proposed toxic and hypoxic impairment of a brainstem locus in autism

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ID: 172988
2013
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Abstract
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, nitrates/nitrites, organophosphates, monosodium glutamate), competition for hemoglobin (carbon monoxide, nitrates/nitrites), and higher blood viscosity (net systemic oxidative stress) are suggested to potentiate microcirculatory insufficiency of the NTS, and thus autism.
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mcginnis2013internationalproposed Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Woody R. McGinnis;Tapan Audhya;Stephen M. Edelson
Journal archives of biochemistry and biophysics
Year 2013
DOI
10.3390/ijerph10126955
URL
http://www.mdpi.com/1660-4601/10/12/6955
Keywords
Hypoxia autism perfusion blood-brain barrier adrenergic toxins baroreflex a2 neuronsmedicine

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