Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model
Background: Hypoxic brain injury is a condition caused by restricted oxygen supply to the brain. Several studies have reported cognitive decline, particularly in spatial memory, after exposure to intermittent hypoxia (IH). However, the effect and mechanism of action of IH exposure on cognition have...
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| Veröffentlicht in: | Genes 2022-10, Vol.13 (10), p.1824 |
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| description | Background: Hypoxic brain injury is a condition caused by restricted oxygen supply to the brain. Several studies have reported cognitive decline, particularly in spatial memory, after exposure to intermittent hypoxia (IH). However, the effect and mechanism of action of IH exposure on cognition have not been evaluated by analyzing gene expression after transcranial direct current stimulation (tDCS). Hence, the purpose of this study was to investigate the effects of tDCS on gene regulation and cognition in a rat model of IH-induced brain injury. Methods: Twenty-four 10-week-old male Sprague−Dawley rats were divided into two groups: IH exposed rats with no stimulation and IH-exposed rats that received tDCS. All rats were exposed to a hypoxic chamber containing 10% oxygen for twelve hours a day for five days. The stimulation group received tDCS at an intensity of 200 µA over the frontal bregma areas for 30 min each day for a week. As a behavior test, the escape latency on the Morris water maze (MWM) test was measured to assess spatial memory before and after stimulation. After seven days of stimulation, gene microarray analysis was conducted with a KEGG mapper tool. Results: Although there were no significant differences between the groups before and after stimulation, there was a significant effect of time and a significant time × group interaction on escape latency. In the microarray analysis, significant fold changes in 12 genes related to neurogenesis were found in the stimulation group after tDCS (p < 0.05, fold change > 2 times, the average of the normalized read count (RC) > 6 times). The highly upregulated genes in the stimulation group after tDCS were SOS, Raf, PI3K, Rac1, IRAK, and Bax. The highly downregulated genes in the stimulation group after tDCS were CHK, Crk, Rap1, p38, Ras, and NF-kB. Conclusion: In this study, we confirmed that SOS, Raf, PI3K, Rac1, IRAK, and Bax were upregulated and that CHK, Crk, Rap1, p38, Ras, and NF-kB were downregulated in a rat model of IH-induced brain injury after application of tDCS. |
| doi_str_mv | 10.3390/genes13101824 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9601999</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A745723218</galeid><sourcerecordid>A745723218</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-bd659f55a59d19bdc7f5de5f0a778bc9ec776d9ff258ac939673e7604b1b8b73</originalsourceid><addsrcrecordid>eNptkk1v3CAQhq2oURIlOfZaIfXSi1M-jDGXSum2TSKlqrTNHWE8uKxs2GJcdf99cb6arQoH4J1nXhg0RfGa4AvGJH7fg4eJMIJJQ6uD4oRiwcqqovzVi_1xcT5NG5xHhSnG_Kg4ZjWVVGB5UsAa-nnQyQWPgkVXiyFaQ1agQymgVei9u49qmyCi9Gn1Hbl88ujGZ2F0KYFP6Hq3Db-dQR-jdktoM8cdWuuEvoYOhrPi0OphgvPH9bS4-_L5bnVd3n67ulld3pamIjSVbVdzaTnXXHZEtp0RlnfALdZCNK2RYISoO2kt5Y02kslaMBA1rlrSNq1gp8WHB9vt3I7QmfywqAe1jW7UcaeCdmo_4t0P1YdfStaYSCmzwbtHgxh-zjAlNbrJwDBoD2GeFBVUctpUgmX07T_oJszR5-oWKiOC8-ov1esBlPM25HvNYqouRcUFZZQ0mbr4D5VnB6MzwYN1Wd9LKB8STAzTFME-10iwWjpD7XVG5t-8_Jhn-qkP2B_89bOc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2728477554</pqid></control><display><type>article</type><title>Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Lee, Jin-Won ; Jeong, Won-Hyeong ; Kim, Eun-Jong ; Choi, Insung ; Song, Min-Keun</creator><creatorcontrib>Lee, Jin-Won ; Jeong, Won-Hyeong ; Kim, Eun-Jong ; Choi, Insung ; Song, Min-Keun</creatorcontrib><description>Background: Hypoxic brain injury is a condition caused by restricted oxygen supply to the brain. Several studies have reported cognitive decline, particularly in spatial memory, after exposure to intermittent hypoxia (IH). However, the effect and mechanism of action of IH exposure on cognition have not been evaluated by analyzing gene expression after transcranial direct current stimulation (tDCS). Hence, the purpose of this study was to investigate the effects of tDCS on gene regulation and cognition in a rat model of IH-induced brain injury. Methods: Twenty-four 10-week-old male Sprague−Dawley rats were divided into two groups: IH exposed rats with no stimulation and IH-exposed rats that received tDCS. All rats were exposed to a hypoxic chamber containing 10% oxygen for twelve hours a day for five days. The stimulation group received tDCS at an intensity of 200 µA over the frontal bregma areas for 30 min each day for a week. As a behavior test, the escape latency on the Morris water maze (MWM) test was measured to assess spatial memory before and after stimulation. After seven days of stimulation, gene microarray analysis was conducted with a KEGG mapper tool. Results: Although there were no significant differences between the groups before and after stimulation, there was a significant effect of time and a significant time × group interaction on escape latency. In the microarray analysis, significant fold changes in 12 genes related to neurogenesis were found in the stimulation group after tDCS (p < 0.05, fold change > 2 times, the average of the normalized read count (RC) > 6 times). The highly upregulated genes in the stimulation group after tDCS were SOS, Raf, PI3K, Rac1, IRAK, and Bax. The highly downregulated genes in the stimulation group after tDCS were CHK, Crk, Rap1, p38, Ras, and NF-kB. Conclusion: In this study, we confirmed that SOS, Raf, PI3K, Rac1, IRAK, and Bax were upregulated and that CHK, Crk, Rap1, p38, Ras, and NF-kB were downregulated in a rat model of IH-induced brain injury after application of tDCS.</description><identifier>ISSN: 2073-4425</identifier><identifier>EISSN: 2073-4425</identifier><identifier>DOI: 10.3390/genes13101824</identifier><identifier>PMID: 36292709</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>1-Phosphatidylinositol 3-kinase ; Analysis ; Animal cognition ; Animal experimentation ; Animals ; bcl-2-Associated X Protein ; Brain ; Brain Injuries ; Brain injury ; Cognition ; Cognitive ability ; DNA microarrays ; Electric stimulation ; Electrical stimulation of the brain ; ESB ; Escape behavior ; Gene expression ; Gene regulation ; Genomes ; Hypoxia ; Hypoxia - genetics ; Injuries ; Latency ; Male ; Memory ; Methods ; Mice ; Neurogenesis ; NF-kappa B ; NF-κB protein ; Oxygen ; Phosphatidylinositol 3-Kinases ; Rac1 protein ; Rap1 protein ; Rats ; Rats, Sprague-Dawley ; Rodents ; Spatial memory ; Testing ; Transcranial Direct Current Stimulation ; Traumatic brain injury</subject><ispartof>Genes, 2022-10, Vol.13 (10), p.1824</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-bd659f55a59d19bdc7f5de5f0a778bc9ec776d9ff258ac939673e7604b1b8b73</citedby><cites>FETCH-LOGICAL-c412t-bd659f55a59d19bdc7f5de5f0a778bc9ec776d9ff258ac939673e7604b1b8b73</cites><orcidid>0000-0002-7775-8392 ; 0000-0001-8186-5345 ; 0000-0001-9527-9320</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9601999/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9601999/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36292709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Jin-Won</creatorcontrib><creatorcontrib>Jeong, Won-Hyeong</creatorcontrib><creatorcontrib>Kim, Eun-Jong</creatorcontrib><creatorcontrib>Choi, Insung</creatorcontrib><creatorcontrib>Song, Min-Keun</creatorcontrib><title>Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model</title><title>Genes</title><addtitle>Genes (Basel)</addtitle><description>Background: Hypoxic brain injury is a condition caused by restricted oxygen supply to the brain. Several studies have reported cognitive decline, particularly in spatial memory, after exposure to intermittent hypoxia (IH). However, the effect and mechanism of action of IH exposure on cognition have not been evaluated by analyzing gene expression after transcranial direct current stimulation (tDCS). Hence, the purpose of this study was to investigate the effects of tDCS on gene regulation and cognition in a rat model of IH-induced brain injury. Methods: Twenty-four 10-week-old male Sprague−Dawley rats were divided into two groups: IH exposed rats with no stimulation and IH-exposed rats that received tDCS. All rats were exposed to a hypoxic chamber containing 10% oxygen for twelve hours a day for five days. The stimulation group received tDCS at an intensity of 200 µA over the frontal bregma areas for 30 min each day for a week. As a behavior test, the escape latency on the Morris water maze (MWM) test was measured to assess spatial memory before and after stimulation. After seven days of stimulation, gene microarray analysis was conducted with a KEGG mapper tool. Results: Although there were no significant differences between the groups before and after stimulation, there was a significant effect of time and a significant time × group interaction on escape latency. In the microarray analysis, significant fold changes in 12 genes related to neurogenesis were found in the stimulation group after tDCS (p < 0.05, fold change > 2 times, the average of the normalized read count (RC) > 6 times). The highly upregulated genes in the stimulation group after tDCS were SOS, Raf, PI3K, Rac1, IRAK, and Bax. The highly downregulated genes in the stimulation group after tDCS were CHK, Crk, Rap1, p38, Ras, and NF-kB. Conclusion: In this study, we confirmed that SOS, Raf, PI3K, Rac1, IRAK, and Bax were upregulated and that CHK, Crk, Rap1, p38, Ras, and NF-kB were downregulated in a rat model of IH-induced brain injury after application of tDCS.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Analysis</subject><subject>Animal cognition</subject><subject>Animal experimentation</subject><subject>Animals</subject><subject>bcl-2-Associated X Protein</subject><subject>Brain</subject><subject>Brain Injuries</subject><subject>Brain injury</subject><subject>Cognition</subject><subject>Cognitive ability</subject><subject>DNA microarrays</subject><subject>Electric stimulation</subject><subject>Electrical stimulation of the brain</subject><subject>ESB</subject><subject>Escape behavior</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Genomes</subject><subject>Hypoxia</subject><subject>Hypoxia - genetics</subject><subject>Injuries</subject><subject>Latency</subject><subject>Male</subject><subject>Memory</subject><subject>Methods</subject><subject>Mice</subject><subject>Neurogenesis</subject><subject>NF-kappa B</subject><subject>NF-κB protein</subject><subject>Oxygen</subject><subject>Phosphatidylinositol 3-Kinases</subject><subject>Rac1 protein</subject><subject>Rap1 protein</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Spatial memory</subject><subject>Testing</subject><subject>Transcranial Direct Current Stimulation</subject><subject>Traumatic brain injury</subject><issn>2073-4425</issn><issn>2073-4425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkk1v3CAQhq2oURIlOfZaIfXSi1M-jDGXSum2TSKlqrTNHWE8uKxs2GJcdf99cb6arQoH4J1nXhg0RfGa4AvGJH7fg4eJMIJJQ6uD4oRiwcqqovzVi_1xcT5NG5xHhSnG_Kg4ZjWVVGB5UsAa-nnQyQWPgkVXiyFaQ1agQymgVei9u49qmyCi9Gn1Hbl88ujGZ2F0KYFP6Hq3Db-dQR-jdktoM8cdWuuEvoYOhrPi0OphgvPH9bS4-_L5bnVd3n67ulld3pamIjSVbVdzaTnXXHZEtp0RlnfALdZCNK2RYISoO2kt5Y02kslaMBA1rlrSNq1gp8WHB9vt3I7QmfywqAe1jW7UcaeCdmo_4t0P1YdfStaYSCmzwbtHgxh-zjAlNbrJwDBoD2GeFBVUctpUgmX07T_oJszR5-oWKiOC8-ov1esBlPM25HvNYqouRcUFZZQ0mbr4D5VnB6MzwYN1Wd9LKB8STAzTFME-10iwWjpD7XVG5t-8_Jhn-qkP2B_89bOc</recordid><startdate>20221009</startdate><enddate>20221009</enddate><creator>Lee, Jin-Won</creator><creator>Jeong, Won-Hyeong</creator><creator>Kim, Eun-Jong</creator><creator>Choi, Insung</creator><creator>Song, Min-Keun</creator><general>MDPI AG</general><general>MDPI</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>8FD</scope><scope>8FE</scope><scope>8FH</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>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7775-8392</orcidid><orcidid>https://orcid.org/0000-0001-8186-5345</orcidid><orcidid>https://orcid.org/0000-0001-9527-9320</orcidid></search><sort><creationdate>20221009</creationdate><title>Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model</title><author>Lee, Jin-Won ; Jeong, Won-Hyeong ; Kim, Eun-Jong ; Choi, Insung ; Song, Min-Keun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-bd659f55a59d19bdc7f5de5f0a778bc9ec776d9ff258ac939673e7604b1b8b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Analysis</topic><topic>Animal cognition</topic><topic>Animal experimentation</topic><topic>Animals</topic><topic>bcl-2-Associated X Protein</topic><topic>Brain</topic><topic>Brain Injuries</topic><topic>Brain injury</topic><topic>Cognition</topic><topic>Cognitive ability</topic><topic>DNA microarrays</topic><topic>Electric stimulation</topic><topic>Electrical stimulation of the brain</topic><topic>ESB</topic><topic>Escape behavior</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Genomes</topic><topic>Hypoxia</topic><topic>Hypoxia - genetics</topic><topic>Injuries</topic><topic>Latency</topic><topic>Male</topic><topic>Memory</topic><topic>Methods</topic><topic>Mice</topic><topic>Neurogenesis</topic><topic>NF-kappa B</topic><topic>NF-κB protein</topic><topic>Oxygen</topic><topic>Phosphatidylinositol 3-Kinases</topic><topic>Rac1 protein</topic><topic>Rap1 protein</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Spatial memory</topic><topic>Testing</topic><topic>Transcranial Direct Current Stimulation</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jin-Won</creatorcontrib><creatorcontrib>Jeong, Won-Hyeong</creatorcontrib><creatorcontrib>Kim, Eun-Jong</creatorcontrib><creatorcontrib>Choi, Insung</creatorcontrib><creatorcontrib>Song, Min-Keun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Jin-Won</au><au>Jeong, Won-Hyeong</au><au>Kim, Eun-Jong</au><au>Choi, Insung</au><au>Song, Min-Keun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model</atitle><jtitle>Genes</jtitle><addtitle>Genes (Basel)</addtitle><date>2022-10-09</date><risdate>2022</risdate><volume>13</volume><issue>10</issue><spage>1824</spage><pages>1824-</pages><issn>2073-4425</issn><eissn>2073-4425</eissn><abstract>Background: Hypoxic brain injury is a condition caused by restricted oxygen supply to the brain. Several studies have reported cognitive decline, particularly in spatial memory, after exposure to intermittent hypoxia (IH). However, the effect and mechanism of action of IH exposure on cognition have not been evaluated by analyzing gene expression after transcranial direct current stimulation (tDCS). Hence, the purpose of this study was to investigate the effects of tDCS on gene regulation and cognition in a rat model of IH-induced brain injury. Methods: Twenty-four 10-week-old male Sprague−Dawley rats were divided into two groups: IH exposed rats with no stimulation and IH-exposed rats that received tDCS. All rats were exposed to a hypoxic chamber containing 10% oxygen for twelve hours a day for five days. The stimulation group received tDCS at an intensity of 200 µA over the frontal bregma areas for 30 min each day for a week. As a behavior test, the escape latency on the Morris water maze (MWM) test was measured to assess spatial memory before and after stimulation. After seven days of stimulation, gene microarray analysis was conducted with a KEGG mapper tool. Results: Although there were no significant differences between the groups before and after stimulation, there was a significant effect of time and a significant time × group interaction on escape latency. In the microarray analysis, significant fold changes in 12 genes related to neurogenesis were found in the stimulation group after tDCS (p < 0.05, fold change > 2 times, the average of the normalized read count (RC) > 6 times). The highly upregulated genes in the stimulation group after tDCS were SOS, Raf, PI3K, Rac1, IRAK, and Bax. The highly downregulated genes in the stimulation group after tDCS were CHK, Crk, Rap1, p38, Ras, and NF-kB. Conclusion: In this study, we confirmed that SOS, Raf, PI3K, Rac1, IRAK, and Bax were upregulated and that CHK, Crk, Rap1, p38, Ras, and NF-kB were downregulated in a rat model of IH-induced brain injury after application of tDCS.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36292709</pmid><doi>10.3390/genes13101824</doi><orcidid>https://orcid.org/0000-0002-7775-8392</orcidid><orcidid>https://orcid.org/0000-0001-8186-5345</orcidid><orcidid>https://orcid.org/0000-0001-9527-9320</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Analysis Animal cognition Animal experimentation Animals bcl-2-Associated X Protein Brain Brain Injuries Brain injury Cognition Cognitive ability DNA microarrays Electric stimulation Electrical stimulation of the brain ESB Escape behavior Gene expression Gene regulation Genomes Hypoxia Hypoxia - genetics Injuries Latency Male Memory Methods Mice Neurogenesis NF-kappa B NF-κB protein Oxygen Phosphatidylinositol 3-Kinases Rac1 protein Rap1 protein Rats Rats, Sprague-Dawley Rodents Spatial memory Testing Transcranial Direct Current Stimulation Traumatic brain injury |
| title | Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model |
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