Journal of Neurophysiology, Vol 68, Issue 4 1079-1086, Copyright © 1992 by APS

ARTICLES

Modulation of IK,Ca by phorbol ester-mediated activation of PKC in pleural sensory neurons of Aplysia

S. D. Critz and J. H. Byrne
Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225.

1. The electrophysiological properties of the sensory neurons that mediate withdrawal reflexes in Aplysia are modulated by a number of second messengers. For example, the second messengers adenosine 3',5'-cyclic monophosphate (cAMP) and arachidonic acid modulate the S-K+ current (IK,S) and the calcium-activated K+ current (IK,Ca). Recent evidence suggests that protein kinase C (PKC) may also be an important regulator of cellular plasticity. In the present study we examined the possibility that IK,Ca was modulated by the activation of PKC in the pleural sensory neurons. 2. In voltage-clamped sensory neurons the application of phorbol esters, such as phorbol dibutyrate (PDBu), phorbol myristate (PMA), and phorbol diacetate (PDAc), which activate PKC, caused a dose-dependent increase in a voltage-dependent current with properties that resembled IK,Ca. The inactive isomer of phorbol ester, 4 alpha-phorbol, was without effect. 3. This phorbol ester-sensitive current had the kinetics and pharmacological sensitivity of IK,Ca. The current developed slowly during step depolarizations, showed little inactivation, and was activated at membrane potentials greater than approximately 0 mV. In addition, the current modulated by phorbol esters was blocked by a concentration of tetraethylammonium (TEA) that blocks a component of IK,Ca in the sensory neurons. 4. IK,Ca, which was activated directly by the iontophoretic injection of Ca2+, was also enhanced by PDBu. Moreover, the enhancement of Ca(2+)-elicited responses by PDBu persisted after Ca2+ influx was blocked by cobalt. These results indicate that at least one component of the modulation of IK,Ca by PDBu was independent of the modulation of voltage-dependent Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				W. S. Sossin Isoform specificity of protein kinase Cs in synaptic plasticity Learn. Mem., April 2, 2007; 14(4): 236 - 246. [Abstract] [Full Text] [PDF]

				B. Dumitriu, J. E. Cohen, Q. Wan, A. M. Negroiu, and T. W. Abrams Serotonin Receptor Antagonists Discriminate Between PKA- and PKC-Mediated Plasticity in Aplysia Sensory Neurons J Neurophysiol, April 1, 2006; 95(4): 2713 - 2720. [Abstract] [Full Text] [PDF]

				O. Khabour, J. Levenson, L. C. Lyons, L. S. Kategaya, J. Chin, J. H. Byrne, and A. Eskin Coregulation of Glutamate Uptake and Long-Term Sensitization in Aplysia J. Neurosci., October 6, 2004; 24(40): 8829 - 8837. [Abstract] [Full Text] [PDF]

				Y. Zhang, N. S. Magoski, and L. K. Kaczmarek Prolonged Activation of Ca2+-Activated K+ Current Contributes to the Long-Lasting Refractory Period of Aplysia Bag Cell Neurons J. Neurosci., December 1, 2002; 22(23): 10134 - 10141. [Abstract] [Full Text] [PDF]

				P. F. Van Soest, J. C. Lodder, and K. S. Kits Activation of Protein Kinase C by Oxytocin-Related Conopressin Underlies Pacemaker Current in Lymnaea Central Neurons J Neurophysiol, November 1, 2000; 84(5): 2541 - 2551. [Abstract] [Full Text] [PDF]

				D. A. Baxter, C. C. Canavier, J. W. Clark Jr., and J. H. Byrne Computational Model of the Serotonergic Modulation of Sensory Neurons in Aplysia J Neurophysiol, December 1, 1999; 82(6): 2914 - 2935. [Abstract] [Full Text] [PDF]

				S. Sugita, D. A. Baxter, and J. H. Byrne Modulation of a cAMP/Protein Kinase A Cascade by Protein Kinase C in Sensory Neurons of Aplysia J. Neurosci., October 1, 1997; 17(19): 7237 - 7244. [Abstract] [Full Text] [PDF]