Abstract
The action of a change in the intracellular 3′,5′-cAMP (cAMP) level on steady-state and potential-dependent transmembrane ionic currents was investigated in vertebrate and invertebrate nerve cells. The change was produced by injecting cAMP directly into the cell or indirectly, by stimulating or inhibiting activity of various enzymes of the cyclase system. An increase in the intracellular cAMP concentration was found to cause activation of the steady-state two-component transmembrane current, the early component of which is linked mainly with an increase in sodium and calcium, the latter with an increase in potassium conductance of the membrane (possibly due to the entry of calcium ions inside the cell). A decrease in the intracellular cAMP concentration (by intracellular dialysis) evokes weakening of the potential-activated inward calcium current, whereas an increase leads to its restoration. Restoration of the calcium current can also be achieved by activation of the intracellular adenylate cyclase, inhibition of phosphodiesterase, or through direct injection of the catalytic subunit of cAMP-dependent protein kinase inside the cell. Evidence is presented that the regulatory effects obtained are mediated through cAMP-dependent phosphorylation of proteins in the corresponding ionic channels. Elevation of the intracellular calcium ion level interacts closely with the regulatory system described above through activation of some of its enzymic processes.
Published Version
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