Requirement for α-CaMKII in Experience-Dependent Plasticity of the Barrel Cortex
The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could und...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 1996-04, Vol.272 (5260), p.421-423 |
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| creator | Glazewski, Stanislaw Chen, Chuan-Min Silva, Alcino Fox, Kevin |
| description | The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice. |
| doi_str_mv | 10.1126/science.272.5260.421 |
| format | Article |
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The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.272.5260.421</identifier><identifier>PMID: 8602534</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Adolescents ; Adults ; Anatomy ; Animals ; Biological and medical sciences ; Body Weight ; Brain ; Brain Mapping ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases - genetics ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Depression (Psychology) ; Developmental neurology ; Electric Stimulation ; Experiential learning ; Feedback (Response) ; Fundamental and applied biological sciences. Psychology ; Heterozygote ; Heterozygotes ; Histograms ; Homozygote ; Homozygotes ; Long term potentiation ; Mammals ; Mice ; Mutation ; Neocortex ; Neuronal Plasticity ; Neurons ; Neuroplasticity ; Physiological aspects ; Plasticity ; Rodents ; Sensory deprivation ; Sensory Experience ; Somatosensory Cortex - physiology ; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors ; Vertebrates: nervous system and sense organs ; Vibrissae - physiology</subject><ispartof>Science (American Association for the Advancement of Science), 1996-04, Vol.272 (5260), p.421-423</ispartof><rights>Copyright 1996 American Association for the Advancement of Science</rights><rights>1996 INIST-CNRS</rights><rights>COPYRIGHT 1996 American Association for the Advancement of Science</rights><rights>COPYRIGHT 1996 American Association for the Advancement of Science</rights><rights>Copyright American Association for the Advancement of Science Apr 19, 1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c746t-37fff9c273616cf6e962bfffa19f8ddcbcd5eddcface7a5f138ba8fc47ead0e3</citedby><cites>FETCH-LOGICAL-c746t-37fff9c273616cf6e962bfffa19f8ddcbcd5eddcface7a5f138ba8fc47ead0e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2890325$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2890325$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2871,2872,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3054142$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8602534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Glazewski, Stanislaw</creatorcontrib><creatorcontrib>Chen, Chuan-Min</creatorcontrib><creatorcontrib>Silva, Alcino</creatorcontrib><creatorcontrib>Fox, Kevin</creatorcontrib><title>Requirement for α-CaMKII in Experience-Dependent Plasticity of the Barrel Cortex</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.</description><subject>Adolescents</subject><subject>Adults</subject><subject>Anatomy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body Weight</subject><subject>Brain</subject><subject>Brain Mapping</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - genetics</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Depression (Psychology)</subject><subject>Developmental neurology</subject><subject>Electric Stimulation</subject><subject>Experiential learning</subject><subject>Feedback (Response)</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heterozygote</subject><subject>Heterozygotes</subject><subject>Histograms</subject><subject>Homozygote</subject><subject>Homozygotes</subject><subject>Long term potentiation</subject><subject>Mammals</subject><subject>Mice</subject><subject>Mutation</subject><subject>Neocortex</subject><subject>Neuronal Plasticity</subject><subject>Neurons</subject><subject>Neuroplasticity</subject><subject>Physiological aspects</subject><subject>Plasticity</subject><subject>Rodents</subject><subject>Sensory deprivation</subject><subject>Sensory Experience</subject><subject>Somatosensory Cortex - physiology</subject><subject>Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. 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The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>8602534</pmid><doi>10.1126/science.272.5260.421</doi><tpages>3</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0036-8075 |
| ispartof | Science (American Association for the Advancement of Science), 1996-04, Vol.272 (5260), p.421-423 |
| issn | 0036-8075 1095-9203 |
| language | eng |
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| source | American Association for the Advancement of Science; Jstor Complete Legacy; MEDLINE |
| subjects | Adolescents Adults Anatomy Animals Biological and medical sciences Body Weight Brain Brain Mapping Calcium-Calmodulin-Dependent Protein Kinase Type 2 Calcium-Calmodulin-Dependent Protein Kinases - genetics Calcium-Calmodulin-Dependent Protein Kinases - metabolism Depression (Psychology) Developmental neurology Electric Stimulation Experiential learning Feedback (Response) Fundamental and applied biological sciences. Psychology Heterozygote Heterozygotes Histograms Homozygote Homozygotes Long term potentiation Mammals Mice Mutation Neocortex Neuronal Plasticity Neurons Neuroplasticity Physiological aspects Plasticity Rodents Sensory deprivation Sensory Experience Somatosensory Cortex - physiology Somesthesis and somesthetic pathways (proprioception, exteroception, nociception) interoception electrolocation. Sensory receptors Vertebrates: nervous system and sense organs Vibrissae - physiology |
| title | Requirement for α-CaMKII in Experience-Dependent Plasticity of the Barrel Cortex |
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