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The Journal of Neuroscience, June 15, 2002, 22(12):5034-5041

Calcineurin Plays Different Roles in Group II Metabotropic Glutamate Receptor- and NMDA Receptor-Dependent Long-Term Depression

Sheng-Tian Li^{1, 3}, Kunio Kato², Kazuhito Tomizawa³, Masayuki Matsushita³, Akiyoshi Moriwaki³, Hideki Matsui³, and Katsuhiko Mikoshiba^{1, 4, 5, 6}

¹ Mikoshiba Calciosignal Net Project, Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, Tokyo 113-0021, Japan, ² Department of Neuropsychiatry, Kochi Medical School, Kochi 783-8505, Japan, ³ Department of Physiology, Graduate School of Medicine and Dentistry, Okayama University, Okayama 700-8558, Japan, ⁴ Division of Molecular Neurobiology, Department of Basic Medical Science, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan, ⁵ Calcium Oscillation Project, Japan Science and Technology Corporation, Tokyo 108-8639, Japan, and ⁶ Laboratory for Developmental Neurobiology, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan

We investigated metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) in hippocampal CA1 pyramidal neurons of 6- to 8-d-old [postnatal days 6-8 (P6-P8)] and 21- to 25-d-old (P21-P25) rats. In P6-P8 rats, induction of LTD depended on the activity of group II mGluRs. In P21-P25 rats, however, this LTD disappeared, and instead, NMDA receptor (NMDAR)-dependent LTD appeared. A bath containing a specific calcineurin (CaN) inhibitor restored the group II mGluR-dependent LTD in the neurons of the P21-P25 rats. Although postsynaptic injection of CaN inhibitors suppressed NMDAR-dependent LTD, it did not affect induction of group II mGluR-dependent LTD. These results demonstrate that CaN plays different roles in the induction of two forms of LTD: presynaptic CaN inhibits group II mGluR-dependent LTD, whereas postsynaptic CaN facilitates NMDAR-dependent LTD. These findings are the first demonstration in vitro of group II mGluR-dependent LTD that is negatively regulated by CaN via an age-dependent mechanism.

Key words: synaptic plasticity; long-term potentiation; LTD; mGluR; NMDA receptor; hippocampus

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22125034-08$05.00/0

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