title: Role of postsynaptic inositol 1, 4, 5-trisphosphate receptors in depotentiation in guinea pig hippocampal CA1 neurons.
abstract: The long-term potentiation (LTP) in the field excitatory postsynaptic potential (EPSP) induced at hippocampal CA1 pyramidal neuron synapses by delivery of high frequency stimulation (HFS), a tetanus of 100 pulses at 100Hz, is decreased (depotentiation) by a train of low frequency stimulation (LFS) of 1000 pulses at 2Hz applied 30min later. Inositol 1, 4, 5-trisphosphate receptors (IP3Rs) activated both during the HFS and after the LFS are involved in this depotentiation, the former triggering, and the latter modifying, LTP induction (decreasing the amplitude of the LTP established by the priming HFS). Furthermore, the decrease in the LTP at CA1 synapses requires activation of IP3Rs during LFS and activation of calcineurin after LFS. These results suggest that, at hippocampal CA1 neuron synapses, HFS-induced IP3R activation, which is modulated by the subsequent LFS, results in postsynaptic protein dephosphorylation after the LFS, leading to a decrease in the field EPSP and in the HFS-induced LTP.
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Sugita
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Yamazaki
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan; Laboratory for Developmental Neurobiology, Riken Brain Science Institute, Wako, Saitama 351-0198, Japan.
authors.forename: Jun-Ichi
authors.initials: JI
authors.lastname: Goto
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Fujiwara
authors.affiliation: Department of Software Science, Tamagawa University, College of Engineering, Machida, Tokyo 194-8610, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Aihara
authors.affiliation: Laboratory for Developmental Neurobiology, Riken Brain Science Institute, Wako, Saitama 351-0198, Japan.
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Mikoshiba
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan; Laboratory for Developmental Neurobiology, Riken Brain Science Institute, Wako, Saitama 351-0198, Japan. Electronic address: sfujii@med.id.yamagata-u.ac.jp.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujii
mesh_terms: D000818:Animals; D056547:CA1 Region, Hippocampal / Q000502:physiology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism; D004558:Electric Stimulation; D006168:Guinea Pigs; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000502:physiology*; D036881:Long-Term Synaptic Depression; D008297:Male; D009474:Neurons / Q000502:physiology*; D010766:Phosphorylation; D011493:Protein Kinase C / Q000378:metabolism; D013569:Synapses / Q000502:physiology*
chemical_list: D053496:Inositol 1,4,5-Trisphosphate Receptors; D011493:Protein Kinase C; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2
keywords: CA1 synapses; Depotentiation; Hippocampus; IP(3) receptors; LTP