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

Brain Res. 2003 Jul 25;979(1-2):225-9. doi: 10.1016/s0006-8993(03)02942-1.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 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

Substances

  • 5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine
  • Neuroprotective Agents
  • Purinergic P1 Receptor Antagonists
  • Pyrimidines
  • Receptor, Adenosine A2A
  • Triazoles
  • Glutamic Acid
  • Quinolinic Acid
  • Adenosine