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The Journal of Neuroscience, March 5, 2008, 28(10):2601-2612; doi:10.1523/JNEUROSCI.4314-07

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Cellular/Molecular
PKC-Induced Intracellular Trafficking of Ca_V2 Precedes Its Rapid Recruitment to the Plasma Membrane

Yalan Zhang,¹ Jessica S. Helm,² Adriano Senatore,³ J. David Spafford,³ Leonard K. Kaczmarek,¹ and Elizabeth A. Jonas²

¹Department of Pharmacology and ²Department of Internal Medicine, Section of Endocrinology, Yale School of Medicine, New Haven, Connecticut 06520, and ³Department of Biology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1

Correspondence should be addressed to Elizabeth A. Jonas, Department of Internal Medicine, Section of Endocrinology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06520. Email: elizabeth.jonas{at}yale.edu

Activation of protein kinase C (PKC) potentiates secretion in Aplysia peptidergic neurons, in part by inducing new sites for peptide release at growth cone terminals. The mechanisms by which ion channels are trafficked to such sites are, however, not well understood. We now show that PKC activation rapidly recruits new Ca_V2 subunits to the plasma membrane, and that recruitment is blocked by latrunculin B, an inhibitor of actin polymerization. In contrast, inhibition of microtubule polymerization selectively prevents the appearance of Ca_V2 subunits only at the distal edge of the growth cone. In resting neurons, Ca_V2-containing organelles reside in the central region of growth cones, but are absent from distal lamellipodia. After activation of PKC, these organelles are transported on microtubules to the lamellipodium. The ability to traffic to the most distal sites of channel insertion inside the lamellipodium does, therefore, not require intact actin but requires intact microtubules. Only after activation of PKC do Ca_V2 channels associate with actin and undergo insertion into the plasma membrane.

Key words: calcium channel; PKC; actin; microtubule; growth cone; Aplysia

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Received Jan. 19, 2007; revised Jan. 24, 2008; accepted Jan. 24, 2008.

Correspondence should be addressed to Elizabeth A. Jonas, Department of Internal Medicine, Section of Endocrinology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06520. Email: elizabeth.jonas{at}yale.edu

This article has been cited by other articles:

				J. E. Geiger and N. S. Magoski Ca2+-Induced Ca2+ Release in Aplysia Bag Cell Neurons Requires Interaction Between Mitochondrial and Endoplasmic Reticulum Stores J Neurophysiol, July 1, 2008; 100(1): 24 - 37. [Abstract] [Full Text] [PDF]

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