Cannabinoid CB1 receptor antagonists cause status epilepticus-like activity in the hippocampal neuronal culture model of acquired epilepsy
Status epilepticus (SE) is a major medical emergency associated with a significant morbidity and mortality. Little is known about the mechanisms that terminate seizure activity and prevent the development of status epilepticus. Cannabinoids possess anticonvulsant properties and the endocannabinoid s...
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| Veröffentlicht in: | Neuroscience letters 2007-01, Vol.411 (1), p.11-16 |
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| creator | Deshpande, Laxmikant S. Sombati, Sompong Blair, Robert E. Carter, Dawn S. Martin, Billy R. DeLorenzo, Robert J. |
| description | Status epilepticus (SE) is a major medical emergency associated with a significant morbidity and mortality. Little is known about the mechanisms that terminate seizure activity and prevent the development of status epilepticus. Cannabinoids possess anticonvulsant properties and the endocannabinoid system has been implicated in regulating seizure duration and frequency. Endocannabinoids regulate synaptic transmission and dampen seizure activity via activation of the presynaptic cannabinoid receptor 1 (CB1). This study was initiated to evaluate the role of CB1 receptor-dependent endocannabinoid synaptic transmission towards preventing the development of status epilepticus-like activity in the well-characterized hippocampal neuronal culture model of acquired epilepsy using patch clamp electrophysiology. Application of the CB1 receptor antagonists SR141716A (1
μM) or AM251 (1
μM) to “epileptic” neurons caused the development of continuous epileptiform activity, resembling electrographic status epilepticus. The induction of status epilepticus-like activity by CB1 receptor antagonists was reversible and could be overcome by maximal concentrations of CB1 agonists. Similar treatment of control neurons with CB1 receptor antagonists did not produce status epilepticus or hyperexcitability. These findings suggest that CB1 receptor-dependent endocannabinoid endogenous tone plays an important role in modulating seizure frequency and duration and preventing the development of status epilepticus-like activity in populations of epileptic neurons. The regulation of seizure activity and prevention of status epilepticus by the endocannabinoid system offers an important insight into understanding the basic mechanisms that control the development of continuous epileptiform discharges. |
| doi_str_mv | 10.1016/j.neulet.2006.09.046 |
| format | Article |
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μM) or AM251 (1
μM) to “epileptic” neurons caused the development of continuous epileptiform activity, resembling electrographic status epilepticus. The induction of status epilepticus-like activity by CB1 receptor antagonists was reversible and could be overcome by maximal concentrations of CB1 agonists. Similar treatment of control neurons with CB1 receptor antagonists did not produce status epilepticus or hyperexcitability. These findings suggest that CB1 receptor-dependent endocannabinoid endogenous tone plays an important role in modulating seizure frequency and duration and preventing the development of status epilepticus-like activity in populations of epileptic neurons. The regulation of seizure activity and prevention of status epilepticus by the endocannabinoid system offers an important insight into understanding the basic mechanisms that control the development of continuous epileptiform discharges.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2006.09.046</identifier><identifier>PMID: 17110038</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Action Potentials - drug effects ; Action Potentials - physiology ; Action Potentials - radiation effects ; Animals ; Animals, Newborn ; Benzoxazines ; Biological and medical sciences ; Cannabinoid ; CB1 receptor ; Cells, Cultured ; Disease Models, Animal ; Drug Interactions ; Endocannabinoid tone ; Epilepsy ; Epilepsy - chemically induced ; Epilepsy - pathology ; Fundamental and applied biological sciences. Psychology ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Hippocampus - pathology ; Medical sciences ; Morpholines - pharmacology ; Naphthalenes - pharmacology ; Nervous system (semeiology, syndromes) ; Neurology ; Neurons - drug effects ; Neurons - physiology ; Patch-Clamp Techniques - methods ; Piperidines - pharmacology ; Pyrazoles - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1 - antagonists & inhibitors ; Rimonabant ; Status epilepticus ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2007-01, Vol.411 (1), p.11-16</ispartof><rights>2006 Elsevier Ireland Ltd</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-e06d872e44c65153880a12be08937a6afc24a368bc6ec7b5c7c8cc00e86eb4643</citedby><cites>FETCH-LOGICAL-c557t-e06d872e44c65153880a12be08937a6afc24a368bc6ec7b5c7c8cc00e86eb4643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neulet.2006.09.046$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18332247$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17110038$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deshpande, Laxmikant S.</creatorcontrib><creatorcontrib>Sombati, Sompong</creatorcontrib><creatorcontrib>Blair, Robert E.</creatorcontrib><creatorcontrib>Carter, Dawn S.</creatorcontrib><creatorcontrib>Martin, Billy R.</creatorcontrib><creatorcontrib>DeLorenzo, Robert J.</creatorcontrib><title>Cannabinoid CB1 receptor antagonists cause status epilepticus-like activity in the hippocampal neuronal culture model of acquired epilepsy</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Status epilepticus (SE) is a major medical emergency associated with a significant morbidity and mortality. Little is known about the mechanisms that terminate seizure activity and prevent the development of status epilepticus. Cannabinoids possess anticonvulsant properties and the endocannabinoid system has been implicated in regulating seizure duration and frequency. Endocannabinoids regulate synaptic transmission and dampen seizure activity via activation of the presynaptic cannabinoid receptor 1 (CB1). This study was initiated to evaluate the role of CB1 receptor-dependent endocannabinoid synaptic transmission towards preventing the development of status epilepticus-like activity in the well-characterized hippocampal neuronal culture model of acquired epilepsy using patch clamp electrophysiology. Application of the CB1 receptor antagonists SR141716A (1
μM) or AM251 (1
μM) to “epileptic” neurons caused the development of continuous epileptiform activity, resembling electrographic status epilepticus. The induction of status epilepticus-like activity by CB1 receptor antagonists was reversible and could be overcome by maximal concentrations of CB1 agonists. Similar treatment of control neurons with CB1 receptor antagonists did not produce status epilepticus or hyperexcitability. These findings suggest that CB1 receptor-dependent endocannabinoid endogenous tone plays an important role in modulating seizure frequency and duration and preventing the development of status epilepticus-like activity in populations of epileptic neurons. The regulation of seizure activity and prevention of status epilepticus by the endocannabinoid system offers an important insight into understanding the basic mechanisms that control the development of continuous epileptiform discharges.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Action Potentials - radiation effects</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Benzoxazines</subject><subject>Biological and medical sciences</subject><subject>Cannabinoid</subject><subject>CB1 receptor</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Drug Interactions</subject><subject>Endocannabinoid tone</subject><subject>Epilepsy</subject><subject>Epilepsy - chemically induced</subject><subject>Epilepsy - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Hippocampus - pathology</subject><subject>Medical sciences</subject><subject>Morpholines - pharmacology</subject><subject>Naphthalenes - pharmacology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Patch-Clamp Techniques - methods</subject><subject>Piperidines - pharmacology</subject><subject>Pyrazoles - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Cannabinoid, CB1 - antagonists & inhibitors</subject><subject>Rimonabant</subject><subject>Status epilepticus</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2O0zAUhSMEYsrAGyDkDcuE68RxnA0SVPxJI7GBteXc3ExdUjvYTqW-Ak-NR60obFjZks85vud-RfGSQ8WByzf7ytE6U6pqAFlBX4GQj4oNV11ddn1XPy420IAom17ATfEsxj0AtLwVT4sb3nEO0KhN8WtrnDODdd6ObPues0BIS_KBGZfMvXc2psjQrJFYTCatkdFi5yyxuMZytj-IGUz2aNOJWcfSjtjOLotHc1jMzPKMwbt8wXVOayB28CPNzE_Z9XO1gcZLXjw9L55MZo704nLeFt8_fvi2_Vzeff30ZfvursS27VJJIMfckYRAmes0SoHh9UCg-qYz0kxYC9NINaAk7IYWO1SIAKQkDUKK5rZ4e85d1uFAI5JLwcx6CfZgwkl7Y_W_L87u9L0_aq5AiV7mAHEOwOBjDDT98XLQD2z0Xp_Z6Ac2Gnqd2WTbq7__vZouMLLg9UVgIpp5CsahjVedapq6Ft21AOUtHS0FHdGSQxrzPjHp0dv_T_IbtKu0Tw</recordid><startdate>20070103</startdate><enddate>20070103</enddate><creator>Deshpande, Laxmikant S.</creator><creator>Sombati, Sompong</creator><creator>Blair, Robert E.</creator><creator>Carter, Dawn S.</creator><creator>Martin, Billy R.</creator><creator>DeLorenzo, Robert J.</creator><general>Elsevier Ireland Ltd</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>5PM</scope></search><sort><creationdate>20070103</creationdate><title>Cannabinoid CB1 receptor antagonists cause status epilepticus-like activity in the hippocampal neuronal culture model of acquired epilepsy</title><author>Deshpande, Laxmikant S. ; Sombati, Sompong ; Blair, Robert E. ; Carter, Dawn S. ; Martin, Billy R. ; DeLorenzo, Robert J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-e06d872e44c65153880a12be08937a6afc24a368bc6ec7b5c7c8cc00e86eb4643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Action Potentials - radiation effects</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Benzoxazines</topic><topic>Biological and medical sciences</topic><topic>Cannabinoid</topic><topic>CB1 receptor</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Drug Interactions</topic><topic>Endocannabinoid tone</topic><topic>Epilepsy</topic><topic>Epilepsy - chemically induced</topic><topic>Epilepsy - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hippocampus - pathology</topic><topic>Medical sciences</topic><topic>Morpholines - pharmacology</topic><topic>Naphthalenes - pharmacology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Patch-Clamp Techniques - methods</topic><topic>Piperidines - pharmacology</topic><topic>Pyrazoles - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Cannabinoid, CB1 - antagonists & inhibitors</topic><topic>Rimonabant</topic><topic>Status epilepticus</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deshpande, Laxmikant S.</creatorcontrib><creatorcontrib>Sombati, Sompong</creatorcontrib><creatorcontrib>Blair, Robert E.</creatorcontrib><creatorcontrib>Carter, Dawn S.</creatorcontrib><creatorcontrib>Martin, Billy R.</creatorcontrib><creatorcontrib>DeLorenzo, Robert J.</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>PubMed Central (Full Participant titles)</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deshpande, Laxmikant S.</au><au>Sombati, Sompong</au><au>Blair, Robert E.</au><au>Carter, Dawn S.</au><au>Martin, Billy R.</au><au>DeLorenzo, Robert J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cannabinoid CB1 receptor antagonists cause status epilepticus-like activity in the hippocampal neuronal culture model of acquired epilepsy</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2007-01-03</date><risdate>2007</risdate><volume>411</volume><issue>1</issue><spage>11</spage><epage>16</epage><pages>11-16</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Status epilepticus (SE) is a major medical emergency associated with a significant morbidity and mortality. Little is known about the mechanisms that terminate seizure activity and prevent the development of status epilepticus. Cannabinoids possess anticonvulsant properties and the endocannabinoid system has been implicated in regulating seizure duration and frequency. Endocannabinoids regulate synaptic transmission and dampen seizure activity via activation of the presynaptic cannabinoid receptor 1 (CB1). This study was initiated to evaluate the role of CB1 receptor-dependent endocannabinoid synaptic transmission towards preventing the development of status epilepticus-like activity in the well-characterized hippocampal neuronal culture model of acquired epilepsy using patch clamp electrophysiology. Application of the CB1 receptor antagonists SR141716A (1
μM) or AM251 (1
μM) to “epileptic” neurons caused the development of continuous epileptiform activity, resembling electrographic status epilepticus. The induction of status epilepticus-like activity by CB1 receptor antagonists was reversible and could be overcome by maximal concentrations of CB1 agonists. Similar treatment of control neurons with CB1 receptor antagonists did not produce status epilepticus or hyperexcitability. These findings suggest that CB1 receptor-dependent endocannabinoid endogenous tone plays an important role in modulating seizure frequency and duration and preventing the development of status epilepticus-like activity in populations of epileptic neurons. The regulation of seizure activity and prevention of status epilepticus by the endocannabinoid system offers an important insight into understanding the basic mechanisms that control the development of continuous epileptiform discharges.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>17110038</pmid><doi>10.1016/j.neulet.2006.09.046</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neuroscience letters, 2007-01, Vol.411 (1), p.11-16 |
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| language | eng |
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| subjects | Action Potentials - drug effects Action Potentials - physiology Action Potentials - radiation effects Animals Animals, Newborn Benzoxazines Biological and medical sciences Cannabinoid CB1 receptor Cells, Cultured Disease Models, Animal Drug Interactions Endocannabinoid tone Epilepsy Epilepsy - chemically induced Epilepsy - pathology Fundamental and applied biological sciences. Psychology Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hippocampus - pathology Medical sciences Morpholines - pharmacology Naphthalenes - pharmacology Nervous system (semeiology, syndromes) Neurology Neurons - drug effects Neurons - physiology Patch-Clamp Techniques - methods Piperidines - pharmacology Pyrazoles - pharmacology Rats Rats, Sprague-Dawley Receptor, Cannabinoid, CB1 - antagonists & inhibitors Rimonabant Status epilepticus Synaptic Transmission - drug effects Synaptic Transmission - physiology Vertebrates: nervous system and sense organs |
| title | Cannabinoid CB1 receptor antagonists cause status epilepticus-like activity in the hippocampal neuronal culture model of acquired epilepsy |
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