In vivo MRS and histochemistry of status epilepticus-induced hippocampal pathology in a juvenile model of temporal lobe epilepsy
Childhood status epilepticus (SE) initiates an epileptogenic process that leads to spontaneous seizures and hippocampal pathology characterized by neuronal loss, gliosis and an imbalance between excitatory and inhibitory neurotransmission. It remains unclear whether these changes are a cause or cons...
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| creator | van der Hel, W. Saskia van Eijsden, Pieter Bos, Ineke W. M. de Graaf, Robin A. Behar, Kevin L. van Nieuwenhuizen, Onno de Graan, Pierre N. E. Braun, Kees P. J. |
| description | Childhood status epilepticus (SE) initiates an epileptogenic process that leads to spontaneous seizures and hippocampal pathology characterized by neuronal loss, gliosis and an imbalance between excitatory and inhibitory neurotransmission. It remains unclear whether these changes are a cause or consequence of chronic epilepsy. In this study, in vivo MRS was used in a post‐SE juvenile rat model of temporal lobe epilepsy (TLE) to establish the temporal evolution of hippocampal injury and neurotransmitter imbalance. SE was induced in P21 rats by injection of lithium and pilocarpine. Four and eight weeks after SE, in vivo 1H and γ‐aminobutyric acid (GABA)‐edited MRS of the hippocampus was performed in combination with dedicated ex vivo immunohistochemistry for the interpretation and validation of MRS findings. MRS showed a 12% decrease (p |
| doi_str_mv | 10.1002/nbm.2828 |
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In this study, in vivo MRS was used in a juvenile rat model of temporal lobe epilepsy to establish the evolution of status epilepticus‐induced hippocampal injury and neurotransmitter imbalance. In vivo MRS showed gliosis and (predominantly γ‐aminobutyric acid‐ergic) neuronal loss, confirmed by histology. Furthermore, an increase in glutamine was detected, accompanied by a decrease in glutamine synthase immunoreactivity and the normalization of glutamine levels. These changes occurred before spontaneous seizures were present, but created a hyperexcitable state, which may play a role in the facilitation of these seizures.]]></description><identifier>ISSN: 0952-3480</identifier><identifier>EISSN: 1099-1492</identifier><identifier>DOI: 10.1002/nbm.2828</identifier><identifier>PMID: 22806932</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Biomarkers - metabolism ; Children ; Choline - metabolism ; Epilepsy, Temporal Lobe - metabolism ; Epilepsy, Temporal Lobe - pathology ; epileptogenesis ; gamma-Aminobutyric Acid - metabolism ; Glutamine - metabolism ; glutamine synthase ; Hippocampus - metabolism ; Hippocampus - pathology ; immunohistochemistry ; lithium-pilocarpine ; Magnetic Resonance Spectroscopy - methods ; Male ; MRS ; Neurons - metabolism ; Neurons - pathology ; Neurotransmitter Agents - metabolism ; postnatal day 21 ; rat ; Rats ; Rats, Wistar ; status epilepticus ; temporal lobe epilepsy</subject><ispartof>NMR in biomedicine, 2013-02, Vol.26 (2), p.132-140</ispartof><rights>Copyright © 2012 John Wiley & Sons, Ltd.</rights><rights>Copyright © 2013 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4208-abf002fc1aeb5244dc04f92b634d0310096a5bf1b955cef76bb669ca2aed56163</citedby><cites>FETCH-LOGICAL-c4208-abf002fc1aeb5244dc04f92b634d0310096a5bf1b955cef76bb669ca2aed56163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fnbm.2828$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fnbm.2828$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22806932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Hel, W. Saskia</creatorcontrib><creatorcontrib>van Eijsden, Pieter</creatorcontrib><creatorcontrib>Bos, Ineke W. M.</creatorcontrib><creatorcontrib>de Graaf, Robin A.</creatorcontrib><creatorcontrib>Behar, Kevin L.</creatorcontrib><creatorcontrib>van Nieuwenhuizen, Onno</creatorcontrib><creatorcontrib>de Graan, Pierre N. E.</creatorcontrib><creatorcontrib>Braun, Kees P. J.</creatorcontrib><title>In vivo MRS and histochemistry of status epilepticus-induced hippocampal pathology in a juvenile model of temporal lobe epilepsy</title><title>NMR in biomedicine</title><addtitle>NMR Biomed</addtitle><description><![CDATA[Childhood status epilepticus (SE) initiates an epileptogenic process that leads to spontaneous seizures and hippocampal pathology characterized by neuronal loss, gliosis and an imbalance between excitatory and inhibitory neurotransmission. It remains unclear whether these changes are a cause or consequence of chronic epilepsy. In this study, in vivo MRS was used in a post‐SE juvenile rat model of temporal lobe epilepsy (TLE) to establish the temporal evolution of hippocampal injury and neurotransmitter imbalance. SE was induced in P21 rats by injection of lithium and pilocarpine. Four and eight weeks after SE, in vivo 1H and γ‐aminobutyric acid (GABA)‐edited MRS of the hippocampus was performed in combination with dedicated ex vivo immunohistochemistry for the interpretation and validation of MRS findings. MRS showed a 12% decrease (p < 0.0001) in N‐acetylaspartate and a 15% increase (p = 0.0226) in choline‐containing compound concentrations, indicating neuronal death and gliosis, respectively. These results were confirmed by FluoroJade and vimentin staining. Furthermore, severe and progressive decreases in GABA (−41%, p < 0.001) and glutamate (Glu) (−17%, p < 0.001) were found. The specific severity of GABAergic cell death was confirmed by parvalbumin immunoreactivity (−68%, p < 0.001). Unexpectedly, we found changes in glutamine (Gln), the metabolic precursor of both GABA and Glu. Gln increased at 4 weeks (+36%, p < 0.001), but returned to control levels at 8 weeks. This decrease was consistent with the simultaneous decrease in glutamine synthase immunoreactivity (−32%, p = 0.037). In vivo MRS showed gliosis and (predominantly GABAergic) neuronal loss. In addition, an increase in Gln was detected, accompanied by a decrease in glutamine synthase immunoreactivity. This may reflect glutamine synthase downregulation in order to normalize Gln levels. These changes occurred before spontaneous recurrent seizures were present but, by creating a pre‐epileptic state, may play a role in epileptogenesis. MRS can be applied in a clinical setting and may be used as a noninvasive tool to monitor the development of TLE. Copyright © 2012 John Wiley & Sons, Ltd.
In this study, in vivo MRS was used in a juvenile rat model of temporal lobe epilepsy to establish the evolution of status epilepticus‐induced hippocampal injury and neurotransmitter imbalance. In vivo MRS showed gliosis and (predominantly γ‐aminobutyric acid‐ergic) neuronal loss, confirmed by histology. Furthermore, an increase in glutamine was detected, accompanied by a decrease in glutamine synthase immunoreactivity and the normalization of glutamine levels. These changes occurred before spontaneous seizures were present, but created a hyperexcitable state, which may play a role in the facilitation of these seizures.]]></description><subject>Animals</subject><subject>Biomarkers - metabolism</subject><subject>Children</subject><subject>Choline - metabolism</subject><subject>Epilepsy, Temporal Lobe - metabolism</subject><subject>Epilepsy, Temporal Lobe - pathology</subject><subject>epileptogenesis</subject><subject>gamma-Aminobutyric Acid - metabolism</subject><subject>Glutamine - metabolism</subject><subject>glutamine synthase</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>immunohistochemistry</subject><subject>lithium-pilocarpine</subject><subject>Magnetic Resonance Spectroscopy - methods</subject><subject>Male</subject><subject>MRS</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>postnatal day 21</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>status epilepticus</subject><subject>temporal lobe epilepsy</subject><issn>0952-3480</issn><issn>1099-1492</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAURS0EotOCxC9AltiwSfFXPPESKihFMwXBIJaW7bwwGZI42MmU7PjpOGooEhJi9TbnHenei9ATSs4pIexFZ9tzVrDiHlpRolRGhWL30YqonGVcFOQEncZ4IIQUgrOH6ISxgkjF2Qr9vOrwsT56vP34CZuuxPs6Dt7toU03TNhXOA5mGCOGvm6gH2o3xqzuytHBDPe9d6btTYN7M-x9479OuO6wwYfxCF36wK0voZk9A7S9D4lsvIVFF6dH6EFlmgiPl3uGPr95vbt4m23eX15dvNxkTjBSZMZWKWjlqAGbMyFKR0SlmJVclISnEpQ0ua2oVXnuoFpLa6VUzjADZS6p5Gfo-a23D_77CHHQKaGDpjEd-DHquTKZRJT9H2VrnhdSkBl99hd68GPoUpAklJIJmUr_I3TBxxig0n2oWxMmTYmeB9RpQD0PmNCni3C0LZR34O_FEpDdAjepv-mfIn39arsIFz7tCT_ueBO-abnm61x_ub7UO7H9IDbvdlryX3c7tGA</recordid><startdate>201302</startdate><enddate>201302</enddate><creator>van der Hel, W. 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Saskia</creatorcontrib><creatorcontrib>van Eijsden, Pieter</creatorcontrib><creatorcontrib>Bos, Ineke W. M.</creatorcontrib><creatorcontrib>de Graaf, Robin A.</creatorcontrib><creatorcontrib>Behar, Kevin L.</creatorcontrib><creatorcontrib>van Nieuwenhuizen, Onno</creatorcontrib><creatorcontrib>de Graan, Pierre N. E.</creatorcontrib><creatorcontrib>Braun, Kees P. J.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>NMR in biomedicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van der Hel, W. Saskia</au><au>van Eijsden, Pieter</au><au>Bos, Ineke W. M.</au><au>de Graaf, Robin A.</au><au>Behar, Kevin L.</au><au>van Nieuwenhuizen, Onno</au><au>de Graan, Pierre N. E.</au><au>Braun, Kees P. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vivo MRS and histochemistry of status epilepticus-induced hippocampal pathology in a juvenile model of temporal lobe epilepsy</atitle><jtitle>NMR in biomedicine</jtitle><addtitle>NMR Biomed</addtitle><date>2013-02</date><risdate>2013</risdate><volume>26</volume><issue>2</issue><spage>132</spage><epage>140</epage><pages>132-140</pages><issn>0952-3480</issn><eissn>1099-1492</eissn><abstract><![CDATA[Childhood status epilepticus (SE) initiates an epileptogenic process that leads to spontaneous seizures and hippocampal pathology characterized by neuronal loss, gliosis and an imbalance between excitatory and inhibitory neurotransmission. It remains unclear whether these changes are a cause or consequence of chronic epilepsy. In this study, in vivo MRS was used in a post‐SE juvenile rat model of temporal lobe epilepsy (TLE) to establish the temporal evolution of hippocampal injury and neurotransmitter imbalance. SE was induced in P21 rats by injection of lithium and pilocarpine. Four and eight weeks after SE, in vivo 1H and γ‐aminobutyric acid (GABA)‐edited MRS of the hippocampus was performed in combination with dedicated ex vivo immunohistochemistry for the interpretation and validation of MRS findings. MRS showed a 12% decrease (p < 0.0001) in N‐acetylaspartate and a 15% increase (p = 0.0226) in choline‐containing compound concentrations, indicating neuronal death and gliosis, respectively. These results were confirmed by FluoroJade and vimentin staining. Furthermore, severe and progressive decreases in GABA (−41%, p < 0.001) and glutamate (Glu) (−17%, p < 0.001) were found. The specific severity of GABAergic cell death was confirmed by parvalbumin immunoreactivity (−68%, p < 0.001). Unexpectedly, we found changes in glutamine (Gln), the metabolic precursor of both GABA and Glu. Gln increased at 4 weeks (+36%, p < 0.001), but returned to control levels at 8 weeks. This decrease was consistent with the simultaneous decrease in glutamine synthase immunoreactivity (−32%, p = 0.037). In vivo MRS showed gliosis and (predominantly GABAergic) neuronal loss. In addition, an increase in Gln was detected, accompanied by a decrease in glutamine synthase immunoreactivity. This may reflect glutamine synthase downregulation in order to normalize Gln levels. These changes occurred before spontaneous recurrent seizures were present but, by creating a pre‐epileptic state, may play a role in epileptogenesis. MRS can be applied in a clinical setting and may be used as a noninvasive tool to monitor the development of TLE. Copyright © 2012 John Wiley & Sons, Ltd.
In this study, in vivo MRS was used in a juvenile rat model of temporal lobe epilepsy to establish the evolution of status epilepticus‐induced hippocampal injury and neurotransmitter imbalance. In vivo MRS showed gliosis and (predominantly γ‐aminobutyric acid‐ergic) neuronal loss, confirmed by histology. Furthermore, an increase in glutamine was detected, accompanied by a decrease in glutamine synthase immunoreactivity and the normalization of glutamine levels. These changes occurred before spontaneous seizures were present, but created a hyperexcitable state, which may play a role in the facilitation of these seizures.]]></abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>22806932</pmid><doi>10.1002/nbm.2828</doi><tpages>9</tpages></addata></record> |
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| ispartof | NMR in biomedicine, 2013-02, Vol.26 (2), p.132-140 |
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| subjects | Animals Biomarkers - metabolism Children Choline - metabolism Epilepsy, Temporal Lobe - metabolism Epilepsy, Temporal Lobe - pathology epileptogenesis gamma-Aminobutyric Acid - metabolism Glutamine - metabolism glutamine synthase Hippocampus - metabolism Hippocampus - pathology immunohistochemistry lithium-pilocarpine Magnetic Resonance Spectroscopy - methods Male MRS Neurons - metabolism Neurons - pathology Neurotransmitter Agents - metabolism postnatal day 21 rat Rats Rats, Wistar status epilepticus temporal lobe epilepsy |
| title | In vivo MRS and histochemistry of status epilepticus-induced hippocampal pathology in a juvenile model of temporal lobe epilepsy |
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