Adenosine modulates methylmercuric chloride (MeHgCl)-inducedd-aspartate release from neonatal rat primary astrocyte cultures

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 ofd-[³H]aspartate release were unchanged upon treatment with adenosine or selective A₁ receptor agonists, N⁶-cyclopentyladenosine (CPA), cyclohexyladenosine (CHA), and R-phenylisopropyladenosine (R-PIA), all partially reversed the MeHg-induced release ofd-aspartate. Treatment of astrocytes with the xanthine derivative, theophylline, an adenosine antagonist, reversed the inhibitory effect of adenosine on MeHg-inducedd-[³H]aspartate release. Since the effect of MeHg ond-[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 A₁ agonists CPA and CHP, and the adenosine antagonist, theophylline, on astrocytic [GSH]_i. Attenuation of the stimulatory effect of MeHg ond-[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-inducedd-[³H]aspartate release is not known, the data suggest a role for adenosine in its regulation.