Piracetam prevents memory deficit induced by postnatal propofol exposure in mice
Postnatal propofol exposure impairs hippocampal synaptic development and memory. However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months a...
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| Veröffentlicht in: | European journal of pharmacology 2016-05, Vol.779, p.59-65 |
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| container_title | European journal of pharmacology |
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| creator | Wang, Yuan-Lin Li, Feng Chen, Xin |
| description | Postnatal propofol exposure impairs hippocampal synaptic development and memory. However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months after propofol administration, hippocampal long-term potentiation (LTP) and long-term memory decreased, while intraperitoneal injection of piracetam at doses of 100mg/kg and 50mg/kg following last propofol exposure reversed the impairments of memory and LTP. Mechanically, piracetam reversed propofol exposure-induced decrease of BDNF and phosphorylation of mTor. Similar as piracetam, BDNF supplementary also ameliorated propofol-induced abnormalities of synaptic plasticity-related protein expressions, hippocampal LTP and long-term memory. These results suggest that piracetam prevents detrimental effects of propofol, likely via activating BDNF synthesis. |
| doi_str_mv | 10.1016/j.ejphar.2016.03.013 |
| format | Article |
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However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months after propofol administration, hippocampal long-term potentiation (LTP) and long-term memory decreased, while intraperitoneal injection of piracetam at doses of 100mg/kg and 50mg/kg following last propofol exposure reversed the impairments of memory and LTP. Mechanically, piracetam reversed propofol exposure-induced decrease of BDNF and phosphorylation of mTor. Similar as piracetam, BDNF supplementary also ameliorated propofol-induced abnormalities of synaptic plasticity-related protein expressions, hippocampal LTP and long-term memory. These results suggest that piracetam prevents detrimental effects of propofol, likely via activating BDNF synthesis.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2016.03.013</identifier><identifier>PMID: 26957054</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; BDNF ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Disks Large Homolog 4 Protein ; Enzyme Activation - drug effects ; Gene Expression Regulation - drug effects ; Guanylate Kinases - metabolism ; Hippocampus - drug effects ; Hippocampus - physiopathology ; Long-term Potentiation ; Long-Term Potentiation - drug effects ; Male ; Membrane Proteins - metabolism ; Memory ; Memory Disorders - chemically induced ; Memory Disorders - metabolism ; Memory Disorders - physiopathology ; Memory Disorders - prevention & control ; Mice ; Piracetam ; Piracetam - pharmacology ; Propofol ; Propofol - administration & dosage ; Propofol - adverse effects</subject><ispartof>European journal of pharmacology, 2016-05, Vol.779, p.59-65</ispartof><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. 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However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months after propofol administration, hippocampal long-term potentiation (LTP) and long-term memory decreased, while intraperitoneal injection of piracetam at doses of 100mg/kg and 50mg/kg following last propofol exposure reversed the impairments of memory and LTP. Mechanically, piracetam reversed propofol exposure-induced decrease of BDNF and phosphorylation of mTor. Similar as piracetam, BDNF supplementary also ameliorated propofol-induced abnormalities of synaptic plasticity-related protein expressions, hippocampal LTP and long-term memory. These results suggest that piracetam prevents detrimental effects of propofol, likely via activating BDNF synthesis.</description><subject>Animals</subject><subject>BDNF</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Disks Large Homolog 4 Protein</subject><subject>Enzyme Activation - drug effects</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Guanylate Kinases - metabolism</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - physiopathology</subject><subject>Long-term Potentiation</subject><subject>Long-Term Potentiation - drug effects</subject><subject>Male</subject><subject>Membrane Proteins - metabolism</subject><subject>Memory</subject><subject>Memory Disorders - chemically induced</subject><subject>Memory Disorders - metabolism</subject><subject>Memory Disorders - physiopathology</subject><subject>Memory Disorders - prevention & control</subject><subject>Mice</subject><subject>Piracetam</subject><subject>Piracetam - pharmacology</subject><subject>Propofol</subject><subject>Propofol - administration & dosage</subject><subject>Propofol - adverse effects</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkElLxDAUgIMozrj8A5EevbRmaSbNRRBxA0EPeg5ZXjFDN5N2cP69Gaoe9fR4j-9tH0JnBBcEk9XluoD18K5DQVNWYFZgwvbQklRC5lgQuo-WGJMyp1LKBTqKcY0x5pLyQ7SgK8kF5uUSvbz4oC2Mus2GABvoxpi10PZhmzmovfVj5js3WXCZ2WZDH8dOj7pJcD_0dd9k8JmKU4CEZa23cIIOat1EOP2Ox-jt7vb15iF_er5_vLl-yi2TfMydppw7QrkxpgJbSqaNFSUXgghiHRGCp7sdN3jlWM0wA2lrK5gzUFLDHDtGF_PcdMnHBHFUrY8WmkZ30E9RkSr9J6tSiP9RURFeMlqxhJYzakMfY4BaDcG3OmwVwWqnXa3VrF3ttCvMVNKe2s6_N0ymBffb9OM5AVczAEnJxkNQ0XroklYfwI7K9f7vDV_BEpYK</recordid><startdate>20160515</startdate><enddate>20160515</enddate><creator>Wang, Yuan-Lin</creator><creator>Li, Feng</creator><creator>Chen, Xin</creator><general>Elsevier B.V</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>7X8</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20160515</creationdate><title>Piracetam prevents memory deficit induced by postnatal propofol exposure in mice</title><author>Wang, Yuan-Lin ; Li, Feng ; Chen, Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c395t-da255d125bbb8ec493abc74577171cd1775999d5b06d3f303e9cfc73dbe42b3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>BDNF</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Disks Large Homolog 4 Protein</topic><topic>Enzyme Activation - drug effects</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Guanylate Kinases - metabolism</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - physiopathology</topic><topic>Long-term Potentiation</topic><topic>Long-Term Potentiation - drug effects</topic><topic>Male</topic><topic>Membrane Proteins - metabolism</topic><topic>Memory</topic><topic>Memory Disorders - chemically induced</topic><topic>Memory Disorders - metabolism</topic><topic>Memory Disorders - physiopathology</topic><topic>Memory Disorders - prevention & control</topic><topic>Mice</topic><topic>Piracetam</topic><topic>Piracetam - pharmacology</topic><topic>Propofol</topic><topic>Propofol - administration & dosage</topic><topic>Propofol - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yuan-Lin</creatorcontrib><creatorcontrib>Li, Feng</creatorcontrib><creatorcontrib>Chen, Xin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yuan-Lin</au><au>Li, Feng</au><au>Chen, Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Piracetam prevents memory deficit induced by postnatal propofol exposure in mice</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2016-05-15</date><risdate>2016</risdate><volume>779</volume><spage>59</spage><epage>65</epage><pages>59-65</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Postnatal propofol exposure impairs hippocampal synaptic development and memory. However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months after propofol administration, hippocampal long-term potentiation (LTP) and long-term memory decreased, while intraperitoneal injection of piracetam at doses of 100mg/kg and 50mg/kg following last propofol exposure reversed the impairments of memory and LTP. Mechanically, piracetam reversed propofol exposure-induced decrease of BDNF and phosphorylation of mTor. Similar as piracetam, BDNF supplementary also ameliorated propofol-induced abnormalities of synaptic plasticity-related protein expressions, hippocampal LTP and long-term memory. These results suggest that piracetam prevents detrimental effects of propofol, likely via activating BDNF synthesis.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26957054</pmid><doi>10.1016/j.ejphar.2016.03.013</doi><tpages>7</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 2016-05, Vol.779, p.59-65 |
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| subjects | Animals BDNF Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Cyclic AMP-Dependent Protein Kinases - metabolism Disks Large Homolog 4 Protein Enzyme Activation - drug effects Gene Expression Regulation - drug effects Guanylate Kinases - metabolism Hippocampus - drug effects Hippocampus - physiopathology Long-term Potentiation Long-Term Potentiation - drug effects Male Membrane Proteins - metabolism Memory Memory Disorders - chemically induced Memory Disorders - metabolism Memory Disorders - physiopathology Memory Disorders - prevention & control Mice Piracetam Piracetam - pharmacology Propofol Propofol - administration & dosage Propofol - adverse effects |
| title | Piracetam prevents memory deficit induced by postnatal propofol exposure in mice |
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