Valproate suppresses N-methyl- d-aspartate-evoked, transient depolarizations in the rat neocortex in vitro
Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1–1 mm) in a dose-related manner suppressed the characteristic transient depolarizations induced by N-methyl- d-aspartate (NMDA)...
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| Veröffentlicht in: | Brain research 1991-03, Vol.544 (2), p.345-348 |
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| creator | Zeise, M.L. Kasparow, S. Zieglgänsberger, W. |
| description | Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1–1 mm) in a dose-related manner suppressed the characteristic transient depolarizations induced by
N-methyl-
d-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5–10 mM) also reduced
l-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation. |
| doi_str_mv | 10.1016/0006-8993(91)90078-A |
| format | Article |
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N-methyl-
d-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5–10 mM) also reduced
l-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/0006-8993(91)90078-A</identifier><identifier>PMID: 2039949</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Animals ; Anticonvulsant ; Anticonvulsants. Antiepileptics. Antiparkinson agents ; Biological and medical sciences ; Diencephalon - physiology ; Glutamates - pharmacology ; In Vitro Techniques ; Inhibitory postsynaptic potential ; l-Glutamate ; Medical sciences ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; N-Methyl- d-aspartate ; N-Methylaspartate ; Neocortex slice ; Neuropharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred Strains ; Repetitive firing ; Synapses - physiology ; Telencephalon - physiology ; Valproate ; Valproic Acid - pharmacology</subject><ispartof>Brain research, 1991-03, Vol.544 (2), p.345-348</ispartof><rights>1991 Elsevier Science Publishers B.V. (Biomedical Division)</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c333t-b854fbb7c5962e466df9c597c0a91348f643f2c31e9bb920d28a90186fc5b7593</citedby><cites>FETCH-LOGICAL-c333t-b854fbb7c5962e466df9c597c0a91348f643f2c31e9bb920d28a90186fc5b7593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/000689939190078A$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19613965$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2039949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeise, M.L.</creatorcontrib><creatorcontrib>Kasparow, S.</creatorcontrib><creatorcontrib>Zieglgänsberger, W.</creatorcontrib><title>Valproate suppresses N-methyl- d-aspartate-evoked, transient depolarizations in the rat neocortex in vitro</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1–1 mm) in a dose-related manner suppressed the characteristic transient depolarizations induced by
N-methyl-
d-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5–10 mM) also reduced
l-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation.</description><subject>Animals</subject><subject>Anticonvulsant</subject><subject>Anticonvulsants. Antiepileptics. Antiparkinson agents</subject><subject>Biological and medical sciences</subject><subject>Diencephalon - physiology</subject><subject>Glutamates - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Inhibitory postsynaptic potential</subject><subject>l-Glutamate</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>N-Methyl- d-aspartate</subject><subject>N-Methylaspartate</subject><subject>Neocortex slice</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Repetitive firing</subject><subject>Synapses - physiology</subject><subject>Telencephalon - physiology</subject><subject>Valproate</subject><subject>Valproic Acid - pharmacology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2P1DAMQCMEWoaFfwBSLyCQCCRNm8YXpNGKL2kFF-AapamrzdJpSpwZsfx6Uma03OCUxH62nGfGHkvxSgqpXwshNDcA6jnIFyBEZ_j2DttI09Vc1424yza3yH32gOi6PJUCccbOaqEAGtiw629uWlJ0GSvaL0tCIqTqE99hvrqZeDVwR4tLuQAcD_E7Di-rnNxMAedcDbjEyaXwy-UQZ6rCXOUrrJLL1YzRx5Tx5xo8hJziQ3ZvdBPho9N5zr6-e_vl4gO__Pz-48X2knulVOa9aZux7zvfgq6x0XoYodw7LxxI1ZhRN2qsvZIIfQ-1GGrjQEijR9_2XQvqnD079i3_-rFHynYXyOM0uTLTnqwRrVGN-D8oWxBamxVsjqBPkSjhaJcUdi7dWCnsugu7iraraAvS_tmF3ZayJ6f--36Hw23RSX7JPz3lHXk3jUWrD_S3N2ipQLeFe3PksFg7BEyWfNHvcQgJfbZDDP8e5DfKCqaW</recordid><startdate>19910329</startdate><enddate>19910329</enddate><creator>Zeise, M.L.</creator><creator>Kasparow, S.</creator><creator>Zieglgänsberger, W.</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>7X8</scope></search><sort><creationdate>19910329</creationdate><title>Valproate suppresses N-methyl- d-aspartate-evoked, transient depolarizations in the rat neocortex in vitro</title><author>Zeise, M.L. ; Kasparow, S. ; Zieglgänsberger, W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c333t-b854fbb7c5962e466df9c597c0a91348f643f2c31e9bb920d28a90186fc5b7593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Animals</topic><topic>Anticonvulsant</topic><topic>Anticonvulsants. Antiepileptics. Antiparkinson agents</topic><topic>Biological and medical sciences</topic><topic>Diencephalon - physiology</topic><topic>Glutamates - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Inhibitory postsynaptic potential</topic><topic>l-Glutamate</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>N-Methyl- d-aspartate</topic><topic>N-Methylaspartate</topic><topic>Neocortex slice</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Repetitive firing</topic><topic>Synapses - physiology</topic><topic>Telencephalon - physiology</topic><topic>Valproate</topic><topic>Valproic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeise, M.L.</creatorcontrib><creatorcontrib>Kasparow, S.</creatorcontrib><creatorcontrib>Zieglgänsberger, W.</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>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeise, M.L.</au><au>Kasparow, S.</au><au>Zieglgänsberger, W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Valproate suppresses N-methyl- d-aspartate-evoked, transient depolarizations in the rat neocortex in vitro</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1991-03-29</date><risdate>1991</risdate><volume>544</volume><issue>2</issue><spage>345</spage><epage>348</epage><pages>345-348</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1–1 mm) in a dose-related manner suppressed the characteristic transient depolarizations induced by
N-methyl-
d-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5–10 mM) also reduced
l-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>2039949</pmid><doi>10.1016/0006-8993(91)90078-A</doi><tpages>4</tpages></addata></record> |
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| ispartof | Brain research, 1991-03, Vol.544 (2), p.345-348 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Anticonvulsant Anticonvulsants. Antiepileptics. Antiparkinson agents Biological and medical sciences Diencephalon - physiology Glutamates - pharmacology In Vitro Techniques Inhibitory postsynaptic potential l-Glutamate Medical sciences Membrane Potentials - drug effects Membrane Potentials - physiology N-Methyl- d-aspartate N-Methylaspartate Neocortex slice Neuropharmacology Pharmacology. Drug treatments Rats Rats, Inbred Strains Repetitive firing Synapses - physiology Telencephalon - physiology Valproate Valproic Acid - pharmacology |
| title | Valproate suppresses N-methyl- d-aspartate-evoked, transient depolarizations in the rat neocortex in vitro |
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