Adenosine A(2A) antagonism increases striatal glutamate outflow in the quinolinic acid rat model of Huntington's disease

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 p...

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Veröffentlicht in:	Brain research 2003-07, Vol.979 (1-2), p.225
Hauptverfasser:	Gianfriddo, Marco, Corsi, Claudia, Melani, Alessia, Pèzzola, Antonella, Reggio, Rosaria, Popoli, Patrizia, Pedata, Felicita
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenosine - analysis Animals Chromatography, High Pressure Liquid Corpus Striatum - chemistry Corpus Striatum - drug effects Corpus Striatum - metabolism Extracellular Space - chemistry Glutamic Acid - analysis Glutamic Acid - drug effects Glutamic Acid - metabolism Huntington Disease - chemically induced Huntington Disease - physiopathology Male Microdialysis Models, Animal Neuroprotective Agents - pharmacology Purinergic P1 Receptor Antagonists Pyrimidines - pharmacology Quinolinic Acid - pharmacology Rats Rats, Wistar Receptor, Adenosine A2A Time Factors Triazoles - pharmacology
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Zusammenfassung:	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.
ISSN:	0006-8993
DOI:	10.1016/S0006-8993(03)02942-1