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Journal of Neuroscience, Vol 7, 700-707, Copyright © 1987 by Society for Neuroscience
Activators of adenylate cyclase and cyclic AMP prolong calcium- dependent action potentials of mouse sensory neurons in culture by reducing a voltage-dependent potassium conductance
DS Grega and RL Macdonald
The effects of compounds that activate adenylate cyclase and of cAMP on
calcium-dependent action potentials recorded from mouse dorsal root
ganglion neurons were assessed. Application of compounds that stimulate the
adenylate cyclase system (forskolin, cholera toxin, and prostaglandin E1)
increased action potential duration with an associated decrease in
afterhyperpolarization. An adenylate cyclase inhibitor,
2',5'-dideoxyadenosine, partially inhibited the responses to forskolin and
cholera toxin. cAMP analogs mimicked the effect of forskolin, and the
phosphodiesterase inhibitor theophylline enhanced the response to
forskolin. Following intracellular injection of the potassium channel
blocker cesium, the forskolin response was reduced. Forskolin did not
significantly alter resting membrane potential or conductance. The action
potential responses to forskolin were voltage dependent, being reduced when
the membrane was held at less negative (less than -50 mV) potentials. The
data suggest that activators of adenylate cyclase and cAMP prolong
calcium-dependent action potentials by blocking a voltage-dependent
potassium conductance that is responsible, in part, for action potential
repolarization and that inactivates at membrane potentials less negative
than -50 mV.
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