Excitatory effects of adenosine are not mediated by inhibition of GABAergic system in slices of superior colliculus and hippocampus from guinea pig

Abstract

Neurotransmission in the superior colliculus (SC) and the hippocampus is enhanced by application of adenosine. To investigate the possibie involvement of disinhibition by adenosine on γ-aminobutyric acid (GABA) -ergic action, the effects of adenosine and picrotoxin, a GABA antagonist, were studied using slices of SC and hippocampus of the guinea pig. Application of adenosine on SC slices (concentration at 100 μM) and hippocampus (concentration at 0.1 μM) enhanced the amplitude of population spikes (PS) in the superficial gray layer (SGL) of SC and in the granule cell layer of dentate gyrus of hippocampus. The application of picrotoxin at 100 μM increased the amplitude of both slices even after previous treatment with adenosine which once increased the amplitude. This was also true for adenosine with the previous treatment of picrotoxin. In SC slices, the increased amplitude by adenosine was reduced to the original amplitude after application of 3-[1-[3-(Dimetylamino) propyl]-1H-indol-3-yl-]4-(1H-indol-3-yl)-1H-pyrrole-2,5-dione (GF109203X) a protein kinase C inhibitor, the previous treatment by the drug counteracted the excitatory action of adenosine. However GF109203X failed to counteract the excitatory effects of picrotoxin. These results indicate that the excitatory mechanism of adenosine is different from that of picrotoxin and is not mediated by disinhibition of the GABAergic system through inhibitory action of adenosine on GABAergic interneurons.