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Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice
Background The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail...
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| Published in: | Chinese medical journal 2011-05, Vol.124 (10), p.1540-1544 |
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| description | Background The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone8 （SAMP8） mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia.Methods Mice were either sham-operated or subjected to complete molar removal. The animals＇ body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1 st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor （BDNF） and the tropomyosin related kinase B （TrkB）, the high affinity receptor of BDNF.Results Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups （P〉0.05）. Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group （P〈0.05）; but the expression of its receptor, TrkB, was not significantly affected.Conclusion These results suggested that the molarless condition impaired learning and memory abilities in SAMP8mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus. |
| doi_str_mv | 10.3760/cma.j.issn.0366-6999.2011.10.019 |
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However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone8 （SAMP8） mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia.Methods Mice were either sham-operated or subjected to complete molar removal. The animals＇ body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1 st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor （BDNF） and the tropomyosin related kinase B （TrkB）, the high affinity receptor of BDNF.Results Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups （P〉0.05）. Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group （P〈0.05）; but the expression of its receptor, TrkB, was not significantly affected.Conclusion These results suggested that the molarless condition impaired learning and memory abilities in SAMP8mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus.</description><identifier>ISSN: 0366-6999</identifier><identifier>EISSN: 2542-5641</identifier><identifier>DOI: 10.3760/cma.j.issn.0366-6999.2011.10.019</identifier><identifier>PMID: 21740813</identifier><language>eng</language><publisher>China: Department of Prosthodontics, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, China%Department of Pharmacology, Institute of Materia Medica Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China%School and Hospital of Stomatology, Peking University, Beijing 100081, China</publisher><subject>Animals ; Blotting, Western ; Body Weight - physiology ; Brain-Derived Neurotrophic Factor - metabolism ; Cerebral Cortex - metabolism ; Hippocampus - metabolism ; Male ; Maze Learning ; Memory Disorders - metabolism ; Mice ; Motor Activity - physiology ; Protein-Tyrosine Kinases - metabolism ; 学习能力 ; 小鼠 ; 海马 ; 皮层 ; 老年痴呆症 ; 脑源性神经营养因子 ; 记忆体 ; 高亲和力受体</subject><ispartof>Chinese medical journal, 2011-05, Vol.124 (10), p.1540-1544</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c330t-a979fc5e23a759247a7a9cbe9cf237f8b9a2c79be733cc5c3337c1e97c8d828e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85656X/85656X.jpg</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21740813$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Qing-Song</creatorcontrib><creatorcontrib>Liang, Zi-Liang</creatorcontrib><creatorcontrib>Wu, Min-Jie</creatorcontrib><creatorcontrib>Feng, Lin</creatorcontrib><creatorcontrib>Liu, Li-Li</creatorcontrib><creatorcontrib>Zhang, Jian-Jun</creatorcontrib><title>Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice</title><title>Chinese medical journal</title><addtitle>Chinese Medical Journal</addtitle><description>Background The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone8 （SAMP8） mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia.Methods Mice were either sham-operated or subjected to complete molar removal. The animals＇ body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1 st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor （BDNF） and the tropomyosin related kinase B （TrkB）, the high affinity receptor of BDNF.Results Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups （P〉0.05）. Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group （P〈0.05）; but the expression of its receptor, TrkB, was not significantly affected.Conclusion These results suggested that the molarless condition impaired learning and memory abilities in SAMP8mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Body Weight - physiology</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Cerebral Cortex - metabolism</subject><subject>Hippocampus - metabolism</subject><subject>Male</subject><subject>Maze Learning</subject><subject>Memory Disorders - metabolism</subject><subject>Mice</subject><subject>Motor Activity - physiology</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>学习能力</subject><subject>小鼠</subject><subject>海马</subject><subject>皮层</subject><subject>老年痴呆症</subject><subject>脑源性神经营养因子</subject><subject>记忆体</subject><subject>高亲和力受体</subject><issn>0366-6999</issn><issn>2542-5641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNo90Ntu1DAQBmALgei28ArI3EBvEnzYxPFlVZWDVATicB05k8nGq9hO7aS0PAZPjJctvbJG_uYf6SfknLNSqpq9A2fKfWlT8iWTdV3UWutSMM7LLBjXT8hGVFtRVPWWPyWbR3NCTlPaMyaqStXPyYngassaLjfkzzfsV8CedtFYX_QY7W2ePK4xLDHMowU6GFhCpHg3R0zJBk-tpxDignfU-J6Odp4DGDevKf_chumQkMkyIp3QRG_97h906EK8pz0OFuxyIC5MJk45lX6_-Py1oc4CviDPBjMlfPnwnpGf769-XH4srr98-HR5cV2AlGwpjFZ6gAqFNKrSYquMMho61DAIqYam00aA0h0qKQGqvCQVcNQKmr4RDcoz8uaY-8v4wfhduw9r9Pli-3sEtz_UylkuNcO3RzjHcLNiWlpnE-A0GY9hTW2jat7oWrIsXz3ItXPYt3O0zsT79n_fGbw-AhiD393kYh6NbDiXQlbyL_BolKY</recordid><startdate>20110520</startdate><enddate>20110520</enddate><creator>Jiang, Qing-Song</creator><creator>Liang, Zi-Liang</creator><creator>Wu, Min-Jie</creator><creator>Feng, Lin</creator><creator>Liu, Li-Li</creator><creator>Zhang, Jian-Jun</creator><general>Department of Prosthodontics, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, China%Department of Pharmacology, Institute of Materia Medica Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China%School and Hospital of Stomatology, Peking University, Beijing 100081, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>20110520</creationdate><title>Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice</title><author>Jiang, Qing-Song ; Liang, Zi-Liang ; Wu, Min-Jie ; Feng, Lin ; Liu, Li-Li ; Zhang, Jian-Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c330t-a979fc5e23a759247a7a9cbe9cf237f8b9a2c79be733cc5c3337c1e97c8d828e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>Body Weight - physiology</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Cerebral Cortex - metabolism</topic><topic>Hippocampus - metabolism</topic><topic>Male</topic><topic>Maze Learning</topic><topic>Memory Disorders - metabolism</topic><topic>Mice</topic><topic>Motor Activity - physiology</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>学习能力</topic><topic>小鼠</topic><topic>海马</topic><topic>皮层</topic><topic>老年痴呆症</topic><topic>脑源性神经营养因子</topic><topic>记忆体</topic><topic>高亲和力受体</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Qing-Song</creatorcontrib><creatorcontrib>Liang, Zi-Liang</creatorcontrib><creatorcontrib>Wu, Min-Jie</creatorcontrib><creatorcontrib>Feng, Lin</creatorcontrib><creatorcontrib>Liu, Li-Li</creatorcontrib><creatorcontrib>Zhang, Jian-Jun</creatorcontrib><collection>维普_期刊</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>维普中文期刊数据库</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Chinese medical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Qing-Song</au><au>Liang, Zi-Liang</au><au>Wu, Min-Jie</au><au>Feng, Lin</au><au>Liu, Li-Li</au><au>Zhang, Jian-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice</atitle><jtitle>Chinese medical journal</jtitle><addtitle>Chinese Medical Journal</addtitle><date>2011-05-20</date><risdate>2011</risdate><volume>124</volume><issue>10</issue><spage>1540</spage><epage>1544</epage><pages>1540-1544</pages><issn>0366-6999</issn><eissn>2542-5641</eissn><notes>Background The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone8 （SAMP8） mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia.Methods Mice were either sham-operated or subjected to complete molar removal. The animals＇ body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1 st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor （BDNF） and the tropomyosin related kinase B （TrkB）, the high affinity receptor of BDNF.Results Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups （P〉0.05）. Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group （P〈0.05）; but the expression of its receptor, TrkB, was not significantly affected.Conclusion These results suggested that the molarless condition impaired learning and memory abilities in SAMP8mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus.</notes><notes>molarless; learning and memory; water maze; brain-derived neurotrophic Jactor; TrkB</notes><notes>11-2154/R</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Background The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone8 （SAMP8） mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia.Methods Mice were either sham-operated or subjected to complete molar removal. The animals＇ body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1 st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor （BDNF） and the tropomyosin related kinase B （TrkB）, the high affinity receptor of BDNF.Results Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups （P〉0.05）. Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group （P〈0.05）; but the expression of its receptor, TrkB, was not significantly affected.Conclusion These results suggested that the molarless condition impaired learning and memory abilities in SAMP8mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus.</abstract><cop>China</cop><pub>Department of Prosthodontics, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, China%Department of Pharmacology, Institute of Materia Medica Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China%School and Hospital of Stomatology, Peking University, Beijing 100081, China</pub><pmid>21740813</pmid><doi>10.3760/cma.j.issn.0366-6999.2011.10.019</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Blotting, Western Body Weight - physiology Brain-Derived Neurotrophic Factor - metabolism Cerebral Cortex - metabolism Hippocampus - metabolism Male Maze Learning Memory Disorders - metabolism Mice Motor Activity - physiology Protein-Tyrosine Kinases - metabolism 学习能力 小鼠 海马 皮层 老年痴呆症 脑源性神经营养因子 记忆体 高亲和力受体 |
| title | Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice |
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