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Elevated GDNF levels following viral vector-mediated gene transfer can increase neuronal death after stroke in rats.

Abstract：

:Previous studies have indicated that administration of glial cell line-derived neurotrophic factor (GDNF) counteracts neuronal death after stroke. However, in these studies damage was evaluated at most a few days after the insult. Here, we have explored the long-term consequences of two routes of GDNF delivery to the rat striatum prior to stroke induced by 30 min of middle cerebral artery occlusion (MCAO): striatal transduction with a recombinant lentiviral vector or transduction of the substantia nigra with a recombinant adeno-associated viral vector and subsequent anterograde transport of GDNF to striatum. Despite high GDNF levels, stereological quantification of striatal neuron numbers revealed no protection at 5 or 8 weeks after MCAO. In fact, anterograde GDNF delivery exacerbated neuronal loss. Moreover, supply of GDNF did not alleviate the striatum-related behavioral deficits. Thus, we demonstrate that the actions of GDNF after stroke are more complex than previously believed and that high levels of this factor, which are neuroprotective in models of Parkinson's disease, can increase ischemic damage. Our findings also underscore the need for quantitative assessment of long-term neuronal survival and behavioral changes to evaluate the therapeutic potential of factors such as GDNF.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Arvidsson A,Kirik D,Lundberg C,Mandel RJ,Andsberg G,Kokaia Z,Lindvall O

doi

10.1016/j.nbd.2003.08.002

keywords:

subject

Has Abstract

pub_date

2003-12-01 00:00:00

pages

542-56

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969996103001542

journal_volume

14

pub_type

杂志文章

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