한빛사논문
- 조회4,658
Abstract
Sue-Hyun Leea,1, Chuljung Kwaka,1, Jaehoon Shima,b,1, Jung-Eun Kima, Sun-Lim Choia, Hyoung F. Kima, Deok-Jin Jangc, Jin-A Leed, Kyungmin Leee, Chi-Hoon Leef, Young-Don Leef, Maria Concetta Miniacig, Craig H. Baileyh,i,k, Eric R. Kandelh,i,j,k,2, and Bong-Kiun Kaanga,b,2
aDepartment of Biological Sciences, National Creative Research Initiative Center for Memory and
bDepartment of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea;
cDepartment of Applied Biology, College of Ecology and Environment, Kyungpook National University, Sangju 742-711, Korea;
dDepartment of Biotechnology, College of Life Science and Nanotechnology, Hannam University, Daejeon 305-811, Korea;
eDepartment of Anatomy, Graduate School of Medicine, Brain Science and Engineering Institute, Kyungpook National University, Daegu 700-422, Korea;
fMarine and Environmental Research Institute, Jeju National University, Jeju, 695-965, Korea;
gDepartment of Experimental Pharmacology, University of Naples Federico II, Naples 80131, Italy; and
hDepartment of Neuroscience,
iKavli Institute for Brain Science, and
jHoward Hughes Medical Institute,
kCollege of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, New York, NY 10032
Abstract
The memory reconsolidation hypothesis suggests that a memory trace becomes labile after retrieval and needs to be reconsolidated before it can be stabilized. However, it is unclear from earlier studies whether the same synapses involved in encoding the memory trace are those that are destabilized and restabilized after the synaptic reactivation that accompanies memory retrieval, or whether new and different synapses are recruited. To address this issue, we studied a simple nonassociative form of memory, long-term sensitization of the gill- and siphon-withdrawal reflex in Aplysia, and its cellular analog, long-term facilitation at the sensory-to-motor neuron synapse. We found that after memory retrieval, behavioral long-term sensitization in Aplysia becomes labile via ubiquitin/proteasome-dependent protein degradation and is reconsolidated by means of de novo protein synthesis. In parallel, we found that on the cellular level, long-term facilitation at the sensory-to-motor neuron synapse that mediates long-term sensitization is also destabilized by protein degradation and is restabilized by protein synthesis after synaptic reactivation, a procedure that parallels memory retrieval or retraining evident on the behavioral level. These results provide direct evidence that the same synapses that store the long-term memory trace encoded by changes in the strength of synaptic connections critical for sensitization are disrupted and reconstructed after signal retrieval.
memory reorganization, memory recall, 5-HT, local protein synthesis, clasto-lactacystin beta-lactone
Footnotes
1S.-H.L., C.K., and J.S. contributed equally to this work.
2To whom correspondence may be addressed.
Author contributions: S.-H.L., D.-J.J., C.H.B., E.R.K., and B.-K.K. designed research; S.-H.L., C.K., J.S., J.-E.K., S.-L.C., and M.C.M. performed research; H.F.K., J.-A.L., K.L., C.-H.L., Y.-D.L., and B.-K.K. contributed new reagents/analytic tools; S.-H.L., C.K., J.S., J.-E.K., D.-J.J., J.-A.L., K.L., and B.-K.K. analyzed data; and S.-H.L., C.K., C.H.B., E.R.K., and B.-K.K. wrote the paper.
논문정보
- Research article
- 2012년 08월 (BRIC 등록일 )
- 국내(교신)+국외 연구진
- 생명과학 > 신경생물학
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