title: JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1.
abstract: 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.
authors.affiliation: Department of Neurobiology and Biophysics, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, PR China.
authors.forename: Xin-Mei
authors.initials: XM
authors.lastname: Li
authors.forename: Chen-Chen
authors.initials: CC
authors.lastname: Li
authors.forename: Shan-Shan
authors.initials: SS
authors.lastname: Yu
authors.forename: Ju-Tao
authors.initials: JT
authors.lastname: Chen
authors.forename: Kanaga
authors.initials: K
authors.lastname: Sabapathy
authors.forename: Di-Yun
authors.initials: DY
authors.lastname: Ruan
mesh_terms: D051698:Activating Transcription Factor 2 / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D000873:Anthracenes / Q000494:pharmacology; D004307:Dose-Response Relationship, Radiation; D004558:Electric Stimulation; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006624:Hippocampus / Q000502:physiology*; D066298:In Vitro Techniques; D036881:Long-Term Synaptic Depression / Q000502:physiology*; D008734:Methoxyhydroxyphenylglycol / Q000031:analogs & derivatives / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D048055:Mitogen-Activated Protein Kinase 8 / Q000172:deficiency / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D018094:Receptors, Metabotropic Glutamate / Q000502:physiology*
chemical_list: D051698:Activating Transcription Factor 2; D000873:Anthracenes; C497107:Atf2 protein, rat; D004791:Enzyme Inhibitors; D018094:Receptors, Metabotropic Glutamate; C432165:pyrazolanthrone; D008734:Methoxyhydroxyphenylglycol; D048055:Mitogen-Activated Protein Kinase 8; C010117:3,4-dihydroxyphenylglycol