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We investigated whether PKA-induced phosphorylation was involved in regulation of hyperpolarization-activated current (I(h)) in rat dorsal root ganglion (DRG) cells. We examined the effect of the catalytic subunit of PKA (PKAc) on I(h) and confirmed an effect of PKAc on Ca(2+) channel currents carried by Ba(2+) (I(Ba)) in identical neurons as a positive control of PKA activity. After the start of recording, amplitudes of I(Ba) gradually decreased (rundown). An intracellular application of ATP reduced the rundown of I(Ba) and induced a depolarizing shift of I(h) activation. The former was partially reversed by PKI but the latter was not affected. An intracellular application of PKAc also prevented the rundown of I(Ba) and this effect was potentiated by okadaic acid (OA). The application of PKAc and OA in combination did not change the electrophysiological properties of I(h) although a potentiating effect on I(Ba) was observed in the same neurons. The application of 2-mM ATP in addition to PKAc and OA did not result in an additional potentiation of I(Ba), but shifted the activation curve of I(h) positively. These results suggested that PKA-induced phosphorylation was not involved in the modulatory mechanisms of I(h) in rat DRG neurons.

Comparison of effects of PKA catalytic subunit on Ih and calcium channel currents in rat dorsal root ganglion cells