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The Journal of Neuroscience, April 22, 2009, 29(16):5100-5107; doi:10.1523/JNEUROSCI.4149-08.2009

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Behavioral/Systems/Cognitive
Role of Protein Kinase C in the Induction and Maintenance of Serotonin-Dependent Enhancement of the Glutamate Response in Isolated Siphon Motor Neurons of Aplysia californica

Greg Villareal,^1 * Quan Li,^4 * Diancai Cai,⁴ Ann E. Fink,² Travis Lim,⁵ Joanna K. Bougie,⁵ Wayne S. Sossin,⁵ and David L. Glanzman^1,3,4

¹Department of Neurobiology, ²Interdepartmental Graduate Program in Neuroscience, and ³Brain Research Institute, David Geffen School of Medicine at UCLA, University of California, Los Angeles, Los Angeles, California 90095-1761, ⁴Department of Physiological Science, UCLA College of Letters and Science, University of California, Los Angeles, Los Angeles, California 90095-1606, and ⁵Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada

Correspondence should be addressed to Dr. David L. Glanzman, Gonda (Goldschmied) Neuroscience and Genetics Research Center, University of California, Los Angeles, 695 Young Drive South, Box 951761, Los Angeles, CA 90095-1761. Email: dglanzman{at}physci.ucla.edu

Serotonin (5-HT) mediates learning-related facilitation of sensorimotor synapses in Aplysia californica. Under some circumstances 5-HT-dependent facilitation requires the activity of protein kinase C (PKC). One critical site of PKC's contribution to 5-HT-dependent synaptic facilitation is the presynaptic sensory neuron. Here, we provide evidence that postsynaptic PKC also contributes to synaptic facilitation. We investigated the contribution of PKC to enhancement of the glutamate-evoked potential (Glu-EP) in isolated siphon motor neurons in cell culture. A 10 min application of either 5-HT or phorbol ester, which activates PKC, produced persistent (> 50 min) enhancement of the Glu-EP. Chelerythrine and bisindolylmaleimide-1 (Bis), two inhibitors of PKC, both blocked the induction of 5-HT-dependent enhancement. An inhibitor of calpain, a calcium-dependent protease, also blocked 5-HT's effect. Interestingly, whereas chelerythrine blocked maintenance of the enhancement, Bis did not. Because Bis has greater selectivity for conventional and novel isoforms of PKC than for atypical isoforms, this result implicates an atypical isoform in the maintenance of 5-HT's effect. Although induction of enhancement of the Glu-EP requires protein synthesis (Villareal et al., 2007), we found that maintenance of the enhancement does not. Maintenance of 5-HT-dependent enhancement appears to be mediated by a PKM-type fragment generated by calpain-dependent proteolysis of atypical PKC. Together, our results suggest that 5-HT treatment triggers two phases of PKC activity within the motor neuron, an early phase that may involve conventional, novel or atypical isoforms of PKC, and a later phase that selectively involves an atypical isoform.

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Received Aug. 30, 2008; revised March 9, 2009; accepted March 9, 2009.

Correspondence should be addressed to Dr. David L. Glanzman, Gonda (Goldschmied) Neuroscience and Genetics Research Center, University of California, Los Angeles, 695 Young Drive South, Box 951761, Los Angeles, CA 90095-1761. Email: dglanzman{at}physci.ucla.edu

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				C. A. Farah, D. Weatherill, T. W. Dunn, and W. S. Sossin PKC Differentially Translocates during Spaced and Massed Training in Aplysia J. Neurosci., August 19, 2009; 29(33): 10281 - 10286. [Abstract] [Full Text] [PDF]

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