Expression and subcellular localization of multifunctional calmodulin-dependent protein kinases-I, -II and -IV are altered in rat hippocampal CA1 neurons after induction of long-term potentiation

被引:15
作者
Ahmed, BY
Yamaguchi, F
Tsumura, T
Gotoh, T
Sugimoto, K
Tai, YJ
Konishi, R
Kobayashi, R
Tokuda, M
机构
[1] Kagawa Med Univ, Fac Med, Dept Physiol, Miki, Kagawa 7610793, Japan
[2] Kagawa Med Univ, Fac Med, Dept Ophthalmol, Miki, Kagawa 7610793, Japan
[3] Kagawa Med Univ, Fac Med, Dept Pharmacobioinformat, Miki, Kagawa 7610793, Japan
[4] Kagawa Med Univ, Fac Med, Dept Chem, Miki, Kagawa 7610793, Japan
关键词
long-term potentiation; calmodulin-dependent protein kinase; hippocampus; translocation; nuclear distribution; immunohistochemistry; electronmicroscopy;
D O I
10.1016/S0304-3940(00)01347-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Long-term potentiation (LTP) is considered to be associated with an increase in expression as well as activity of Ca2+/calmodulin-dependent protein kinases (CaMKs). LTP-induced and control hippocampal slices were studied by immunohistochemical and electronmicroscopic analyses using anti-CaMK-I, -II and -IV antibodies. All three kinases were demonstrated to increase their expression in CA1 neurons. CaMK-I was shown to mainly localize in the cytoplasm of the control and LTP-induced neurons, and a significant increase of immunoreactivity was observed in the latter neurons. A part of CaMK-I was found to translocate to the nuclei of LTP-induced hippocampal CA1 neu ro ns. Direct evidence of the translocation of CaMK-II from cytoplasm to nuclei in LTP was demonstrated by immuno-electronmicroscopy. A significant increase in expression of CaMK-IV in the nuclei was also observed. Our data suggest that all the th ree CaMKs were actively involved in nuclear Ca2+-signaling in LTP. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:149 / 153
页数:5
相关论文
共 20 条
[1]   A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[2]  
BROCKE L, 1995, J NEUROSCI, V15, P6797
[3]  
De Crombrugghe B, 1971, Nat New Biol, V231, P139
[4]   CaM kinase II in long-term potentiation [J].
Fukunaga, K ;
Muller, D ;
Miyamoto, E .
NEUROCHEMISTRY INTERNATIONAL, 1996, 28 (04) :343-358
[5]   Phosphorylation at the nuclear localization signal of Ca2+/calmodulin-dependent protein kinase II blocks its nuclear targeting [J].
Heist, EK ;
Srinivasan, M ;
Schulman, H .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (31) :19763-19771
[6]   Mice lacking the gene encoding tissue-type plasminogen activator show a selective interference with late-phase long-term potentiation in both Schaffer collateral and mossy fiber pathways [J].
Huang, YY ;
Bach, ME ;
Lipp, HP ;
Zhuo, M ;
Wolfer, DP ;
Hawkins, RD ;
Schoonjans, L ;
Kandel, ER ;
Godfraind, JM ;
Mulligan, R ;
Collen, D ;
Carmeliet, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (16) :8699-8704
[7]   NUCLEAR AND AXONAL LOCALIZATION OF CA2+ CALMODULIN-DEPENDENT PROTEIN-KINASE TYPE-GR IN RAT CEREBELLAR CORTEX [J].
JENSEN, KF ;
OHMSTEDE, CA ;
FISHER, RS ;
SAHYOUN, N .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (07) :2850-2853
[8]  
KLANN E, 1991, J BIOL CHEM, V266, P24253
[9]   SYNAPTIC PLASTICITY IN THE HIPPOCAMPUS - LTP AND LTD [J].
MALENKA, RC .
CELL, 1994, 78 (04) :535-538
[10]   AN ESSENTIAL ROLE FOR POSTSYNAPTIC CALMODULIN AND PROTEIN-KINASE ACTIVITY IN LONG-TERM POTENTIATION [J].
MALENKA, RC ;
KAUER, JA ;
PERKEL, DJ ;
MAUK, MD ;
KELLY, PT ;
NICOLL, RA ;
WAXHAM, MN .
NATURE, 1989, 340 (6234) :554-557