS facilitates normal cerebrovascular perfusion, and is the seminal point for an ascending noradrenergic system that modulates many complex behaviors. Microvascular configuration predisposes the NTS to focal hypoxia. A subregion—the “pNTS”—permits exposure to all blood-borne neurotoxins, including those that do not readily transit the blood-brain barrier. Impairment of acetylcholinesterase (mercury and cadmium cations, nitratesitrites, organophosphates, monosodium glutamate), competition for hemoglobin (carbon monoxide, nitratesitrites), and higher blood viscosity (net systemic oxidative stress) are suggested to potentiate microcirculatory insufficiency of the NTS, and thus autism.
机译：电生理检查结果提示孤独症中孤束核（NTS）的位点特异性损伤。这就要求对这种小的脑干结构起重要作用的假设进行考虑，以作为自闭症看似脱节的行为和躯体特征的基础。 NTS是大脑进入内脏的切入点，是迷走神经反射的传递点，是循环，免疫，胃肠道和喉功能自主控制的整合中心。 NTS有助于正常的脑血管灌注，并且是升华的去甲肾上腺素能系统的精髓，它调节许多复杂的行为。微血管结构使NTS容易发生局灶性缺氧。一个子区域（pNTS）允许接触所有血液传播的神经毒素，包括那些不易通过血脑屏障的神经毒素。建议破坏乙酰胆碱酯酶（汞和镉阳离子，硝酸盐/亚硝酸盐，有机磷酸酯，谷氨酸钠），竞争血红蛋白（一氧化碳，硝酸盐/亚硝酸盐）和更高的血液粘度（净系统氧化应激），以加强NTS的微循环功能不全。 ，因此是自闭症。

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