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. Author manuscript; available in PMC: 2019 Dec 5.
Published in final edited form as: Drug Dev Res. 1999 Mar 1;45(3-4):113–124. doi: 10.1002/(SICI)1098-2299(199811/12)45:3/4<113::AID-DDR5>3.0.CO;2-S

Fig. 1.

Fig. 1.

Processes resulting from activation of A3 adenosine receptors. The dashed line indicates activity only at micromolar concentrations of IB-MECA [Kohno et al., 1996; Casavola et al., 1998]. Presynaptic hippocampal A3 receptor activation induces inhibition of the effects of A1 receptors [Dunwiddie et al., 1997] and a PKC-dependent inhibition of mGlu receptors [Macek et al., 1998]. In CA3 pyramidal neurons, potentiated calcium current through a protein kinase A (PKA)-dependent mechanism [Fleming and Mogul, 1997]. In cardiac myocytes, A3 receptor activation is proposed to induce PKC-dependent activation of ATP-sensitive K+ channels, which results in cardioprotection [Stambaugh et al., 1997]. PI, phosphatidyl inositol; PKC, protein kinase C; DAG, diacylglycerol; NT, neurotransmitter; GRKs, G-protein-coupled receptor kinases.