Abstract

The application of dibutyryl cyclic adenosine monophosphate (d-cAMP) to an isolated, voltage clamped node of Ranvier resulted in an increase in the peak inward and steady-state outward current amplitudes. Blocking K + channels with TEA abolished the effects of d-cAMP on Na + currents. Blocking Na + channels with TTX revealed an increase in K + current amplitude in response to d-cAMP. Application of a potent phosphodiesterase inhibitor, SQ20009, reproduced the effects of d-cAMP in the intact node, but with a latency in onset. These results suggest a physiological role for cAMP in the modulation of Na + and K + currents in myelinated peripheral nerve.

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