The weaver mutant mouse as a model of nigrostriatal dysfunction |
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Authors: | J R Simon B Ghetti |
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Institution: | (1) Department of Psychiatry, Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN;(2) Department of Pathology (Neuropathology) and Program in Medical Neurobiology, Indiana University School of Medicine, Indianapolis, IN |
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Abstract: | The weaver mutant mouse has a genetic defect that results in the loss of dopamine neurons in the nigrostriatal pathway. Striatal
tyrosine hydroxylase and dopamine content are reduced by 60–70%, and dopamine uptake is reduced by as much as 95%. Deficits
in all three of these striatal dopamine markers are seen as early as postnatal d 3. The striatal dopamine systems in the weaver
apparently have the ability to compensate for this dopamine deficit. Thus, in the weaver, in vitro resting release, as well
as amphetamine-evoked fractional release of endogenous dopamine are increased. An additional change seen in the weaver striatum
is an elevated serotonin content. These alterations may play an adaptive role in attempting to compensate for the dopamine
loss. In summary, the weaver mutant mouse has dramatic deficits in the nigrostriatal pathway, but also seems to develop certain
adaptive mechanisms in dopaminergic and other transmitter systems that may compensate functionally for the dopamine deficit.
Thus, the weaver mouse provides a unique animal model for studying naturally induced neuronal degeneration that complements
those models using surgical and pharmacological protocols. |
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Keywords: | Striatum dopamine weaver mouse neuronal degeneration |
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