Model of CaV1.2 regulation in DRG neurons. Depolarization of DRG neurons results in CaV1.2 and calcium-dependent activation of PKA-II. The induction of PKA-II activity is not sensitive to opioids or inhibitors of calcium-stimulated ACs, phosphodiesterases (PDEs), and cAMP antagonists such as Rp-cAMPS, indicating a cAMP-independent activation mechanism (red shadow). In addition, inhibition of CaMKII or ERK1/2 is not affecting the induction of PKA-II activity after depolarization, excluding that PKA-II is downstream of these kinases. Depolarization sensitizes CaV1.2 by PKA-dependent phosphorylation of Ser1928. Dephosphorylation of CaV1.2 by the phosphatase calcineurin (CaN) inactivates the channel. CsA, cyclosporine A; MOR, µ opioid receptor.
Figure 9.

Model of CaV1.2 regulation in DRG neurons. Depolarization of DRG neurons results in CaV1.2 and calcium-dependent activation of PKA-II. The induction of PKA-II activity is not sensitive to opioids or inhibitors of calcium-stimulated ACs, phosphodiesterases (PDEs), and cAMP antagonists such as Rp-cAMPS, indicating a cAMP-independent activation mechanism (red shadow). In addition, inhibition of CaMKII or ERK1/2 is not affecting the induction of PKA-II activity after depolarization, excluding that PKA-II is downstream of these kinases. Depolarization sensitizes CaV1.2 by PKA-dependent phosphorylation of Ser1928. Dephosphorylation of CaV1.2 by the phosphatase calcineurin (CaN) inactivates the channel. CsA, cyclosporine A; MOR, µ opioid receptor.

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