The role of GSK‐3 in synaptic plasticity
Glycogen synthase kinase‐3 (GSK‐3), an important component of the glycogen metabolism pathway, is highly expressed in the CNS. It has been implicated in major neurological disorders including Alzheimer's disease, schizophrenia and bipolar disorders. Despite its central role in these conditions...
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| Veröffentlicht in: | British journal of pharmacology 2008-03, Vol.153 (S1), p.S428-S437 |
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| creator | Peineau, S Bradley, C Taghibiglou, C Doherty, A Bortolotto, Z A Wang, Y T Collingridge, G L |
| description | Glycogen synthase kinase‐3 (GSK‐3), an important component of the glycogen metabolism pathway, is highly expressed in the CNS. It has been implicated in major neurological disorders including Alzheimer's disease, schizophrenia and bipolar disorders. Despite its central role in these conditions it was not known until recently whether GSK‐3 has neuronal‐specific functions under normal conditions. However recent work has shown that GSK‐3 is involved in the regulation of, and cross‐talk between, two major forms of synaptic plasticity, N‐methyl‐D‐aspartate receptor (NMDAR)‐dependent long‐term potentiation (LTP) and NMDAR‐dependent long‐term depression (LTD). The present article summarizes this recent work and discusses its potential relevance to the treatment of neurological disorders.
British Journal of Pharmacology (2008) 153, S428–S437; doi:10.1038/bjp.2008.2 |
| doi_str_mv | 10.1038/bjp.2008.2 |
| format | Article |
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British Journal of Pharmacology (2008) 153, S428–S437; doi:10.1038/bjp.2008.2</description><subject>Akt</subject><subject>Alzheimer's disease</subject><subject>AMPA receptor</subject><subject>Animals</subject><subject>Bipolar disorder</subject><subject>Central nervous system</subject><subject>Glutamic acid receptors</subject><subject>Glycogen</subject><subject>glycogen synthase kinase</subject><subject>Glycogen Synthase Kinase 3</subject><subject>Glycogen Synthase Kinase 3 - drug effects</subject><subject>Glycogen Synthase Kinase 3 - physiology</subject><subject>hippocampus</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Long-term depression</subject><subject>Long-term potentiation</subject><subject>Mental disorders</subject><subject>Metabolism</subject><subject>metaplasticity</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Neurodegenerative diseases</subject><subject>Neurological diseases</subject><subject>Neuronal Plasticity</subject><subject>Neuronal Plasticity - drug effects</subject><subject>Neuronal Plasticity - physiology</subject><subject>Neurons and Cognition</subject><subject>NMDA receptor</subject><subject>Pharmacology</subject><subject>PI3K</subject><subject>Plasticity (synaptic)</subject><subject>PP1</subject><subject>Receptors, N-Methyl-D-Aspartate</subject><subject>Receptors, N-Methyl-D-Aspartate - drug effects</subject><subject>Receptors, N-Methyl-D-Aspartate - physiology</subject><subject>Review</subject><subject>Schizophrenia</subject><subject>Synapses</subject><subject>Synapses - drug effects</subject><subject>Synapses - physiology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFksFOGzEQhi3UCtLAhQdAqx5Qhbrp2F6vZy9IFNEENRKVCmfL6zjE0WZ3sRNQbn0EnpEnwatELXCgpznM5_-fGf-EHFIYUOD4rZy3AwaAA7ZDejSTeSo40g-kBwAypRRxj3wKYQ4Qm1Lskj2KnFIqZI-cXM9s4pvKJs00Gf7--fTnkSeuTsK61u3SmaStdIjVLdf75ONUV8EebGuf3Py4uD4fpeOr4eX52Tg1ORSYFkzY6GSEZhaNRjASy4nNJ0Whpc4MlpgJkXE00qIUubbFxOjY0DQvdcl4n5xudNtVubATY-ul15VqvVtov1aNdup1p3YzddvcK8ZyBEmjwNeNwOzNs9HZWLk6WL9Q8TJSgsD7Dj_e-vnmbmXDUi1cMLaqdG2bVVASeJZJDv8FGeRM5tht8OVdkAKLgyIvMKKf36DzZuXreF_FqGSQRcUInWwg45sQvJ3-3YqC6iKgYgRUFwHVmR-9PN8_dPvnERhsgAdX2fU7Uur7rxHGMZ8BLbK5WA</recordid><startdate>200803</startdate><enddate>200803</enddate><creator>Peineau, S</creator><creator>Bradley, C</creator><creator>Taghibiglou, C</creator><creator>Doherty, A</creator><creator>Bortolotto, Z A</creator><creator>Wang, Y T</creator><creator>Collingridge, G L</creator><general>Blackwell Publishing Ltd</general><general>Wiley</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4721-6795</orcidid><orcidid>https://orcid.org/0000-0002-3117-5263</orcidid></search><sort><creationdate>200803</creationdate><title>The role of GSK‐3 in synaptic plasticity</title><author>Peineau, S ; Bradley, C ; Taghibiglou, C ; Doherty, A ; Bortolotto, Z A ; Wang, Y T ; Collingridge, G L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6098-925e001c5a2e8ca80c78bde6d99a7a4c8b8455438c7e8756ae9dcaa4ca16bab23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Akt</topic><topic>Alzheimer's disease</topic><topic>AMPA receptor</topic><topic>Animals</topic><topic>Bipolar disorder</topic><topic>Central nervous system</topic><topic>Glutamic acid receptors</topic><topic>Glycogen</topic><topic>glycogen synthase kinase</topic><topic>Glycogen Synthase Kinase 3</topic><topic>Glycogen Synthase Kinase 3 - drug effects</topic><topic>Glycogen Synthase Kinase 3 - physiology</topic><topic>hippocampus</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Long-term depression</topic><topic>Long-term potentiation</topic><topic>Mental disorders</topic><topic>Metabolism</topic><topic>metaplasticity</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Neurodegenerative diseases</topic><topic>Neurological diseases</topic><topic>Neuronal Plasticity</topic><topic>Neuronal Plasticity - drug effects</topic><topic>Neuronal Plasticity - physiology</topic><topic>Neurons and Cognition</topic><topic>NMDA receptor</topic><topic>Pharmacology</topic><topic>PI3K</topic><topic>Plasticity (synaptic)</topic><topic>PP1</topic><topic>Receptors, N-Methyl-D-Aspartate</topic><topic>Receptors, N-Methyl-D-Aspartate - drug effects</topic><topic>Receptors, N-Methyl-D-Aspartate - physiology</topic><topic>Review</topic><topic>Schizophrenia</topic><topic>Synapses</topic><topic>Synapses - drug effects</topic><topic>Synapses - 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Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peineau, S</au><au>Bradley, C</au><au>Taghibiglou, C</au><au>Doherty, A</au><au>Bortolotto, Z A</au><au>Wang, Y T</au><au>Collingridge, G L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of GSK‐3 in synaptic plasticity</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2008-03</date><risdate>2008</risdate><volume>153</volume><issue>S1</issue><spage>S428</spage><epage>S437</epage><pages>S428-S437</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>Glycogen synthase kinase‐3 (GSK‐3), an important component of the glycogen metabolism pathway, is highly expressed in the CNS. It has been implicated in major neurological disorders including Alzheimer's disease, schizophrenia and bipolar disorders. Despite its central role in these conditions it was not known until recently whether GSK‐3 has neuronal‐specific functions under normal conditions. However recent work has shown that GSK‐3 is involved in the regulation of, and cross‐talk between, two major forms of synaptic plasticity, N‐methyl‐D‐aspartate receptor (NMDAR)‐dependent long‐term potentiation (LTP) and NMDAR‐dependent long‐term depression (LTD). The present article summarizes this recent work and discusses its potential relevance to the treatment of neurological disorders.
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| subjects | Akt Alzheimer's disease AMPA receptor Animals Bipolar disorder Central nervous system Glutamic acid receptors Glycogen glycogen synthase kinase Glycogen Synthase Kinase 3 Glycogen Synthase Kinase 3 - drug effects Glycogen Synthase Kinase 3 - physiology hippocampus Humans Life Sciences Long-term depression Long-term potentiation Mental disorders Metabolism metaplasticity N-Methyl-D-aspartic acid receptors Neurodegenerative diseases Neurological diseases Neuronal Plasticity Neuronal Plasticity - drug effects Neuronal Plasticity - physiology Neurons and Cognition NMDA receptor Pharmacology PI3K Plasticity (synaptic) PP1 Receptors, N-Methyl-D-Aspartate Receptors, N-Methyl-D-Aspartate - drug effects Receptors, N-Methyl-D-Aspartate - physiology Review Schizophrenia Synapses Synapses - drug effects Synapses - physiology |
| title | The role of GSK‐3 in synaptic plasticity |
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