Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat
Although electroconvulsive therapy (ECT) is regarded as one of the efficient treatments for intractable psychiatric disorders, the mechanism of therapeutic action remains unclear. Recently, many studies indicate that ECT affects the immune-related cells, such as microglia, astrocytes, and lymphocyte...
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| Veröffentlicht in: | Journal of neuroinflammation 2016-09, Vol.13 (1), p.230-230, Article 230 |
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| creator | Limoa, Erlyn Hashioka, Sadayuki Miyaoka, Tsuyoshi Tsuchie, Keiko Arauchi, Ryosuke Azis, Ilhamuddin A Wake, Rei Hayashida, Maiko Araki, Tomoko Furuya, Motohide Liaury, Kristian Tanra, Andi J Horiguchi, Jun |
| description | Although electroconvulsive therapy (ECT) is regarded as one of the efficient treatments for intractable psychiatric disorders, the mechanism of therapeutic action remains unclear. Recently, many studies indicate that ECT affects the immune-related cells, such as microglia, astrocytes, and lymphocytes. Moreover, microglial activation and astrocytic activation have been implicated in the postmortem brains of schizophrenia patients. We previously demonstrated that Gunn rats showed schizophrenia-like behavior and microglial activation in their brains. The present study examined the effects of electroconvulsive shock (ECS), an animal counterpart of ECT, on schizophrenia-like behavior, microgliosis, and astrogliosis in the brain of Gunn rats.
The rats were divided into four groups, i.e., Wistar sham, Wistar ECS, Gunn sham, and Gunn ECS. ECS groups received ECS once daily for six consecutive days. Subsequently, prepulse inhibition (PPI) test was performed, and immunohistochemistry analysis was carried out to determine the activation degree of microglia and astrocytes in the hippocampus by using anti-CD11b and anti-glial fibrillary acidic protein (GFAP) antibody, respectively.
We found PPI deficit in Gunn rats compared to Wistar rats, and it was significantly improved by ECS. Immunohistochemistry analysis revealed that immunoreactivity of CD11b and GFAP was significantly increased in Gunn rats compared to Wistar rats. ECS significantly attenuated the immunoreactivity of both CD11b and GFAP in Gunn rats.
ECS ameliorated schizophrenia-like behavior of Gunn rats and attenuated microgliosis and astrogliosis in the hippocampus of Gunn rats. Accordingly, therapeutic effects of ECT may be exerted, at least in part, by inhibition of glial activation. These results may provide crucial information to elucidate the role of activated glia in the pathogenesis of schizophrenia and to determine whether future therapeutic interventions should attempt to up-regulate or down-regulate glial functions. |
| doi_str_mv | 10.1186/s12974-016-0688-2 |
| format | Article |
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The rats were divided into four groups, i.e., Wistar sham, Wistar ECS, Gunn sham, and Gunn ECS. ECS groups received ECS once daily for six consecutive days. Subsequently, prepulse inhibition (PPI) test was performed, and immunohistochemistry analysis was carried out to determine the activation degree of microglia and astrocytes in the hippocampus by using anti-CD11b and anti-glial fibrillary acidic protein (GFAP) antibody, respectively.
We found PPI deficit in Gunn rats compared to Wistar rats, and it was significantly improved by ECS. Immunohistochemistry analysis revealed that immunoreactivity of CD11b and GFAP was significantly increased in Gunn rats compared to Wistar rats. ECS significantly attenuated the immunoreactivity of both CD11b and GFAP in Gunn rats.
ECS ameliorated schizophrenia-like behavior of Gunn rats and attenuated microgliosis and astrogliosis in the hippocampus of Gunn rats. Accordingly, therapeutic effects of ECT may be exerted, at least in part, by inhibition of glial activation. These results may provide crucial information to elucidate the role of activated glia in the pathogenesis of schizophrenia and to determine whether future therapeutic interventions should attempt to up-regulate or down-regulate glial functions.</description><identifier>ISSN: 1742-2094</identifier><identifier>EISSN: 1742-2094</identifier><identifier>DOI: 10.1186/s12974-016-0688-2</identifier><identifier>PMID: 27590010</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Acoustic Stimulation ; Analysis ; Animals ; Astrocytes - pathology ; Astrocytes - physiology ; Astrocytoma ; Care and treatment ; CD11b Antigen - metabolism ; Disease Models, Animal ; Electroshock ; Glial Fibrillary Acidic Protein - metabolism ; Gliosis - etiology ; Gliosis - therapy ; Hearing Disorders - genetics ; Hippocampus - pathology ; Immunohistochemistry ; Male ; Microglia - pathology ; Prepulse Inhibition - physiology ; Psychoacoustics ; Rats ; Rats, Gunn ; Rats, Wistar ; Schizophrenia ; Schizophrenia - complications ; Schizophrenia - genetics ; Schizophrenia - pathology</subject><ispartof>Journal of neuroinflammation, 2016-09, Vol.13 (1), p.230-230, Article 230</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c604t-3b7b9323ad8aaa11a543ca8716c44dfdab90f804a67c3a4045fe53367b260fbc3</citedby><cites>FETCH-LOGICAL-c604t-3b7b9323ad8aaa11a543ca8716c44dfdab90f804a67c3a4045fe53367b260fbc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5009533/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5009533/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27590010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Limoa, Erlyn</creatorcontrib><creatorcontrib>Hashioka, Sadayuki</creatorcontrib><creatorcontrib>Miyaoka, Tsuyoshi</creatorcontrib><creatorcontrib>Tsuchie, Keiko</creatorcontrib><creatorcontrib>Arauchi, Ryosuke</creatorcontrib><creatorcontrib>Azis, Ilhamuddin A</creatorcontrib><creatorcontrib>Wake, Rei</creatorcontrib><creatorcontrib>Hayashida, Maiko</creatorcontrib><creatorcontrib>Araki, Tomoko</creatorcontrib><creatorcontrib>Furuya, Motohide</creatorcontrib><creatorcontrib>Liaury, Kristian</creatorcontrib><creatorcontrib>Tanra, Andi J</creatorcontrib><creatorcontrib>Horiguchi, Jun</creatorcontrib><title>Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat</title><title>Journal of neuroinflammation</title><addtitle>J Neuroinflammation</addtitle><description>Although electroconvulsive therapy (ECT) is regarded as one of the efficient treatments for intractable psychiatric disorders, the mechanism of therapeutic action remains unclear. Recently, many studies indicate that ECT affects the immune-related cells, such as microglia, astrocytes, and lymphocytes. Moreover, microglial activation and astrocytic activation have been implicated in the postmortem brains of schizophrenia patients. We previously demonstrated that Gunn rats showed schizophrenia-like behavior and microglial activation in their brains. The present study examined the effects of electroconvulsive shock (ECS), an animal counterpart of ECT, on schizophrenia-like behavior, microgliosis, and astrogliosis in the brain of Gunn rats.
The rats were divided into four groups, i.e., Wistar sham, Wistar ECS, Gunn sham, and Gunn ECS. ECS groups received ECS once daily for six consecutive days. Subsequently, prepulse inhibition (PPI) test was performed, and immunohistochemistry analysis was carried out to determine the activation degree of microglia and astrocytes in the hippocampus by using anti-CD11b and anti-glial fibrillary acidic protein (GFAP) antibody, respectively.
We found PPI deficit in Gunn rats compared to Wistar rats, and it was significantly improved by ECS. Immunohistochemistry analysis revealed that immunoreactivity of CD11b and GFAP was significantly increased in Gunn rats compared to Wistar rats. ECS significantly attenuated the immunoreactivity of both CD11b and GFAP in Gunn rats.
ECS ameliorated schizophrenia-like behavior of Gunn rats and attenuated microgliosis and astrogliosis in the hippocampus of Gunn rats. Accordingly, therapeutic effects of ECT may be exerted, at least in part, by inhibition of glial activation. These results may provide crucial information to elucidate the role of activated glia in the pathogenesis of schizophrenia and to determine whether future therapeutic interventions should attempt to up-regulate or down-regulate glial functions.</description><subject>Acoustic Stimulation</subject><subject>Analysis</subject><subject>Animals</subject><subject>Astrocytes - pathology</subject><subject>Astrocytes - physiology</subject><subject>Astrocytoma</subject><subject>Care and treatment</subject><subject>CD11b Antigen - metabolism</subject><subject>Disease Models, Animal</subject><subject>Electroshock</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Gliosis - etiology</subject><subject>Gliosis - therapy</subject><subject>Hearing Disorders - genetics</subject><subject>Hippocampus - pathology</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Microglia - pathology</subject><subject>Prepulse Inhibition - physiology</subject><subject>Psychoacoustics</subject><subject>Rats</subject><subject>Rats, Gunn</subject><subject>Rats, Wistar</subject><subject>Schizophrenia</subject><subject>Schizophrenia - complications</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenia - pathology</subject><issn>1742-2094</issn><issn>1742-2094</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNptks1u1DAUhSMEoqXwAGyQJTZsUvxvZ4NUVW1BqsQG1taN40zcJnawk5HgFXjpepihPwh5Yev6O8e6vqeq3hJ8SoiWHzOhjeI1JrLGUuuaPquOieK0prjhzx-dj6pXOd9gzKiQ9GV1RJVoMCb4uPp9MTq7pGhj2K5j9luH8hDtLYJlcWGFxXVo8jbFzehj9hlB6BDk5aHgA1oGhwY_z9HCNK8HZnIFSH8Msh38rzgPyQUP9ehvHWrdANtyj2KPrtYQUCFfVy96GLN7c9hPqu-XF9_OP9fXX6--nJ9d11ZivtSsVW3DKINOAwAhIDizoBWRlvOu76BtcK8xB6ksA4656J1gTKqWSty3lp1Un_a-89pOrrMuLAlGMyc_QfppInjz9Cb4wWzi1giMm-JUDD4cDFL8sbq8mMln68YRgotrNkQTJYRmmhf0_T_oTVxTKO0ViopGaSzVA7WB0Rkf-ljetTtTc8alFLJMqynU6X-osjpXRhSD632pPxGQvaDML-fk-vseCTa7BJl9gkxJkNklyNCieff4c-4VfyPD7gBFMMSI</recordid><startdate>20160902</startdate><enddate>20160902</enddate><creator>Limoa, Erlyn</creator><creator>Hashioka, Sadayuki</creator><creator>Miyaoka, Tsuyoshi</creator><creator>Tsuchie, Keiko</creator><creator>Arauchi, Ryosuke</creator><creator>Azis, Ilhamuddin A</creator><creator>Wake, Rei</creator><creator>Hayashida, Maiko</creator><creator>Araki, Tomoko</creator><creator>Furuya, Motohide</creator><creator>Liaury, Kristian</creator><creator>Tanra, Andi J</creator><creator>Horiguchi, Jun</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160902</creationdate><title>Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat</title><author>Limoa, Erlyn ; Hashioka, Sadayuki ; Miyaoka, Tsuyoshi ; Tsuchie, Keiko ; Arauchi, Ryosuke ; Azis, Ilhamuddin A ; Wake, Rei ; Hayashida, Maiko ; Araki, Tomoko ; Furuya, Motohide ; Liaury, Kristian ; Tanra, Andi J ; Horiguchi, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c604t-3b7b9323ad8aaa11a543ca8716c44dfdab90f804a67c3a4045fe53367b260fbc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acoustic Stimulation</topic><topic>Analysis</topic><topic>Animals</topic><topic>Astrocytes - pathology</topic><topic>Astrocytes - physiology</topic><topic>Astrocytoma</topic><topic>Care and treatment</topic><topic>CD11b Antigen - metabolism</topic><topic>Disease Models, Animal</topic><topic>Electroshock</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Gliosis - etiology</topic><topic>Gliosis - therapy</topic><topic>Hearing Disorders - genetics</topic><topic>Hippocampus - pathology</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Microglia - pathology</topic><topic>Prepulse Inhibition - physiology</topic><topic>Psychoacoustics</topic><topic>Rats</topic><topic>Rats, Gunn</topic><topic>Rats, Wistar</topic><topic>Schizophrenia</topic><topic>Schizophrenia - complications</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenia - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Limoa, Erlyn</creatorcontrib><creatorcontrib>Hashioka, Sadayuki</creatorcontrib><creatorcontrib>Miyaoka, Tsuyoshi</creatorcontrib><creatorcontrib>Tsuchie, Keiko</creatorcontrib><creatorcontrib>Arauchi, Ryosuke</creatorcontrib><creatorcontrib>Azis, Ilhamuddin A</creatorcontrib><creatorcontrib>Wake, Rei</creatorcontrib><creatorcontrib>Hayashida, Maiko</creatorcontrib><creatorcontrib>Araki, Tomoko</creatorcontrib><creatorcontrib>Furuya, Motohide</creatorcontrib><creatorcontrib>Liaury, Kristian</creatorcontrib><creatorcontrib>Tanra, Andi J</creatorcontrib><creatorcontrib>Horiguchi, Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuroinflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Limoa, Erlyn</au><au>Hashioka, Sadayuki</au><au>Miyaoka, Tsuyoshi</au><au>Tsuchie, Keiko</au><au>Arauchi, Ryosuke</au><au>Azis, Ilhamuddin A</au><au>Wake, Rei</au><au>Hayashida, Maiko</au><au>Araki, Tomoko</au><au>Furuya, Motohide</au><au>Liaury, Kristian</au><au>Tanra, Andi J</au><au>Horiguchi, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat</atitle><jtitle>Journal of neuroinflammation</jtitle><addtitle>J Neuroinflammation</addtitle><date>2016-09-02</date><risdate>2016</risdate><volume>13</volume><issue>1</issue><spage>230</spage><epage>230</epage><pages>230-230</pages><artnum>230</artnum><issn>1742-2094</issn><eissn>1742-2094</eissn><abstract>Although electroconvulsive therapy (ECT) is regarded as one of the efficient treatments for intractable psychiatric disorders, the mechanism of therapeutic action remains unclear. Recently, many studies indicate that ECT affects the immune-related cells, such as microglia, astrocytes, and lymphocytes. Moreover, microglial activation and astrocytic activation have been implicated in the postmortem brains of schizophrenia patients. We previously demonstrated that Gunn rats showed schizophrenia-like behavior and microglial activation in their brains. The present study examined the effects of electroconvulsive shock (ECS), an animal counterpart of ECT, on schizophrenia-like behavior, microgliosis, and astrogliosis in the brain of Gunn rats.
The rats were divided into four groups, i.e., Wistar sham, Wistar ECS, Gunn sham, and Gunn ECS. ECS groups received ECS once daily for six consecutive days. Subsequently, prepulse inhibition (PPI) test was performed, and immunohistochemistry analysis was carried out to determine the activation degree of microglia and astrocytes in the hippocampus by using anti-CD11b and anti-glial fibrillary acidic protein (GFAP) antibody, respectively.
We found PPI deficit in Gunn rats compared to Wistar rats, and it was significantly improved by ECS. Immunohistochemistry analysis revealed that immunoreactivity of CD11b and GFAP was significantly increased in Gunn rats compared to Wistar rats. ECS significantly attenuated the immunoreactivity of both CD11b and GFAP in Gunn rats.
ECS ameliorated schizophrenia-like behavior of Gunn rats and attenuated microgliosis and astrogliosis in the hippocampus of Gunn rats. Accordingly, therapeutic effects of ECT may be exerted, at least in part, by inhibition of glial activation. These results may provide crucial information to elucidate the role of activated glia in the pathogenesis of schizophrenia and to determine whether future therapeutic interventions should attempt to up-regulate or down-regulate glial functions.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27590010</pmid><doi>10.1186/s12974-016-0688-2</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acoustic Stimulation Analysis Animals Astrocytes - pathology Astrocytes - physiology Astrocytoma Care and treatment CD11b Antigen - metabolism Disease Models, Animal Electroshock Glial Fibrillary Acidic Protein - metabolism Gliosis - etiology Gliosis - therapy Hearing Disorders - genetics Hippocampus - pathology Immunohistochemistry Male Microglia - pathology Prepulse Inhibition - physiology Psychoacoustics Rats Rats, Gunn Rats, Wistar Schizophrenia Schizophrenia - complications Schizophrenia - genetics Schizophrenia - pathology |
| title | Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat |
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