The contribution of PKA to the excitatory mechanism of adenosine in guinea pig superior colliculus slices.

The involvement of cyclic AMP-dependent protein kinase (PKA) for excitatory action of adenosine on neurotransmission was investigated using superior colliculus slices. The postsynaptic potential was elicited in the superficial gray layer after optic layer stimulation. Application of dibutyryl cyclic AMP to the medium enhanced the postsynaptic potential, but additional application of adenosine at 100 microM did not change the amplitude. Treatment of slices with a non-selective protein kinase inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) or a selective PKA inhibitor, N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide (H-8) blocked the excitatory action of adenosine. Forskolin enhanced the postsynaptic potential, which was counteracted by treatment with a highly selective PKA inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H-89) and subsequent application of 100 microM adenosine did not potentiate the postsynaptic potential. These results indicate that the excitatory effect of adenosine on neurotransmission in the superior colliculus involves PKA system.