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doi: 10.1242/jcs.00854


Journal of Cell Science 117, 163-175 (2004)
Published by The Company of Biologists 2004
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Research Article

Kinesin dependent, rapid, bi-directional transport of ER sub-compartment in dendrites of hippocampal neurons

Hiroko Bannai1,2, Takafumi Inoue2,4,*, Tomohiro Nakayama2,3, Mitsuharu Hattori2 and Katsuhiko Mikoshiba1,2,4

1 Laboratory for Developmental Neurobiology, Brain Science Institute, RIKEN, Saitama 351-0198, Japan
2 Division of Molecular Neurobiology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
3 Department of Pediatrics, Tokyo Women's Medical University, Tokyo 162-8666, Japan
4 Calcium Oscillation Project, ICORP, Japan Science and Technology Corporation (JST), Tokyo 108-0071, Japan

* Author for correspondence (e-mail: tinoue{at}ims.u-tokyo.ac.jp)

Accepted 4 September 2003

Although spatially restricted Ca2+ release from the endoplasmic reticulum (ER) through intracellular Ca2+ channels plays important roles in various neuronal activities, the accurate distribution and dynamics of ER in the dendrite of living neurons still remain unknown. To elucidate these, we expressed fluorescent protein-tagged ER proteins in cultured mouse hippocampal neurons, and monitored their movements using time-lapse microscopy. We report here that a sub-compartment of ER forms in relatively large vesicles that are capable, similarly to the reticular ER, of taking up and releasing Ca2+. The vesicular sub-compartment of ER moved rapidly along the dendrites in both anterograde and retrograde directions at a velocity of 0.2-0.3 µm/second. Depletion of microtubules, overexpression of dominant-negative kinesin and kinesin depletion by antisense DNA reduced the number and velocity of the moving vesicles, suggesting that kinesin may drive the transport of the vesicular sub-compartment of ER along microtubules in the dendrite. Rapid transport of the Ca2+-releasable sub-compartment of ER might contribute to rapid supply of fresh ER proteins to the distal part of the dendrite, or to the spatial regulation of intracellular Ca2+ signaling.

Key words: Endoplasmic reticulum, Ins(1,4,5)P3R, Neuron, Dendrite, Kinesin, Microtubule




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