Abstract
In the quinolinic acid (QA)-rat model of Huntington's disease (HD), 15 days after QA injection, striatal glutamate, measured by in vivo microdialysis, was unchanged while a significant decrease in adenosine occurred. The decrease in adenosine may depend on QA-induced striatal cell loss. Probe perfusion of the adenosine A(2A) receptor antagonist SCH 58261 significantly increased striatal glutamate outflow, suggesting a potential detrimental effect of A(2A) antagonism at later stages of the neurodegenerative process induced by QA.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine / analysis
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Animals
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Chromatography, High Pressure Liquid
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Corpus Striatum / chemistry*
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Corpus Striatum / drug effects
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Corpus Striatum / metabolism
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Extracellular Space / chemistry
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Glutamic Acid / analysis
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Glutamic Acid / drug effects
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Glutamic Acid / metabolism*
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Huntington Disease / chemically induced
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Huntington Disease / physiopathology*
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Male
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Microdialysis
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Models, Animal
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Neuroprotective Agents / pharmacology
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Purinergic P1 Receptor Antagonists*
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Pyrimidines / pharmacology
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Quinolinic Acid / pharmacology
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Rats
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Rats, Wistar
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Receptor, Adenosine A2A
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Time Factors
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Triazoles / pharmacology
Substances
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5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine
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Neuroprotective Agents
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Purinergic P1 Receptor Antagonists
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Pyrimidines
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Receptor, Adenosine A2A
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Triazoles
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Glutamic Acid
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Quinolinic Acid
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Adenosine