Adenosine facilitates glutamate release in a protein kinase-dependent manner in superior colliculus slices.

Experiments were performed to clarify the excitatory mechanism of adenosine in superior colliculus slices. Postsynaptic field potential was recorded in the superficial gray layer after stimulation to the optic layer. Application of adenosine to the perfusion medium at a concentration of 0.2 microM or 100 microM enhanced the amplitude of the postsynaptic field potential and the excitatory effect of adenosine was counteracted by application of 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) (100 microM), a non-selective protein kinase inhibitor or N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA1004) (100 microM), a selective protein kinase A inhibitor. The presence of adenosine at a concentration of 0.2 microM or 100 microM during electrical stimulation to slices of the superficial gray layer increased the release of glutamate 2.5 and 2.3 times, respectively, and this increase was suppressed in Ca(2+)-free medium or by applying tetrodotoxin (1 microM) to the medium. Application of H-7 or HA1004 to the incubation medium inhibited the enhancement of the glutamate release. These results suggest that the excitatory effect of adenosine in the superior colliculus is due to an increase in glutamate release and involves the protein kinase system.