X.-M.L. and C.-C.L. contributed equally to this work.
JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1
Article first published online: 24 JAN 2007
European Journal of Neuroscience
Volume 25, Issue 2, pages 391–396, January 2007
How to Cite
Li, X.-M., Li, C.-C., Yu, S.-S., Chen, J.-T., Sabapathy, K. and Ruan, D.-Y. (2007), JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1. European Journal of Neuroscience, 25: 391–396. doi: 10.1111/j.1460-9568.2006.05300.x
- Issue published online: 24 JAN 2007
- Article first published online: 24 JAN 2007
- Received 18 August 2006, revised 13 November 2006, accepted 15 November 2006
- c-Jun N-terminal kinases;
- long-term depression;
- synaptic plasticity
Several recent reports implicate an important role played by c-Jun N-terminal kinases (JNKs) in long-term potentiation (LTP). However, little is known about how the isoforms of JNKs participate in synaptic plasticity. Here we showed that short-term synaptic plasticity was impaired in the hippocampal area CA1 of JNK1-deficient (JNK1–/–) mice; these mice showed normal LTP in response to a strong tetanus and no alteration of N-methyl-d-aspartate receptor-dependent long-term depression (LTD) in the hippocampus. However, LTD induced either by group I metabotropic glutamate receptors (mGluRs) agonist dihydroxyphenylglycine or by paired-pulse low-frequency stimulation was absent in both the JNK1–/– slices and in JNK inhibitor anthrax [1, 9-cd] pyrazol-6(2H)-1 (SP600125)-pretreated slices. Induction of mGluR-dependent LTD resulted in an increase in phosphorylation of JNK1 substrates, including p-c-Jun and p-ATF2 in wild-type (WT) mice, and these increases failed to occur in the JNK1–/– or SP600125-pretreated mice. These results demonstrated that JNK1 played a crucial role in the short-term synaptic plasticity and mGluR-dependent LTD, whereas hippocampus LTP was not affected by JNK1 deficiency.