Combined diazepam and HDAC inhibitor treatment protects against seizures and neuronal damage caused by soman exposure
► In this work we are studying the status epilepticus after soman exposure. ► EEGraphical and neuropathological effects were analyzed after 72h. ► DZP alone or combined with SAHA and VPA was administered after SE onset. ► DZP plus VPA 100mg/kg showed more anticonvulsive effects. The occurrence of st...
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| creator | Rossetti, Franco de Araujo Furtado, Marcio Pak, Thomas Bailey, Keenan Shields, Mallory Chanda, Soma Addis, Michael Robertson, Benjamin D. Moffett, Mark Lumley, Lucille A. Yourick, Debra L. |
| description | ► In this work we are studying the status epilepticus after soman exposure. ► EEGraphical and neuropathological effects were analyzed after 72h. ► DZP alone or combined with SAHA and VPA was administered after SE onset. ► DZP plus VPA 100mg/kg showed more anticonvulsive effects.
The occurrence of status epilepticus (SE) is considered the main cause of brain lesions and morphological alterations, such as hippocampal neuron loss, that result in chronic epilepsy. Previous work demonstrated the convulsive and widespread neuropathological effects of soman, an organophosphorus compound that causes SE and severe recurrent seizures as a result of exposure. Seizures begin rapidly after exposure, can continue for hours, and contribute to prolonged physical incapacitation of the victim. This study attempts to identify anticonvulsive and neuroprotective drugs against soman exposure. Male Sprague-Dawley rats were exposed to 1.0LD50 soman. EEGraphical and neuropathological (Fluoro-Jade B staining) effects were analyzed at 72h post-exposure to soman and subsequent treatments with diazepam (DZP) alone or in combination with histone deacetylase inhibitors, suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA). The extent of brain damage was dependent on the length of SE and not on the number of recurrent seizures. DZP treatment alone decreased SE time and damage in hippocampus, amygdala, thalamus and cortex, but not in piriform nuclei. The combination of DZP and VPA 100mg/kg showed more anticonvulsive effects, decreased SE time, and afforded more neuroprotection in the hippocampus, mainly the ventral portion. The combination DZP and SAHA 25mg/kg was more neuroprotective, but not more anticonvulsant than DZP alone. The DZP combination with VPA HDAC inhibitor proved to be a good treatment for SE and neuronal damage caused by soman exposure. |
| doi_str_mv | 10.1016/j.neuro.2012.02.010 |
| format | Article |
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The occurrence of status epilepticus (SE) is considered the main cause of brain lesions and morphological alterations, such as hippocampal neuron loss, that result in chronic epilepsy. Previous work demonstrated the convulsive and widespread neuropathological effects of soman, an organophosphorus compound that causes SE and severe recurrent seizures as a result of exposure. Seizures begin rapidly after exposure, can continue for hours, and contribute to prolonged physical incapacitation of the victim. This study attempts to identify anticonvulsive and neuroprotective drugs against soman exposure. Male Sprague-Dawley rats were exposed to 1.0LD50 soman. EEGraphical and neuropathological (Fluoro-Jade B staining) effects were analyzed at 72h post-exposure to soman and subsequent treatments with diazepam (DZP) alone or in combination with histone deacetylase inhibitors, suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA). The extent of brain damage was dependent on the length of SE and not on the number of recurrent seizures. DZP treatment alone decreased SE time and damage in hippocampus, amygdala, thalamus and cortex, but not in piriform nuclei. The combination of DZP and VPA 100mg/kg showed more anticonvulsive effects, decreased SE time, and afforded more neuroprotection in the hippocampus, mainly the ventral portion. The combination DZP and SAHA 25mg/kg was more neuroprotective, but not more anticonvulsant than DZP alone. The DZP combination with VPA HDAC inhibitor proved to be a good treatment for SE and neuronal damage caused by soman exposure.</description><identifier>ISSN: 0161-813X</identifier><identifier>EISSN: 1872-9711</identifier><identifier>DOI: 10.1016/j.neuro.2012.02.010</identifier><identifier>PMID: 22387230</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Amygdala ; Animals ; Anticonvulsants ; Anticonvulsants - pharmacology ; Anticonvulsants. Antiepileptics. Antiparkinson agents ; Biological and medical sciences ; Brain - drug effects ; Brain - pathology ; Brain - physiopathology ; Brain injury ; Brain Mapping - methods ; Brain Waves - drug effects ; Chemical and industrial products toxicology. Toxic occupational diseases ; Chemical Warfare Agents - toxicity ; Cortex ; Cortex (piriform) ; Cytoprotection ; Diazepam ; Diazepam - pharmacology ; Drug Therapy, Combination ; Drugs ; Electroencephalography ; Epilepsy ; Fluoro-Jade B ; Gas, fumes ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Hippocampus ; Histone deacetylase ; Histone Deacetylase Inhibitors - pharmacology ; Hydroxamic acid ; Hydroxamic Acids - pharmacology ; Male ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neurology ; Neurons ; Neurons - drug effects ; Neurons - pathology ; Neuropharmacology ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Organophosphorus compounds ; Pharmacology. Drug treatments ; Piriform ; Rats ; Rats, Sprague-Dawley ; Seizures ; Seizures - chemically induced ; Seizures - pathology ; Seizures - physiopathology ; Seizures - prevention & control ; Soman ; Soman - toxicity ; Suberoylanilide hydroxamic acid ; Thalamus ; Time Factors ; Toxicology ; Valproic acid ; Valproic Acid - pharmacology</subject><ispartof>Neurotoxicology (Park Forest South), 2012-06, Vol.33 (3), p.500-511</ispartof><rights>2012</rights><rights>2015 INIST-CNRS</rights><rights>Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-889a47b6602394b8cbe612c561a1f91f19c6e723fa2dace2be9e6736a8c569d13</citedby><cites>FETCH-LOGICAL-c422t-889a47b6602394b8cbe612c561a1f91f19c6e723fa2dace2be9e6736a8c569d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuro.2012.02.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26011784$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22387230$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rossetti, Franco</creatorcontrib><creatorcontrib>de Araujo Furtado, Marcio</creatorcontrib><creatorcontrib>Pak, Thomas</creatorcontrib><creatorcontrib>Bailey, Keenan</creatorcontrib><creatorcontrib>Shields, Mallory</creatorcontrib><creatorcontrib>Chanda, Soma</creatorcontrib><creatorcontrib>Addis, Michael</creatorcontrib><creatorcontrib>Robertson, Benjamin D.</creatorcontrib><creatorcontrib>Moffett, Mark</creatorcontrib><creatorcontrib>Lumley, Lucille A.</creatorcontrib><creatorcontrib>Yourick, Debra L.</creatorcontrib><title>Combined diazepam and HDAC inhibitor treatment protects against seizures and neuronal damage caused by soman exposure</title><title>Neurotoxicology (Park Forest South)</title><addtitle>Neurotoxicology</addtitle><description>► In this work we are studying the status epilepticus after soman exposure. ► EEGraphical and neuropathological effects were analyzed after 72h. ► DZP alone or combined with SAHA and VPA was administered after SE onset. ► DZP plus VPA 100mg/kg showed more anticonvulsive effects.
The occurrence of status epilepticus (SE) is considered the main cause of brain lesions and morphological alterations, such as hippocampal neuron loss, that result in chronic epilepsy. Previous work demonstrated the convulsive and widespread neuropathological effects of soman, an organophosphorus compound that causes SE and severe recurrent seizures as a result of exposure. Seizures begin rapidly after exposure, can continue for hours, and contribute to prolonged physical incapacitation of the victim. This study attempts to identify anticonvulsive and neuroprotective drugs against soman exposure. Male Sprague-Dawley rats were exposed to 1.0LD50 soman. EEGraphical and neuropathological (Fluoro-Jade B staining) effects were analyzed at 72h post-exposure to soman and subsequent treatments with diazepam (DZP) alone or in combination with histone deacetylase inhibitors, suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA). The extent of brain damage was dependent on the length of SE and not on the number of recurrent seizures. DZP treatment alone decreased SE time and damage in hippocampus, amygdala, thalamus and cortex, but not in piriform nuclei. The combination of DZP and VPA 100mg/kg showed more anticonvulsive effects, decreased SE time, and afforded more neuroprotection in the hippocampus, mainly the ventral portion. The combination DZP and SAHA 25mg/kg was more neuroprotective, but not more anticonvulsant than DZP alone. The DZP combination with VPA HDAC inhibitor proved to be a good treatment for SE and neuronal damage caused by soman exposure.</description><subject>Amygdala</subject><subject>Animals</subject><subject>Anticonvulsants</subject><subject>Anticonvulsants - pharmacology</subject><subject>Anticonvulsants. Antiepileptics. Antiparkinson agents</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Brain injury</subject><subject>Brain Mapping - methods</subject><subject>Brain Waves - drug effects</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Chemical Warfare Agents - toxicity</subject><subject>Cortex</subject><subject>Cortex (piriform)</subject><subject>Cytoprotection</subject><subject>Diazepam</subject><subject>Diazepam - pharmacology</subject><subject>Drug Therapy, Combination</subject><subject>Drugs</subject><subject>Electroencephalography</subject><subject>Epilepsy</subject><subject>Fluoro-Jade B</subject><subject>Gas, fumes</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Hippocampus</subject><subject>Histone deacetylase</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Hydroxamic acid</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - pathology</subject><subject>Neuropharmacology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Organophosphorus compounds</subject><subject>Pharmacology. Drug treatments</subject><subject>Piriform</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Seizures</subject><subject>Seizures - chemically induced</subject><subject>Seizures - pathology</subject><subject>Seizures - physiopathology</subject><subject>Seizures - prevention & control</subject><subject>Soman</subject><subject>Soman - toxicity</subject><subject>Suberoylanilide hydroxamic acid</subject><subject>Thalamus</subject><subject>Time Factors</subject><subject>Toxicology</subject><subject>Valproic acid</subject><subject>Valproic Acid - pharmacology</subject><issn>0161-813X</issn><issn>1872-9711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi1ERZfCL0BCviBxydbj7DrJgUO1fBSpUi8gcbMm9qR4ldiL7VS0v77eD-CGNJIvzzt-52HsDYglCFCX26WnOYalFCCXogyIZ2wBbSOrrgF4zhaFgqqF-sc5e5nSVghYN6p7wc6lrAtWiwWbN2HqnSfLrcNH2uHE0Vt-_fFqw53_6XqXQ-Q5EuaJfOa7GDKZnDjeofMp80TucY6UDrFDIY8jtzjhHXGDcyqr-weewoSe0-9dSIV-xc4GHBO9Pr0X7PvnT98219XN7Zevm6ubyqykzFXbdrhqeqWErLtV35qeFEizVoAwdDBAZxSVOwaUFg3JnjpSTa2wLUxnob5g7497S-1fM6WsJ5cMjSN6CnPSIKRo1yUhClofURNDSpEGvYtuwvhQIL33rbf6cJ7e-9aiDOxTb08fzP1E9m_mj-ACvDsBmAyOQ0RvXPrHKQHQtKvCfThyVHTcO4o6GUfekHWx-NY2uP8WeQKYRqDm</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Rossetti, Franco</creator><creator>de Araujo Furtado, Marcio</creator><creator>Pak, Thomas</creator><creator>Bailey, Keenan</creator><creator>Shields, Mallory</creator><creator>Chanda, Soma</creator><creator>Addis, Michael</creator><creator>Robertson, Benjamin D.</creator><creator>Moffett, Mark</creator><creator>Lumley, Lucille A.</creator><creator>Yourick, Debra L.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20120601</creationdate><title>Combined diazepam and HDAC inhibitor treatment protects against seizures and neuronal damage caused by soman exposure</title><author>Rossetti, Franco ; de Araujo Furtado, Marcio ; Pak, Thomas ; Bailey, Keenan ; Shields, Mallory ; Chanda, Soma ; Addis, Michael ; Robertson, Benjamin D. ; Moffett, Mark ; Lumley, Lucille A. ; Yourick, Debra L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-889a47b6602394b8cbe612c561a1f91f19c6e723fa2dace2be9e6736a8c569d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Amygdala</topic><topic>Animals</topic><topic>Anticonvulsants</topic><topic>Anticonvulsants - pharmacology</topic><topic>Anticonvulsants. Antiepileptics. Antiparkinson agents</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - pathology</topic><topic>Brain - physiopathology</topic><topic>Brain injury</topic><topic>Brain Mapping - methods</topic><topic>Brain Waves - drug effects</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Chemical Warfare Agents - toxicity</topic><topic>Cortex</topic><topic>Cortex (piriform)</topic><topic>Cytoprotection</topic><topic>Diazepam</topic><topic>Diazepam - pharmacology</topic><topic>Drug Therapy, Combination</topic><topic>Drugs</topic><topic>Electroencephalography</topic><topic>Epilepsy</topic><topic>Fluoro-Jade B</topic><topic>Gas, fumes</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hippocampus</topic><topic>Histone deacetylase</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Hydroxamic acid</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - pathology</topic><topic>Neuropharmacology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Organophosphorus compounds</topic><topic>Pharmacology. Drug treatments</topic><topic>Piriform</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Seizures</topic><topic>Seizures - chemically induced</topic><topic>Seizures - pathology</topic><topic>Seizures - physiopathology</topic><topic>Seizures - prevention & control</topic><topic>Soman</topic><topic>Soman - toxicity</topic><topic>Suberoylanilide hydroxamic acid</topic><topic>Thalamus</topic><topic>Time Factors</topic><topic>Toxicology</topic><topic>Valproic acid</topic><topic>Valproic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rossetti, Franco</creatorcontrib><creatorcontrib>de Araujo Furtado, Marcio</creatorcontrib><creatorcontrib>Pak, Thomas</creatorcontrib><creatorcontrib>Bailey, Keenan</creatorcontrib><creatorcontrib>Shields, Mallory</creatorcontrib><creatorcontrib>Chanda, Soma</creatorcontrib><creatorcontrib>Addis, Michael</creatorcontrib><creatorcontrib>Robertson, Benjamin D.</creatorcontrib><creatorcontrib>Moffett, Mark</creatorcontrib><creatorcontrib>Lumley, Lucille A.</creatorcontrib><creatorcontrib>Yourick, Debra L.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicology (Park Forest South)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rossetti, Franco</au><au>de Araujo Furtado, Marcio</au><au>Pak, Thomas</au><au>Bailey, Keenan</au><au>Shields, Mallory</au><au>Chanda, Soma</au><au>Addis, Michael</au><au>Robertson, Benjamin D.</au><au>Moffett, Mark</au><au>Lumley, Lucille A.</au><au>Yourick, Debra L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combined diazepam and HDAC inhibitor treatment protects against seizures and neuronal damage caused by soman exposure</atitle><jtitle>Neurotoxicology (Park Forest South)</jtitle><addtitle>Neurotoxicology</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>33</volume><issue>3</issue><spage>500</spage><epage>511</epage><pages>500-511</pages><issn>0161-813X</issn><eissn>1872-9711</eissn><abstract>► In this work we are studying the status epilepticus after soman exposure. ► EEGraphical and neuropathological effects were analyzed after 72h. ► DZP alone or combined with SAHA and VPA was administered after SE onset. ► DZP plus VPA 100mg/kg showed more anticonvulsive effects.
The occurrence of status epilepticus (SE) is considered the main cause of brain lesions and morphological alterations, such as hippocampal neuron loss, that result in chronic epilepsy. Previous work demonstrated the convulsive and widespread neuropathological effects of soman, an organophosphorus compound that causes SE and severe recurrent seizures as a result of exposure. Seizures begin rapidly after exposure, can continue for hours, and contribute to prolonged physical incapacitation of the victim. This study attempts to identify anticonvulsive and neuroprotective drugs against soman exposure. Male Sprague-Dawley rats were exposed to 1.0LD50 soman. EEGraphical and neuropathological (Fluoro-Jade B staining) effects were analyzed at 72h post-exposure to soman and subsequent treatments with diazepam (DZP) alone or in combination with histone deacetylase inhibitors, suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA). The extent of brain damage was dependent on the length of SE and not on the number of recurrent seizures. DZP treatment alone decreased SE time and damage in hippocampus, amygdala, thalamus and cortex, but not in piriform nuclei. The combination of DZP and VPA 100mg/kg showed more anticonvulsive effects, decreased SE time, and afforded more neuroprotection in the hippocampus, mainly the ventral portion. The combination DZP and SAHA 25mg/kg was more neuroprotective, but not more anticonvulsant than DZP alone. The DZP combination with VPA HDAC inhibitor proved to be a good treatment for SE and neuronal damage caused by soman exposure.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>22387230</pmid><doi>10.1016/j.neuro.2012.02.010</doi><tpages>12</tpages></addata></record> |
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| ispartof | Neurotoxicology (Park Forest South), 2012-06, Vol.33 (3), p.500-511 |
| issn | 0161-813X 1872-9711 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Amygdala Animals Anticonvulsants Anticonvulsants - pharmacology Anticonvulsants. Antiepileptics. Antiparkinson agents Biological and medical sciences Brain - drug effects Brain - pathology Brain - physiopathology Brain injury Brain Mapping - methods Brain Waves - drug effects Chemical and industrial products toxicology. Toxic occupational diseases Chemical Warfare Agents - toxicity Cortex Cortex (piriform) Cytoprotection Diazepam Diazepam - pharmacology Drug Therapy, Combination Drugs Electroencephalography Epilepsy Fluoro-Jade B Gas, fumes Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hippocampus Histone deacetylase Histone Deacetylase Inhibitors - pharmacology Hydroxamic acid Hydroxamic Acids - pharmacology Male Medical sciences Nervous system (semeiology, syndromes) Neurology Neurons Neurons - drug effects Neurons - pathology Neuropharmacology Neuroprotection Neuroprotective Agents - pharmacology Organophosphorus compounds Pharmacology. Drug treatments Piriform Rats Rats, Sprague-Dawley Seizures Seizures - chemically induced Seizures - pathology Seizures - physiopathology Seizures - prevention & control Soman Soman - toxicity Suberoylanilide hydroxamic acid Thalamus Time Factors Toxicology Valproic acid Valproic Acid - pharmacology |
| title | Combined diazepam and HDAC inhibitor treatment protects against seizures and neuronal damage caused by soman exposure |
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