Abstract：
:Gene transfer to the central nervous system provides powerful methodology for the study of gene function and gene-environment interactions in vivo, in addition to a vehicle for the delivery of therapeutic transgenes for gene therapy. The aim of the present study was to determine patterns of tropism exhibited by pseudotyped lentiviral vectors in the rat substantia nigra, in order to evaluate their utility for gene transfer in experimental models of Parkinson's disease. Isogenic lentiviral vector particles encoding a GFP reporter were pseudotyped with envelope glycoproteins derived from vesicular stomatitis virus (VSV), Mokola virus (MV), lymphocytic choriomeningitis virus (LCMV), or Moloney murine leukemia virus (MuLV). Adult male Lewis rats received unilateral stereotactic infusions of vector into the substantia nigra; three weeks later, patterns of viral transduction were determined by immunohistological detection of GFP. Different pseudotypes gave rise to transgene expression in restricted and distinct cellular populations. VSV and MV pseudotypes transduced midbrain neurons, including a subset of nigral dopaminergic neurons. In contrast, LCMV- and MuLV-pseudotyped lentivirus produced transgene expression exclusively in astrocytes; the restricted transduction of astroglial cells was not explained by the cellular distribution of receptors previously shown to mediate entry of LCMV or MuLV. These data suggest that pseudotyped lentiviral vectors will be useful for experimental gene transfer to the rat substantia nigra. In particular, the availability of neuronal and astrocytic-targeting vectors will allow dissociation of cell autonomous and cell non-autonomous functions of key gene products in vivo.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Cannon JR,Sew T,Montero L,Burton EA,Greenamyre JTdoi
10.1016/j.expneurol.2010.10.016subject
Has Abstractpub_date
2011-03-01 00:00:00pages
41-52issue
1eissn
0014-4886issn
1090-2430pii
S0014-4886(10)00401-2journal_volume
228pub_type
杂志文章abstract：:Neuropathological studies of human traumatic brain injury (TBI) cases have described amyloid plaques acutely after a single severe TBI, and tau pathology after repeat mild TBI (mTBI). This has helped drive the hypothesis that a single moderate to severe TBI increases the risk of developing late-onset Alzheimer's disea...
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journal_title：Experimental neurology
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doi：10.1016/j.expneurol.2008.05.007
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journal_title：Experimental neurology
pub_type： 杂志文章
doi：10.1006/exnr.1994.1167
更新日期：1994-10-01 00:00:00
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journal_title：Experimental neurology
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doi：10.1016/j.expneurol.2009.03.002
更新日期：2009-06-01 00:00:00
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journal_title：Experimental neurology
pub_type： 杂志文章
doi：10.1016/0014-4886(86)90161-5
更新日期：1986-07-01 00:00:00
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journal_title：Experimental neurology
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journal_title：Experimental neurology
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journal_title：Experimental neurology
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journal_title：Experimental neurology
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journal_title：Experimental neurology
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