LTP inhibits LTD in the hippocampus via regulation of GSK3beta
| Autor: | Peineau, Stéphane, Taghibiglou, Changiz, Bradley, Clarrisa, Wong, Tak Pan, Liu, Lidong, Lu, Jie, Lo, Edmond, Wu, Dongchuan, Saule, Emilia, Bouschet, Tristan, Matthews, Paul, Isaac, John, Bortolotto, Zuner, Wang, Yu Tian, Collingridge, Graham |
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| Přispěvatelé: | Department of Anatomy, University Walk-MRC Centre for Synaptic Plasticity-School of Medical and Sciences, Brain Research Center, Department of Medicine-UBC Hospital-University of British Columbia (UBC), National Institute of Neurological Disorders and Stroke [Bethesda] (NINDS), National Institutes of Health [Bethesda] (NIH), This work was supported by the MRC, Wellcome Trust, CIHR, and NINDS. S.P. was supported by a fellowship from FRM (Fondation pour la Recherche Médicale). C.T. was supported by fellowships from CIHR and MSFHR. G.L.C. is a Royal Society-Wolfson Merit Award Holder. Y.T.W. is an HHMI international scholar. |
| Jazyk: | angličtina |
| Rok vydání: | 2007 |
| Předmět: |
MESH: Signal Transduction
MESH: Enzyme Activation MESH: Hippocampus MESH: Long-Term Synaptic Depression endocrine system diseases MESH: Rats macromolecular substances glycogen synthase kinase PI3K MESH: Dendritic Spines MESH: Long-Term Potentiation MESH: Protein Kinase Inhibitors long-term depression MESH: Animals MESH: Excitatory Postsynaptic Potentials MESH: Glycogen Synthase Kinase 3 MESH: Maleimides synaptic plasticity MESH: Proto-Oncogene Proteins c-akt Akt MESH: Aminophenols MESH: Organ Culture Techniques nervous system NMDA MESH: Phosphatidylinositol 3-Kinases MESH: Receptors AMPA Long-term potentiation [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] hormones hormone substitutes and hormone antagonists |
| Zdroj: | Neuron Neuron, Elsevier, 2007, 53 (5), pp.703-17. ⟨10.1016/j.neuron.2007.01.029⟩ |
| ISSN: | 0896-6273 |
| Popis: | International audience; Glycogen synthase kinase-3 (GSK3) has been implicated in major neurological disorders, but its role in normal neuronal function is largely unknown. Here we show that GSK3beta mediates an interaction between two major forms of synaptic plasticity in the brain, N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) and NMDA receptor-dependent long-term depression (LTD). In rat hippocampal slices, GSK3beta inhibitors block the induction of LTD. Furthermore, the activity of GSK3beta is enhanced during LTD via activation of PP1. Conversely, following the induction of LTP, there is inhibition of GSK3beta activity. This regulation of GSK3beta during LTP involves activation of NMDA receptors and the PI3K-Akt pathway and disrupts the ability of synapses to undergo LTD for up to 1 hr. We conclude that the regulation of GSK3beta activity provides a powerful mechanism to preserve information encoded during LTP from erasure by subsequent LTD, perhaps thereby permitting the initial consolidation of learnt information. |
| Databáze: | OpenAIRE |
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