Propofol exhibits antiepileptic activity in hippocampal pyramidal neurons
Propofol was reported to exhibit an antiepileptic activity. This study was performed to investigate the effect of propofol on evoked and spontaneous seizure-like activity induced by the convulsant veratridine. Studies were performed on rat brain slices using conventional electrophysiological intrace...
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| Veröffentlicht in: | Pharmacology, biochemistry and behavior biochemistry and behavior, 2004-03, Vol.77 (3), p.595-599 |
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| creator | Otoom, Sameer A. Hasan, Zuheir |
| description | Propofol was reported to exhibit an antiepileptic activity. This study was performed to investigate the effect of propofol on evoked and spontaneous seizure-like activity induced by the convulsant veratridine. Studies were performed on rat brain slices using conventional electrophysiological intracellular techniques. The alteration of sodium channel function by veratridine (0.3 μM) induced an evoked and spontaneous seizure-like activity in the hippocampal CA1 pyramidal neurons. Therapeutic concentrations of propofol (10 μM) were ineffective in inhibiting veratridine-induced seizure-like activity. However, higher concentrations (50–100 μM,
n=6) inhibited both evoked and spontaneous bursting, induced by veratridine. The inhibitory effect of propofol (100 μM) was associated with membrane hyperpolarization [after veratridine, −66±0.71 mV (mean±S.E.M.), and after propofol, −77±2.15 mV] and with an increase in input resistance [after veratridine (37.8±1.2 MΩ) and after propofol (43±1.3 MΩ)]. The drug also produced an increase in current threshold. Results from this study are valuable in solving critical questions regarding the antiepileptic activity of propofol and strengthen the validity of the veratridine model in testing for potential antiepileptic drugs. |
| doi_str_mv | 10.1016/j.pbb.2003.12.021 |
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n=6) inhibited both evoked and spontaneous bursting, induced by veratridine. The inhibitory effect of propofol (100 μM) was associated with membrane hyperpolarization [after veratridine, −66±0.71 mV (mean±S.E.M.), and after propofol, −77±2.15 mV] and with an increase in input resistance [after veratridine (37.8±1.2 MΩ) and after propofol (43±1.3 MΩ)]. The drug also produced an increase in current threshold. Results from this study are valuable in solving critical questions regarding the antiepileptic activity of propofol and strengthen the validity of the veratridine model in testing for potential antiepileptic drugs.</description><identifier>ISSN: 0091-3057</identifier><identifier>EISSN: 1873-5177</identifier><identifier>DOI: 10.1016/j.pbb.2003.12.021</identifier><identifier>PMID: 15006471</identifier><identifier>CODEN: PBBHAU</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Anticonvulsants - pharmacology ; Biological and medical sciences ; Brain slice ; CA1 ; Fundamental and applied biological sciences. Psychology ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - physiology ; Male ; Medical sciences ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Neuropharmacology ; Pharmacology. Drug treatments ; Propofol ; Propofol - pharmacology ; Psychology. Psychoanalysis. Psychiatry ; Psychology. Psychophysiology ; Pyramidal Cells - drug effects ; Pyramidal Cells - physiology ; Rats ; Rats, Sprague-Dawley ; Spontaneous and evoked bursting ; Veratridine ; Veratridine - pharmacology</subject><ispartof>Pharmacology, biochemistry and behavior, 2004-03, Vol.77 (3), p.595-599</ispartof><rights>2004 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-9cb1922d5d43d1b1f3f94f5fde021089f7e06c26a2fa26a00d95ff30927c1de73</citedby><cites>FETCH-LOGICAL-c410t-9cb1922d5d43d1b1f3f94f5fde021089f7e06c26a2fa26a00d95ff30927c1de73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.pbb.2003.12.021$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16009000$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15006471$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Otoom, Sameer A.</creatorcontrib><creatorcontrib>Hasan, Zuheir</creatorcontrib><title>Propofol exhibits antiepileptic activity in hippocampal pyramidal neurons</title><title>Pharmacology, biochemistry and behavior</title><addtitle>Pharmacol Biochem Behav</addtitle><description>Propofol was reported to exhibit an antiepileptic activity. This study was performed to investigate the effect of propofol on evoked and spontaneous seizure-like activity induced by the convulsant veratridine. Studies were performed on rat brain slices using conventional electrophysiological intracellular techniques. The alteration of sodium channel function by veratridine (0.3 μM) induced an evoked and spontaneous seizure-like activity in the hippocampal CA1 pyramidal neurons. Therapeutic concentrations of propofol (10 μM) were ineffective in inhibiting veratridine-induced seizure-like activity. However, higher concentrations (50–100 μM,
n=6) inhibited both evoked and spontaneous bursting, induced by veratridine. The inhibitory effect of propofol (100 μM) was associated with membrane hyperpolarization [after veratridine, −66±0.71 mV (mean±S.E.M.), and after propofol, −77±2.15 mV] and with an increase in input resistance [after veratridine (37.8±1.2 MΩ) and after propofol (43±1.3 MΩ)]. The drug also produced an increase in current threshold. Results from this study are valuable in solving critical questions regarding the antiepileptic activity of propofol and strengthen the validity of the veratridine model in testing for potential antiepileptic drugs.</description><subject>Animals</subject><subject>Anticonvulsants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain slice</subject><subject>CA1</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Propofol</subject><subject>Propofol - pharmacology</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Spontaneous and evoked bursting</subject><subject>Veratridine</subject><subject>Veratridine - pharmacology</subject><issn>0091-3057</issn><issn>1873-5177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT1rHDEQhkVIiM9OfkCasE3c7WZG-yGLVME4icEQF0kttNII69hdKdKe8f1767gDd3GjUfHMy8szjH1CaBBw-Lpt4jg2HKBtkDfA8Q3b4JVo6x6FeMs2ABLrFnpxxs5z3gJAxwfxnp1hDzB0Ajfs9j6FGFyYKnp68KNfc6WX1VP0E8XVm0qb1T_6dV_5pXrwMQaj56inKu6Tnr0tv4V2KSz5A3vn9JTp42lesL8_bv5c_6rvfv-8vf5-V5sOYa2lGVFybnvbtRZHdK2TneudpdIfrqQTBIPhg-ZOlxfAyt65FiQXBi2J9oJdHnNjCv92lFc1-2xomvRCYZeVQIH9MPSvgihb2aE8JOIRNCnknMipmPys014hqINotVVFtDqIVshVKVp2Pp_Cd-NM9mXjZLYAX06AzkZPLunF-PzCDeU45SCF-3bkqDh79JRUNp4WQ9YnMquywf-nxjOTQ5t0</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Otoom, Sameer A.</creator><creator>Hasan, Zuheir</creator><general>Elsevier Inc</general><general>Elsevier Science</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>7QG</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20040301</creationdate><title>Propofol exhibits antiepileptic activity in hippocampal pyramidal neurons</title><author>Otoom, Sameer A. ; Hasan, Zuheir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-9cb1922d5d43d1b1f3f94f5fde021089f7e06c26a2fa26a00d95ff30927c1de73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Anticonvulsants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain slice</topic><topic>CA1</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Propofol</topic><topic>Propofol - pharmacology</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. Psychophysiology</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Spontaneous and evoked bursting</topic><topic>Veratridine</topic><topic>Veratridine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Otoom, Sameer A.</creatorcontrib><creatorcontrib>Hasan, Zuheir</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>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Pharmacology, biochemistry and behavior</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Otoom, Sameer A.</au><au>Hasan, Zuheir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Propofol exhibits antiepileptic activity in hippocampal pyramidal neurons</atitle><jtitle>Pharmacology, biochemistry and behavior</jtitle><addtitle>Pharmacol Biochem Behav</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>77</volume><issue>3</issue><spage>595</spage><epage>599</epage><pages>595-599</pages><issn>0091-3057</issn><eissn>1873-5177</eissn><coden>PBBHAU</coden><abstract>Propofol was reported to exhibit an antiepileptic activity. This study was performed to investigate the effect of propofol on evoked and spontaneous seizure-like activity induced by the convulsant veratridine. Studies were performed on rat brain slices using conventional electrophysiological intracellular techniques. The alteration of sodium channel function by veratridine (0.3 μM) induced an evoked and spontaneous seizure-like activity in the hippocampal CA1 pyramidal neurons. Therapeutic concentrations of propofol (10 μM) were ineffective in inhibiting veratridine-induced seizure-like activity. However, higher concentrations (50–100 μM,
n=6) inhibited both evoked and spontaneous bursting, induced by veratridine. The inhibitory effect of propofol (100 μM) was associated with membrane hyperpolarization [after veratridine, −66±0.71 mV (mean±S.E.M.), and after propofol, −77±2.15 mV] and with an increase in input resistance [after veratridine (37.8±1.2 MΩ) and after propofol (43±1.3 MΩ)]. The drug also produced an increase in current threshold. Results from this study are valuable in solving critical questions regarding the antiepileptic activity of propofol and strengthen the validity of the veratridine model in testing for potential antiepileptic drugs.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15006471</pmid><doi>10.1016/j.pbb.2003.12.021</doi><tpages>5</tpages></addata></record> |
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| ispartof | Pharmacology, biochemistry and behavior, 2004-03, Vol.77 (3), p.595-599 |
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| subjects | Animals Anticonvulsants - pharmacology Biological and medical sciences Brain slice CA1 Fundamental and applied biological sciences. Psychology Hippocampus Hippocampus - drug effects Hippocampus - physiology Male Medical sciences Membrane Potentials - drug effects Membrane Potentials - physiology Neuropharmacology Pharmacology. Drug treatments Propofol Propofol - pharmacology Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Pyramidal Cells - drug effects Pyramidal Cells - physiology Rats Rats, Sprague-Dawley Spontaneous and evoked bursting Veratridine Veratridine - pharmacology |
| title | Propofol exhibits antiepileptic activity in hippocampal pyramidal neurons |
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