Intranasal insulin treatment restores cognitive deficits and insulin signaling impairment induced by repeated methamphetamine exposure
Long‐term use of methamphetamine (MA) causes a broad range of cognitive deficits. Recently, it has been reported insulin signaling and mitochondrial biogenesis are involved in cognitive processes. This study aimed to examine whether MA induces cognitive deficits concomitant with insulin signaling im...
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| Veröffentlicht in: | Journal of cellular biochemistry 2018-02, Vol.119 (2), p.2345-2355 |
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| container_title | Journal of cellular biochemistry |
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| creator | Beirami, Elmira Oryan, Shahrbanoo Seyedhosseini Tamijani, Seyedeh Masoumeh Ahmadiani, Abolhassan Dargahi, Leila |
| description | Long‐term use of methamphetamine (MA) causes a broad range of cognitive deficits. Recently, it has been reported insulin signaling and mitochondrial biogenesis are involved in cognitive processes. This study aimed to examine whether MA induces cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions and also intranasal (IN) insulin treatment can reverse cognitive deficits caused by MA. Rats were repeatedly treated with increasing doses of MA (1‐10 mg/kg) twice a day for 10 days, and their cognitive functions were assessed using Y‐maze, novel object recognition and passive avoidance tasks. The expression of components involved in insulin signaling (IR/IRS2/PI3K/Akt/GSK3β) and mitochondrial biogenesis (PGC‐1α, NRF1, and TFAM) was measured in the hippocampus. Therapeutic effects of IN insulin delivery (0.5 IU/day, for 7 days after MA discontinuation) were also investigated in MA‐treated animals. Our results showed that repeated MA exposure induced cognitive deficits, and led to insulin signaling impairment and mitochondrial dysfunction. Interestingly, IN insulin treatment reduced MA‐induced cognitive impairments possibly through activating insulin signaling, particularly PI3K/Akt/GSK3β pathway, and mitochondrial biogenesis. Thus, insulin and insulin signaling pathway can be considered as useful targets for the treatment of abnormalities associated with MA abuse.
Repeated methamphetamine exposure induced cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions. Intranasal insulin treatment alleviated MA‐induced cognitive deficits, insulin signaling impairment, and mitochondrial dysfunctions. |
| doi_str_mv | 10.1002/jcb.26398 |
| format | Article |
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Repeated methamphetamine exposure induced cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions. Intranasal insulin treatment alleviated MA‐induced cognitive deficits, insulin signaling impairment, and mitochondrial dysfunctions.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.26398</identifier><identifier>PMID: 28884876</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Abnormalities ; Administration, Intranasal ; AKT protein ; Amphetamine-Related Disorders - complications ; Amphetamine-Related Disorders - genetics ; Amphetamine-Related Disorders - metabolism ; Animals ; Biosynthesis ; cognition ; Cognition Disorders - chemically induced ; Cognition Disorders - drug therapy ; Cognition Disorders - genetics ; Cognition Disorders - metabolism ; Cognitive ability ; Disease Models, Animal ; Exposure ; Gene Expression Regulation - drug effects ; Gene Regulatory Networks - drug effects ; Glucose ; Growth hormones ; Impairment ; Insulin ; Insulin - administration & dosage ; Insulin - pharmacology ; insulin signaling ; Male ; Memory, Short-Term - drug effects ; Methamphetamine ; Methamphetamine - toxicity ; Mitochondria ; Mitochondria - drug effects ; mitochondrial biogenesis ; Object recognition ; Pattern recognition ; Rats ; Rats, Wistar ; Signal transduction ; Signal Transduction - drug effects ; Signaling</subject><ispartof>Journal of cellular biochemistry, 2018-02, Vol.119 (2), p.2345-2355</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4198-54d40cdc6581680bda06bb2ae7e5e86509be42a6165c86c7b4984fc0c7f9d3303</citedby><cites>FETCH-LOGICAL-c4198-54d40cdc6581680bda06bb2ae7e5e86509be42a6165c86c7b4984fc0c7f9d3303</cites><orcidid>0000-0001-7777-5435 ; 0000-0002-6668-2302</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.26398$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.26398$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,27907,27908,45557,45558</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28884876$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Beirami, Elmira</creatorcontrib><creatorcontrib>Oryan, Shahrbanoo</creatorcontrib><creatorcontrib>Seyedhosseini Tamijani, Seyedeh Masoumeh</creatorcontrib><creatorcontrib>Ahmadiani, Abolhassan</creatorcontrib><creatorcontrib>Dargahi, Leila</creatorcontrib><title>Intranasal insulin treatment restores cognitive deficits and insulin signaling impairment induced by repeated methamphetamine exposure</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Long‐term use of methamphetamine (MA) causes a broad range of cognitive deficits. Recently, it has been reported insulin signaling and mitochondrial biogenesis are involved in cognitive processes. This study aimed to examine whether MA induces cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions and also intranasal (IN) insulin treatment can reverse cognitive deficits caused by MA. Rats were repeatedly treated with increasing doses of MA (1‐10 mg/kg) twice a day for 10 days, and their cognitive functions were assessed using Y‐maze, novel object recognition and passive avoidance tasks. The expression of components involved in insulin signaling (IR/IRS2/PI3K/Akt/GSK3β) and mitochondrial biogenesis (PGC‐1α, NRF1, and TFAM) was measured in the hippocampus. Therapeutic effects of IN insulin delivery (0.5 IU/day, for 7 days after MA discontinuation) were also investigated in MA‐treated animals. Our results showed that repeated MA exposure induced cognitive deficits, and led to insulin signaling impairment and mitochondrial dysfunction. Interestingly, IN insulin treatment reduced MA‐induced cognitive impairments possibly through activating insulin signaling, particularly PI3K/Akt/GSK3β pathway, and mitochondrial biogenesis. Thus, insulin and insulin signaling pathway can be considered as useful targets for the treatment of abnormalities associated with MA abuse.
Repeated methamphetamine exposure induced cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions. Intranasal insulin treatment alleviated MA‐induced cognitive deficits, insulin signaling impairment, and mitochondrial dysfunctions.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Abnormalities</subject><subject>Administration, Intranasal</subject><subject>AKT protein</subject><subject>Amphetamine-Related Disorders - complications</subject><subject>Amphetamine-Related Disorders - genetics</subject><subject>Amphetamine-Related Disorders - metabolism</subject><subject>Animals</subject><subject>Biosynthesis</subject><subject>cognition</subject><subject>Cognition Disorders - chemically induced</subject><subject>Cognition Disorders - drug therapy</subject><subject>Cognition Disorders - genetics</subject><subject>Cognition Disorders - metabolism</subject><subject>Cognitive ability</subject><subject>Disease Models, Animal</subject><subject>Exposure</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Regulatory Networks - drug effects</subject><subject>Glucose</subject><subject>Growth hormones</subject><subject>Impairment</subject><subject>Insulin</subject><subject>Insulin - administration & dosage</subject><subject>Insulin - pharmacology</subject><subject>insulin signaling</subject><subject>Male</subject><subject>Memory, Short-Term - drug effects</subject><subject>Methamphetamine</subject><subject>Methamphetamine - toxicity</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>mitochondrial biogenesis</subject><subject>Object recognition</subject><subject>Pattern recognition</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1v1DAQhi0EokvhwB9AlrjAIa2_4o8jrAoUVeIC58ixJ1uvEifYTmH_QH83brf0gMRlZg7PPNLMi9BrSs4oIex87_ozJrnRT9CGEqMaIYV4ijZEcdIwTtkJepHznhBiDGfP0QnTWgut5AbdXsaSbLTZjjjEvI4h4pLAlgliwQlymWvBbt7FUMINYA9DcKFkbKN_3MhhF20ddjhMiw3pfjlEvzrwuD9Uz1KVdZ6gXNtpuYZipxABw-9lzmuCl-jZYMcMrx76Kfrx6eL79ktz9e3z5fbDVeMENbpphRfEeSdbTaUmvbdE9j2zoKAFLVtiehDMSipbp6VTvTBaDI44NRjPOeGn6N3Ru6T551qv66aQHYyjjTCvuaOGq5YJSXlF3_6D7uc11TPvKGWUrL_UlXp_pFyac04wdEsKk02HjpLuLpyuhtPdh1PZNw_GtZ_AP5J_06jA-RH4FUY4_N_Ufd1-PCr_AHWSm_M</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Beirami, Elmira</creator><creator>Oryan, Shahrbanoo</creator><creator>Seyedhosseini Tamijani, Seyedeh Masoumeh</creator><creator>Ahmadiani, Abolhassan</creator><creator>Dargahi, Leila</creator><general>Wiley Subscription Services, Inc</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7777-5435</orcidid><orcidid>https://orcid.org/0000-0002-6668-2302</orcidid></search><sort><creationdate>201802</creationdate><title>Intranasal insulin treatment restores cognitive deficits and insulin signaling impairment induced by repeated methamphetamine exposure</title><author>Beirami, Elmira ; Oryan, Shahrbanoo ; Seyedhosseini Tamijani, Seyedeh Masoumeh ; Ahmadiani, Abolhassan ; Dargahi, Leila</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4198-54d40cdc6581680bda06bb2ae7e5e86509be42a6165c86c7b4984fc0c7f9d3303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Abnormalities</topic><topic>Administration, Intranasal</topic><topic>AKT protein</topic><topic>Amphetamine-Related Disorders - complications</topic><topic>Amphetamine-Related Disorders - genetics</topic><topic>Amphetamine-Related Disorders - metabolism</topic><topic>Animals</topic><topic>Biosynthesis</topic><topic>cognition</topic><topic>Cognition Disorders - chemically induced</topic><topic>Cognition Disorders - drug therapy</topic><topic>Cognition Disorders - genetics</topic><topic>Cognition Disorders - metabolism</topic><topic>Cognitive ability</topic><topic>Disease Models, Animal</topic><topic>Exposure</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Regulatory Networks - drug effects</topic><topic>Glucose</topic><topic>Growth hormones</topic><topic>Impairment</topic><topic>Insulin</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - pharmacology</topic><topic>insulin signaling</topic><topic>Male</topic><topic>Memory, Short-Term - drug effects</topic><topic>Methamphetamine</topic><topic>Methamphetamine - toxicity</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>mitochondrial biogenesis</topic><topic>Object recognition</topic><topic>Pattern recognition</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beirami, Elmira</creatorcontrib><creatorcontrib>Oryan, Shahrbanoo</creatorcontrib><creatorcontrib>Seyedhosseini Tamijani, Seyedeh Masoumeh</creatorcontrib><creatorcontrib>Ahmadiani, Abolhassan</creatorcontrib><creatorcontrib>Dargahi, Leila</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beirami, Elmira</au><au>Oryan, Shahrbanoo</au><au>Seyedhosseini Tamijani, Seyedeh Masoumeh</au><au>Ahmadiani, Abolhassan</au><au>Dargahi, Leila</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intranasal insulin treatment restores cognitive deficits and insulin signaling impairment induced by repeated methamphetamine exposure</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2018-02</date><risdate>2018</risdate><volume>119</volume><issue>2</issue><spage>2345</spage><epage>2355</epage><pages>2345-2355</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Long‐term use of methamphetamine (MA) causes a broad range of cognitive deficits. Recently, it has been reported insulin signaling and mitochondrial biogenesis are involved in cognitive processes. This study aimed to examine whether MA induces cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions and also intranasal (IN) insulin treatment can reverse cognitive deficits caused by MA. Rats were repeatedly treated with increasing doses of MA (1‐10 mg/kg) twice a day for 10 days, and their cognitive functions were assessed using Y‐maze, novel object recognition and passive avoidance tasks. The expression of components involved in insulin signaling (IR/IRS2/PI3K/Akt/GSK3β) and mitochondrial biogenesis (PGC‐1α, NRF1, and TFAM) was measured in the hippocampus. Therapeutic effects of IN insulin delivery (0.5 IU/day, for 7 days after MA discontinuation) were also investigated in MA‐treated animals. Our results showed that repeated MA exposure induced cognitive deficits, and led to insulin signaling impairment and mitochondrial dysfunction. Interestingly, IN insulin treatment reduced MA‐induced cognitive impairments possibly through activating insulin signaling, particularly PI3K/Akt/GSK3β pathway, and mitochondrial biogenesis. Thus, insulin and insulin signaling pathway can be considered as useful targets for the treatment of abnormalities associated with MA abuse.
Repeated methamphetamine exposure induced cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions. Intranasal insulin treatment alleviated MA‐induced cognitive deficits, insulin signaling impairment, and mitochondrial dysfunctions.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28884876</pmid><doi>10.1002/jcb.26398</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-7777-5435</orcidid><orcidid>https://orcid.org/0000-0002-6668-2302</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Abnormalities Administration, Intranasal AKT protein Amphetamine-Related Disorders - complications Amphetamine-Related Disorders - genetics Amphetamine-Related Disorders - metabolism Animals Biosynthesis cognition Cognition Disorders - chemically induced Cognition Disorders - drug therapy Cognition Disorders - genetics Cognition Disorders - metabolism Cognitive ability Disease Models, Animal Exposure Gene Expression Regulation - drug effects Gene Regulatory Networks - drug effects Glucose Growth hormones Impairment Insulin Insulin - administration & dosage Insulin - pharmacology insulin signaling Male Memory, Short-Term - drug effects Methamphetamine Methamphetamine - toxicity Mitochondria Mitochondria - drug effects mitochondrial biogenesis Object recognition Pattern recognition Rats Rats, Wistar Signal transduction Signal Transduction - drug effects Signaling |
| title | Intranasal insulin treatment restores cognitive deficits and insulin signaling impairment induced by repeated methamphetamine exposure |
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