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The Journal of Neurophysiology Vol. 83 No. 3 March 2000, pp. 1567-1579
Copyright ©2000 by the American Physiological Society
Committee on Neurobiology and Department of Neurobiology, Pharmacology and Physiology, University of Chicago, Chicago, Illinois 60637
Fox, Lyle E. and
Philip E. Lloyd.
Role of cAMP in the Short-Term Modulation of a Neuromuscular
System in Aplysia. J. Neurophysiol. 83: 1567-1579, 2000. Neuromuscular synapses in buccal
muscle I3a of Aplysia are modulated by the small
cardioactive peptide (SCP), a peptide cotransmitter that is intrinsic
to the motor neurons, and by serotonin (5-HT) released from modulatory
neurons that are extrinsic to the motor circuit. Although the
modulation of excitatory junction potentials (EJPs) and contractions by
5-HT and SCP has been studied extensively in this muscle, little is
known about the mechanisms that underlie the modulation. 5-HT and SCP,
at 1 µM, were found to potently increase the level of cAMP in I3a.
Therefore we investigated whether the activation of the cAMP pathway
was sufficient to modulate EJPs and contractions. The direct activation
of adenylyl cyclase with forskolin increased the level of cAMP,
facilitated EJPs, and potentiated contractions. Indeed, the short-term
effects of forskolin were very similar to all aspects of the short-term
effects of 5-HT and SCP. Membrane-permeable cAMP analogues also
mimicked the effects of 5-HT and SCP on EJPs and contractions. However, it seems likely that some effects of 5-HT are also mediated through other second-messenger pathways because low concentrations of 5-HT
modulate EJPs and contractions but do not significantly increase cAMP
levels in I3a. It is possible that lower concentrations of 5-HT
function through receptors linked to protein kinase C (PKC) because
phorbol, an activator of PKC, modulated EJPs and contractions without
increasing the levels of cAMP. In conclusion, we provide evidence that
pharmacological agents that activate the cAMP pathway mimicked most of
the effects of 5-HT or SCP and that more than one second-messenger
system appears to be involved in the modulation of the I3a
neuromuscular system.
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