ATP-evoked potassium currents in rat striatal neurons are mediated by a P2 purinergic receptor.
The effect of ATP on cultured striatal neurons was examined by whole cell voltage clamp recordings. ATP produced outwardly rectifying currents that reversed near the expected equilibrium potential for the potassium ion and the currents were blocked by intracellular Cs+. Purinergic receptor agonists such as ADP, AMP adenosine, and 2-methylthio ATP (2-MeSATP) also evoked similar outward currents. The order of their potencies was ATP >> 2-MeSATP > or = ADP > adenosine > AMP, corresponding to a P2 purinergic receptor. ATP-evoked currents were blocked by a specific protein kinase C ( PKC) inhibitor, GF109203X. In addition, the intracellular perfusion of a G-protein inactivator, GDP beta S abolished ATP-induced currents, whereas pertussis toxin (PTX) had no effect on the currents. These results suggest that ATP activates a potassium channel in striatal neurons, which is regulated by protein kinase C ( PKC) activation through a P2 purinergic receptor linked to PTX-insensitive G protein.[1]References
- ATP-evoked potassium currents in rat striatal neurons are mediated by a P2 purinergic receptor. Ikeuchi, Y., Nishizaki, T. Neurosci. Lett. (1995) [Pubmed]
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