Abstract
The effects of adenosine, and selective adenosine receptor agonists and antagonists on methylmercury (MeHg)-induced aspartate release were studied in neonatal rat primary astrocyte cultures. Whereas basal levels of d-[ 3H]aspartate release were unchanged upon treatment with adenosine or selective A 1 receptor agonists, N 6-cyclopentyladenosine (CPA), cyclohexyladenosine (CHA), and R-phenylisopropyladenosine (R-PIA), all partially reversed the MeHg-induced release of d-aspartate. Treatment of astrocytes with the xanthine derivative, theophylline, an adenosine antagonist, reversed the inhibitory effect of adenosine on MeHg-induced d-[ 3H]aspartate release. Since the effect of MeHg on d-[ 3H]aspartate release is known to be associated with sulfhydryl (-SH) groups which are controlled by intracellular glutathione concentrations [GSH] i, we also evaluated the effects of adenosine, the A 1 agonists CPA and CHP, and the adenosine antagonist, theophylline, on astrocytic [GSH] i. Attenuation of the stimulatory effect of MeHg on d-[ 3H]aspartate release by adenosine and its agonists occurred in the presence of reduced astrocytic [GSH] i, suggesting that other mechanisms must be invoked for this protective effect. Whilst the mechanism of MeHg-induced d-[ 3H]aspartate release is not known, the data suggest a role for adenosine in its regulation.
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