Ontogeny of seizure incidence, latency, and severity in genetically epilepsy prone rats
The Genetically Epilepsy‐Prone Rat (GEPR) is a widely studied model of epileptiform disorders. While there is considerable evidence that neurotransmitter abnormalities contribute to the unusual sensitivity of these animals to seizures, the possibility that seizure susceptibility may reflect developm...
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Veröffentlicht in: | Developmental psychobiology 1987-05, Vol.20 (3), p.355-363 |
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description | The Genetically Epilepsy‐Prone Rat (GEPR) is a widely studied model of epileptiform disorders. While there is considerable evidence that neurotransmitter abnormalities contribute to the unusual sensitivity of these animals to seizures, the possibility that seizure susceptibility may reflect developmental changes in the central nervous system has not been fully addressed. In the present study, 91 GEPR‐9 pups were tested for incidence, latency and severity of an audiogenically induced seizure at 6, 9, 12, 15, 18, 21, 24, 27, 28, 29, or 30 days postpartum (1 test per pup) and retested at 60 days. Seizure incidence, latency, and severity were significantly greater on Days 27, 28, 29, and 30 than on all previous days. The first observation of running fits occurred in Day 18 pups and the first evidence of seizures occurred in Day 21 pups. When retested at Day 60, seizure incidence and severity were significantly greater than on initial tests while latency declined. The results suggest that seizure susceptibility in the GEPR‐9 occurs as the result of developmental events in the CNS occurring on or shortly after Day 18 postpartum. |
doi_str_mv | 10.1002/dev.420200312 |
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While there is considerable evidence that neurotransmitter abnormalities contribute to the unusual sensitivity of these animals to seizures, the possibility that seizure susceptibility may reflect developmental changes in the central nervous system has not been fully addressed. In the present study, 91 GEPR‐9 pups were tested for incidence, latency and severity of an audiogenically induced seizure at 6, 9, 12, 15, 18, 21, 24, 27, 28, 29, or 30 days postpartum (1 test per pup) and retested at 60 days. Seizure incidence, latency, and severity were significantly greater on Days 27, 28, 29, and 30 than on all previous days. The first observation of running fits occurred in Day 18 pups and the first evidence of seizures occurred in Day 21 pups. When retested at Day 60, seizure incidence and severity were significantly greater than on initial tests while latency declined. The results suggest that seizure susceptibility in the GEPR‐9 occurs as the result of developmental events in the CNS occurring on or shortly after Day 18 postpartum.</description><identifier>ISSN: 0012-1630</identifier><identifier>EISSN: 1098-2302</identifier><identifier>DOI: 10.1002/dev.420200312</identifier><identifier>PMID: 3596061</identifier><identifier>CODEN: DEPBA5</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Age Factors ; Animals ; Biological and medical sciences ; Epilepsy - genetics ; Epilepsy - physiopathology ; Female ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Male ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neurology ; Rats ; Rats, Inbred Strains - genetics</subject><ispartof>Developmental psychobiology, 1987-05, Vol.20 (3), p.355-363</ispartof><rights>Copyright © 1987 John Wiley & Sons, Inc.</rights><rights>1987 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4032-8d4b75254c6083be924fa14bf4882b5eae9e0b44ac7672e4c262c99becc0f4863</citedby><cites>FETCH-LOGICAL-c4032-8d4b75254c6083be924fa14bf4882b5eae9e0b44ac7672e4c262c99becc0f4863</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%2Fdev.420200312$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fdev.420200312$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8292630$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3596061$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hjeresen, Dennis L.</creatorcontrib><creatorcontrib>Franck, Joann E.</creatorcontrib><creatorcontrib>Amend, Diane L.</creatorcontrib><title>Ontogeny of seizure incidence, latency, and severity in genetically epilepsy prone rats</title><title>Developmental psychobiology</title><addtitle>Dev. Psychobiol</addtitle><description>The Genetically Epilepsy‐Prone Rat (GEPR) is a widely studied model of epileptiform disorders. While there is considerable evidence that neurotransmitter abnormalities contribute to the unusual sensitivity of these animals to seizures, the possibility that seizure susceptibility may reflect developmental changes in the central nervous system has not been fully addressed. In the present study, 91 GEPR‐9 pups were tested for incidence, latency and severity of an audiogenically induced seizure at 6, 9, 12, 15, 18, 21, 24, 27, 28, 29, or 30 days postpartum (1 test per pup) and retested at 60 days. Seizure incidence, latency, and severity were significantly greater on Days 27, 28, 29, and 30 than on all previous days. The first observation of running fits occurred in Day 18 pups and the first evidence of seizures occurred in Day 21 pups. When retested at Day 60, seizure incidence and severity were significantly greater than on initial tests while latency declined. The results suggest that seizure susceptibility in the GEPR‐9 occurs as the result of developmental events in the CNS occurring on or shortly after Day 18 postpartum.</description><subject>Age Factors</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Epilepsy - genetics</subject><subject>Epilepsy - physiopathology</subject><subject>Female</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Inbred Strains - genetics</subject><issn>0012-1630</issn><issn>1098-2302</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtv1DAURi1UVKaFJUskL6qumnL9iO0s0fQpVdMNdJaW49wgQyYZ7Ewh_fUYTTTqipWv9Z370CHkI4NLBsA_N_h8KTlwAMH4G7JgUJmCC-BHZAHAeMGUgHfkJKUf-cuk0cfkWJSVAsUWZP3Yj8N37Cc6tDRheNlFpKH3ocHe4wXt3JiL6YK6vsn5M8YwThmguQfH4F3XTRS3ocNtmug2Dj3S6Mb0nrxtXZfww_yekm8311-Xd8XD4-398stD4SUIXphG1rrkpfQKjKix4rJ1TNatNIbXJTqsEGopnddKc5SeK-6rqkbvITNKnJLz_dy8-tcO02g3IXnsOtfjsEtW69LoyrAMFnvQxyGliK3dxrBxcbIM7D-RNou0B5GZ_zQP3tUbbA70bC7nZ3PuUrbQRpelpQNmeMWz94zpPfY7K5r-v9NeXT-9PmA-OKQR_xw6XfxplRa6tOvVrV2Z9ZNa3t3YlfgLWZKaxg</recordid><startdate>198705</startdate><enddate>198705</enddate><creator>Hjeresen, Dennis L.</creator><creator>Franck, Joann E.</creator><creator>Amend, Diane L.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>198705</creationdate><title>Ontogeny of seizure incidence, latency, and severity in genetically epilepsy prone rats</title><author>Hjeresen, Dennis L. ; Franck, Joann E. ; Amend, Diane L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4032-8d4b75254c6083be924fa14bf4882b5eae9e0b44ac7672e4c262c99becc0f4863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Epilepsy - genetics</topic><topic>Epilepsy - physiopathology</topic><topic>Female</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Inbred Strains - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hjeresen, Dennis L.</creatorcontrib><creatorcontrib>Franck, Joann E.</creatorcontrib><creatorcontrib>Amend, Diane L.</creatorcontrib><collection>Istex</collection><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>MEDLINE - Academic</collection><jtitle>Developmental psychobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hjeresen, Dennis L.</au><au>Franck, Joann E.</au><au>Amend, Diane L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ontogeny of seizure incidence, latency, and severity in genetically epilepsy prone rats</atitle><jtitle>Developmental psychobiology</jtitle><addtitle>Dev. Psychobiol</addtitle><date>1987-05</date><risdate>1987</risdate><volume>20</volume><issue>3</issue><spage>355</spage><epage>363</epage><pages>355-363</pages><issn>0012-1630</issn><eissn>1098-2302</eissn><coden>DEPBA5</coden><abstract>The Genetically Epilepsy‐Prone Rat (GEPR) is a widely studied model of epileptiform disorders. While there is considerable evidence that neurotransmitter abnormalities contribute to the unusual sensitivity of these animals to seizures, the possibility that seizure susceptibility may reflect developmental changes in the central nervous system has not been fully addressed. In the present study, 91 GEPR‐9 pups were tested for incidence, latency and severity of an audiogenically induced seizure at 6, 9, 12, 15, 18, 21, 24, 27, 28, 29, or 30 days postpartum (1 test per pup) and retested at 60 days. Seizure incidence, latency, and severity were significantly greater on Days 27, 28, 29, and 30 than on all previous days. The first observation of running fits occurred in Day 18 pups and the first evidence of seizures occurred in Day 21 pups. When retested at Day 60, seizure incidence and severity were significantly greater than on initial tests while latency declined. The results suggest that seizure susceptibility in the GEPR‐9 occurs as the result of developmental events in the CNS occurring on or shortly after Day 18 postpartum.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>3596061</pmid><doi>10.1002/dev.420200312</doi><tpages>9</tpages></addata></record> |
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subjects | Age Factors Animals Biological and medical sciences Epilepsy - genetics Epilepsy - physiopathology Female Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Male Medical sciences Nervous system (semeiology, syndromes) Neurology Rats Rats, Inbred Strains - genetics |
title | Ontogeny of seizure incidence, latency, and severity in genetically epilepsy prone rats |
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