Abstract:
:Human immunodeficiency virus-associated distal-symmetric neuropathy (HIV-DSP) is the most common neurological complication of HIV infection. The pathophysiology of HIV-DSP is poorly understood and no treatment is available for this entity. The dorsal root ganglia (DRG) are the principal sites of neuronal damage and are associated with reactive mononuclear phagocytes as well as HIV-infected macrophages. To determine the role of HIV-infected macrophages in the pathogenesis of HIV-DSP, we developed a technique for culturing human DRG's. When the dissociated DRG neurons were exposed to supernatants from macrophages infected with CXCR4 or CCR5 tropic HIV-1 strains axonal retraction was observed without neuronal cell death but there was mitochondrial dysfunction in the neuronal cell body. Even though CXCR4 and CCR5 were expressed on the DRG neurons, the effects were independent of these receptors. Antioxidants rescued the neuronal cell body but not the axon from the toxic effects of the culture supernatants. Further, peripheral nerves of HIV-infected patients obtained at autopsy did not show evidence of increased oxidative stress. These observations suggest a differential effect on the axon and cell body. Different mechanisms of injury may be operative in these two structures.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Hahn K,Robinson B,Anderson C,Li W,Pardo CA,Morgello S,Simpson D,Nath Adoi
10.1016/j.expneurol.2007.06.015subject
Has Abstractpub_date
2008-03-01 00:00:00pages
30-40issue
1eissn
0014-4886issn
1090-2430pii
S0014-4886(07)00246-4journal_volume
210pub_type
杂志文章abstract::Chewing rhythms are set by a putative central pattern generator whose output is influenced by sensory feedback. In this study we assessed how an altered feedback imposed by changing the hardness of a gum bolus modifies the timing of chewing, the maximal gape, and the activity in the masseter muscle on the chewing side...
journal_title:Experimental neurology
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journal_title:Experimental neurology
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doi:10.1016/j.expneurol.2007.02.004
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journal_title:Experimental neurology
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doi:10.1006/exnr.1997.6673
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2006.12.020
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(88)90172-0
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journal_title:Experimental neurology
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pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.2002.7958
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journal_title:Experimental neurology
pub_type: 杂志文章
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