Epileptogenesis Induced by Alternate‐site Kindling in Bilateral Hippocampi
Purpose: Alternate‐site kindling (AK), which has been known to induce so‐called kindling antagonism, was performed in the bilateral hippocampi to reveal neural mechanisms underlying hippocampal kindling. Methods: Ten adult rabbits were used. Daily kindling stimulation consisted of a 1‐ s train of 50...
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| Veröffentlicht in: | Epilepsia (Copenhagen) 2003-03, Vol.44 (3), p.292-298 |
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| creator | Matsuda, Yoshiki Yano, Michiko Kitayama, Masaomi Kogure, Shinichi Yamauchi, Toshio |
| description | Purpose: Alternate‐site kindling (AK), which has been known to induce so‐called kindling antagonism, was performed in the bilateral hippocampi to reveal neural mechanisms underlying hippocampal kindling.
Methods: Ten adult rabbits were used. Daily kindling stimulation consisted of a 1‐ s train of 50 pulses (pulse duration, 1 ms) of 80 to 200 μA (base‐to‐peak), which was higher than the afterdischarge (AD) threshold. The concurrent alternating stimulations were delivered to the right and left hippocampus once every 24 h.
Results: All animals developed a stage 5 convulsion with a mean of 28.1 ± 3.3 (mean ± SEM) stimulations. The right and left hippocampus received 14.8 ± 1.7 and 14.6 ± 1.6 stimulations, respectively. Behavioral stages induced by stimulation of the right or left hippocampus evolved to generalized seizures along a similar course. Kindling antagonism was not observed. The two sides showed similar increases in AD duration, and similar chronologic changes in interictal discharge (IID) frequency. Simple A‐type IID and complex types of IID appeared at higher rates, whereas simple B‐type IID remained at a relatively low level.
Conclusions: The present AK procedure did not induce kindling antagonism, but it induced progression of kindling manifestations. The origin of simple B‐type IID is known to be in the contralateral side, and its intracellular counterpart corresponds to a sequence of small depolarization followed by large hyperpolarization, suggesting that plastic changes in the feed‐forward inhibitory system play an important role in hippocampal kindling. |
| doi_str_mv | 10.1046/j.1528-1157.2003.25802.x |
| format | Article |
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Methods: Ten adult rabbits were used. Daily kindling stimulation consisted of a 1‐ s train of 50 pulses (pulse duration, 1 ms) of 80 to 200 μA (base‐to‐peak), which was higher than the afterdischarge (AD) threshold. The concurrent alternating stimulations were delivered to the right and left hippocampus once every 24 h.
Results: All animals developed a stage 5 convulsion with a mean of 28.1 ± 3.3 (mean ± SEM) stimulations. The right and left hippocampus received 14.8 ± 1.7 and 14.6 ± 1.6 stimulations, respectively. Behavioral stages induced by stimulation of the right or left hippocampus evolved to generalized seizures along a similar course. Kindling antagonism was not observed. The two sides showed similar increases in AD duration, and similar chronologic changes in interictal discharge (IID) frequency. Simple A‐type IID and complex types of IID appeared at higher rates, whereas simple B‐type IID remained at a relatively low level.
Conclusions: The present AK procedure did not induce kindling antagonism, but it induced progression of kindling manifestations. The origin of simple B‐type IID is known to be in the contralateral side, and its intracellular counterpart corresponds to a sequence of small depolarization followed by large hyperpolarization, suggesting that plastic changes in the feed‐forward inhibitory system play an important role in hippocampal kindling.</description><identifier>ISSN: 0013-9580</identifier><identifier>EISSN: 1528-1167</identifier><identifier>DOI: 10.1046/j.1528-1157.2003.25802.x</identifier><identifier>PMID: 12614383</identifier><identifier>CODEN: EPILAK</identifier><language>eng</language><publisher>Boston, MA, USA: Blackwell Science Inc</publisher><subject>Alternate‐site kindling ; Animals ; Bilateral kindling ; Biological and medical sciences ; Circadian Rhythm - physiology ; Disease Models, Animal ; Electric Stimulation - methods ; Electroencephalography - statistics & numerical data ; Epilepsy - etiology ; Epilepsy - physiopathology ; Functional Laterality - physiology ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Hippocampus ; Hippocampus - physiology ; Hippocampus - physiopathology ; Kindling antagonism ; Kindling model ; Kindling, Neurologic - physiology ; Male ; Medical sciences ; Models, Neurological ; Nerve Net - physiology ; Nervous system (semeiology, syndromes) ; Neural Inhibition - physiology ; Neurology ; Neuronal Plasticity - physiology ; Rabbits ; Seizures - etiology ; Seizures - physiopathology</subject><ispartof>Epilepsia (Copenhagen), 2003-03, Vol.44 (3), p.292-298</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5412-72abf2c651b6ab59d2b7ed9f1902bc48a2afde126a2b37cddcbf7981272923ee3</citedby><cites>FETCH-LOGICAL-c5412-72abf2c651b6ab59d2b7ed9f1902bc48a2afde126a2b37cddcbf7981272923ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1528-1157.2003.25802.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1528-1157.2003.25802.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1413,1429,27906,27907,45556,45557,46391,46815</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14869023$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12614383$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsuda, Yoshiki</creatorcontrib><creatorcontrib>Yano, Michiko</creatorcontrib><creatorcontrib>Kitayama, Masaomi</creatorcontrib><creatorcontrib>Kogure, Shinichi</creatorcontrib><creatorcontrib>Yamauchi, Toshio</creatorcontrib><title>Epileptogenesis Induced by Alternate‐site Kindling in Bilateral Hippocampi</title><title>Epilepsia (Copenhagen)</title><addtitle>Epilepsia</addtitle><description>Purpose: Alternate‐site kindling (AK), which has been known to induce so‐called kindling antagonism, was performed in the bilateral hippocampi to reveal neural mechanisms underlying hippocampal kindling.
Methods: Ten adult rabbits were used. Daily kindling stimulation consisted of a 1‐ s train of 50 pulses (pulse duration, 1 ms) of 80 to 200 μA (base‐to‐peak), which was higher than the afterdischarge (AD) threshold. The concurrent alternating stimulations were delivered to the right and left hippocampus once every 24 h.
Results: All animals developed a stage 5 convulsion with a mean of 28.1 ± 3.3 (mean ± SEM) stimulations. The right and left hippocampus received 14.8 ± 1.7 and 14.6 ± 1.6 stimulations, respectively. Behavioral stages induced by stimulation of the right or left hippocampus evolved to generalized seizures along a similar course. Kindling antagonism was not observed. The two sides showed similar increases in AD duration, and similar chronologic changes in interictal discharge (IID) frequency. Simple A‐type IID and complex types of IID appeared at higher rates, whereas simple B‐type IID remained at a relatively low level.
Conclusions: The present AK procedure did not induce kindling antagonism, but it induced progression of kindling manifestations. The origin of simple B‐type IID is known to be in the contralateral side, and its intracellular counterpart corresponds to a sequence of small depolarization followed by large hyperpolarization, suggesting that plastic changes in the feed‐forward inhibitory system play an important role in hippocampal kindling.</description><subject>Alternate‐site kindling</subject><subject>Animals</subject><subject>Bilateral kindling</subject><subject>Biological and medical sciences</subject><subject>Circadian Rhythm - physiology</subject><subject>Disease Models, Animal</subject><subject>Electric Stimulation - methods</subject><subject>Electroencephalography - statistics & numerical data</subject><subject>Epilepsy - etiology</subject><subject>Epilepsy - physiopathology</subject><subject>Functional Laterality - physiology</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Hippocampus</subject><subject>Hippocampus - physiology</subject><subject>Hippocampus - physiopathology</subject><subject>Kindling antagonism</subject><subject>Kindling model</subject><subject>Kindling, Neurologic - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Neurological</subject><subject>Nerve Net - physiology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neural Inhibition - physiology</subject><subject>Neurology</subject><subject>Neuronal Plasticity - physiology</subject><subject>Rabbits</subject><subject>Seizures - etiology</subject><subject>Seizures - physiopathology</subject><issn>0013-9580</issn><issn>1528-1167</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtOwzAQhi0EgvK4AsoGdgl-JHGyQYKqQAUCFrC2_JhUrtwkxImgOyQuwBk5CQmN1C0rj_R_M575EAoIjgiO04tlRBKahYQkPKIYs4gmGabRxw6ajEHKd9EEY8LCvI8O0KH3S4wxTznbRweEpiRmGZugx1ltHdRttYASvPXBvDSdBhOodXDlWmhK2cLP57e3LQT3tjTOlovAlsG1dX3SSPfz-XVn67rSclXbY7RXSOfhZHyP0OvN7GV6Fz483c6nVw-hTmJCQ06lKqhOE6JSqZLcUMXB5AXJMVU6ziSVhYF-S0kV49oYrQqeZ4RymlMGwI7Q-WZu3VRvHfhWrKzX4Jwsoeq84AyneYZZD2YbUDeV9w0Uom7sSjZrQbAYXIqlGJSJwaUYXIo_l-Kjbz0d_-jUCsy2cZTXA2cjIL2Wrmhkqa3fcnGW9vcM3OWGe-9Vr_-9gJg9z_9K9gtytJJV</recordid><startdate>200303</startdate><enddate>200303</enddate><creator>Matsuda, Yoshiki</creator><creator>Yano, Michiko</creator><creator>Kitayama, Masaomi</creator><creator>Kogure, Shinichi</creator><creator>Yamauchi, Toshio</creator><general>Blackwell Science Inc</general><general>Blackwell</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>7X8</scope></search><sort><creationdate>200303</creationdate><title>Epileptogenesis Induced by Alternate‐site Kindling in Bilateral Hippocampi</title><author>Matsuda, Yoshiki ; Yano, Michiko ; Kitayama, Masaomi ; Kogure, Shinichi ; Yamauchi, Toshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5412-72abf2c651b6ab59d2b7ed9f1902bc48a2afde126a2b37cddcbf7981272923ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Alternate‐site kindling</topic><topic>Animals</topic><topic>Bilateral kindling</topic><topic>Biological and medical sciences</topic><topic>Circadian Rhythm - physiology</topic><topic>Disease Models, Animal</topic><topic>Electric Stimulation - methods</topic><topic>Electroencephalography - statistics & numerical data</topic><topic>Epilepsy - etiology</topic><topic>Epilepsy - physiopathology</topic><topic>Functional Laterality - physiology</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hippocampus</topic><topic>Hippocampus - physiology</topic><topic>Hippocampus - physiopathology</topic><topic>Kindling antagonism</topic><topic>Kindling model</topic><topic>Kindling, Neurologic - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Neurological</topic><topic>Nerve Net - physiology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neural Inhibition - physiology</topic><topic>Neurology</topic><topic>Neuronal Plasticity - physiology</topic><topic>Rabbits</topic><topic>Seizures - etiology</topic><topic>Seizures - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsuda, Yoshiki</creatorcontrib><creatorcontrib>Yano, Michiko</creatorcontrib><creatorcontrib>Kitayama, Masaomi</creatorcontrib><creatorcontrib>Kogure, Shinichi</creatorcontrib><creatorcontrib>Yamauchi, Toshio</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>MEDLINE - Academic</collection><jtitle>Epilepsia (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsuda, Yoshiki</au><au>Yano, Michiko</au><au>Kitayama, Masaomi</au><au>Kogure, Shinichi</au><au>Yamauchi, Toshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epileptogenesis Induced by Alternate‐site Kindling in Bilateral Hippocampi</atitle><jtitle>Epilepsia (Copenhagen)</jtitle><addtitle>Epilepsia</addtitle><date>2003-03</date><risdate>2003</risdate><volume>44</volume><issue>3</issue><spage>292</spage><epage>298</epage><pages>292-298</pages><issn>0013-9580</issn><eissn>1528-1167</eissn><coden>EPILAK</coden><abstract>Purpose: Alternate‐site kindling (AK), which has been known to induce so‐called kindling antagonism, was performed in the bilateral hippocampi to reveal neural mechanisms underlying hippocampal kindling.
Methods: Ten adult rabbits were used. Daily kindling stimulation consisted of a 1‐ s train of 50 pulses (pulse duration, 1 ms) of 80 to 200 μA (base‐to‐peak), which was higher than the afterdischarge (AD) threshold. The concurrent alternating stimulations were delivered to the right and left hippocampus once every 24 h.
Results: All animals developed a stage 5 convulsion with a mean of 28.1 ± 3.3 (mean ± SEM) stimulations. The right and left hippocampus received 14.8 ± 1.7 and 14.6 ± 1.6 stimulations, respectively. Behavioral stages induced by stimulation of the right or left hippocampus evolved to generalized seizures along a similar course. Kindling antagonism was not observed. The two sides showed similar increases in AD duration, and similar chronologic changes in interictal discharge (IID) frequency. Simple A‐type IID and complex types of IID appeared at higher rates, whereas simple B‐type IID remained at a relatively low level.
Conclusions: The present AK procedure did not induce kindling antagonism, but it induced progression of kindling manifestations. The origin of simple B‐type IID is known to be in the contralateral side, and its intracellular counterpart corresponds to a sequence of small depolarization followed by large hyperpolarization, suggesting that plastic changes in the feed‐forward inhibitory system play an important role in hippocampal kindling.</abstract><cop>Boston, MA, USA</cop><pub>Blackwell Science Inc</pub><pmid>12614383</pmid><doi>10.1046/j.1528-1157.2003.25802.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alternate‐site kindling Animals Bilateral kindling Biological and medical sciences Circadian Rhythm - physiology Disease Models, Animal Electric Stimulation - methods Electroencephalography - statistics & numerical data Epilepsy - etiology Epilepsy - physiopathology Functional Laterality - physiology Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hippocampus Hippocampus - physiology Hippocampus - physiopathology Kindling antagonism Kindling model Kindling, Neurologic - physiology Male Medical sciences Models, Neurological Nerve Net - physiology Nervous system (semeiology, syndromes) Neural Inhibition - physiology Neurology Neuronal Plasticity - physiology Rabbits Seizures - etiology Seizures - physiopathology |
| title | Epileptogenesis Induced by Alternate‐site Kindling in Bilateral Hippocampi |
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