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No immediate clinical implications; hypothesis-generating for purinergic signaling in central neurons.
Adenosine evoked whole-cell potassium currents and enhanced intracellular free Ca2+ concentration ([Ca2+]i) in superior colliculus neurons through a P2Y purinoceptor linked to a pertussis toxin-insensitive G-protein, possibly Gq-protein, which is involved in a protein kinase C (PKC) activation pathway. The [Ca2+]i increase was inhibited by a phospholipase C (PLC) inhibitor, whereas the evoked currents were not affected by a PLC inhibitor or a phospholipase A2 (PLA2) inhibitor. Adenosine elicited single channel currents via PKC activation in cell-attached patches and furthermore, those currents with conductances of the same slope were induced even in excised patches, suggesting that PKC can be activated only by cell membrane factors without intracellular components. These results thus indicate that the P2Y purinoceptor-coupled potassium channel is regulated via a novel PKC activation pathway independent of PLC or PLA2.
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Nishizaki et al. (1996) studied this question.
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