Abstract:
:Systemically-administered inorganic mercury localizes to motor neurons, but it is not known if mercury injures these neurons. We therefore looked for signs of damage to the motor and sensory neurons of mice that had been exposed to inorganic mercury. Young adult mice were injected intraperitoneally with either 1 or 2 microg/g of mercuric chloride and perfused 1 or 30 weeks later. The cellular distribution of mercury in the spinal cord was examined with silver nitrate autometallography. The numbers and sizes of myelinated axons in the L5 anterior and posterior roots were quantitated using an image analysis program. Mercury was found throughout the cytoplasm of motor neuron cell bodies after 1 week and in paranuclear aggregations after 30 weeks. Thirty weeks after exposure to either 1 or 2 microg/g of mercury, fewer large myelinated axons were seen in mercury-injected groups than in controls, though total numbers of myelinated axons did not differ between groups. A slight increase in numbers of small axons was seen in the posterior roots of mice exposed to 1 microg/g of mercury. In conclusion, inorganic mercury remains within mouse neurons for prolonged periods and causes a reduction in the size of myelinated axons in the anterior root and to a lesser extent the posterior spinal root. Inorganic mercury within motor neurons therefore appears to behave as a slowly-acting neurotoxin that shrinks motor axons.
journal_name
J Neuropathol Exp Neuroljournal_title
Journal of neuropathology and experimental neurologyauthors
Pamphlett R,Png FYdoi
10.1097/00005072-199804000-00009subject
Has Abstractpub_date
1998-04-01 00:00:00pages
360-6issue
4eissn
0022-3069issn
1554-6578journal_volume
57pub_type
杂志文章abstract::Spinal muscular atrophy (SMA) is characterized by loss of motor neurons in the spinal cord that results in muscle denervation and profound weakness in affected patients. We sought evidence for primary muscle involvement in the disease during human development by analyzing the expression of several muscle cytoskeletal ...
journal_title:Journal of neuropathology and experimental neurology
pub_type: 杂志文章
doi:10.1097/NEN.0000000000000078
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abstract::Vascular dementia (VaD) is cognitive decline linked to reduced cerebral blood perfusion, yet there are few therapeutic options to protect cognitive function following cerebrovascular accidents. The purpose of this study was to profile gene expression changes unique to VaD to identify and characterize disease relevant ...
journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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doi:10.1097/00005072-198809000-00001
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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更新日期:2004-02-01 00:00:00
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
pub_type: 杂志文章
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journal_title:Journal of neuropathology and experimental neurology
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doi:10.1093/jnen/60.6.637
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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doi:10.1097/00005072-198005000-00006
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
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journal_title:Journal of neuropathology and experimental neurology
pub_type: 杂志文章
doi:10.1097/00005072-198511000-00007
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journal_title:Journal of neuropathology and experimental neurology
pub_type: 杂志文章
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