Activation of N-methyl-D-aspartate-sensitive glutamate receptors stimulates arachidonic acid release in primary cultures of cerebellar granule cells
In cultured granule cells prelabeled with [ 3H]arachidonate the activation of excitatory amino acid receptors by various agonists results in a dose-dependent stimulation of [ 3H]arachidonic acid release. Glutamate and aspartate were the most potent agonists, whereas N-methyl-D-aspartate, kainate and...
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| Veröffentlicht in: | Neuropharmacology 1988-07, Vol.27 (7), p.765-769 |
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| container_title | Neuropharmacology |
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| creator | Lazarewicz, J.W. Wroblewski, J.T. Palmer, M.E. Costa, E. |
| description | In cultured granule cells prelabeled with [
3H]arachidonate the activation of excitatory amino acid receptors by various agonists results in a dose-dependent stimulation of [
3H]arachidonic acid release. Glutamate and aspartate were the most potent agonists, whereas N-methyl-D-aspartate, kainate and quisqualate were less potent. Other neurotransmitter receptor agonists — GABA, baclofen and norepinephrine — were inactive, while carbachol induced only a slight effect. Since the transmitter-mediated release of [
3H]arachidonate was blocked by phencyclidine, a selective inhibitor of NMDA-sensitive glutamate receptors, it can be inferred that the effects of all other receptor agonists were indirectly mediated via the release of glutamate from granule cells. Aspartate-evoked release was Ca
2+-dependent and was abolished by the glutamate receptor inhibitors: Mg
2+ ions and 2-amino-5-phosphonovalerate. The inhibitors of phospholipase A
2, quinacrine and p-bromophenacyi bromide, decreased the release of [
3H]arachidonate in a dose-related manner. |
| doi_str_mv | 10.1016/0028-3908(88)90088-3 |
| format | Article |
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3H]arachidonate the activation of excitatory amino acid receptors by various agonists results in a dose-dependent stimulation of [
3H]arachidonic acid release. Glutamate and aspartate were the most potent agonists, whereas N-methyl-D-aspartate, kainate and quisqualate were less potent. Other neurotransmitter receptor agonists — GABA, baclofen and norepinephrine — were inactive, while carbachol induced only a slight effect. Since the transmitter-mediated release of [
3H]arachidonate was blocked by phencyclidine, a selective inhibitor of NMDA-sensitive glutamate receptors, it can be inferred that the effects of all other receptor agonists were indirectly mediated via the release of glutamate from granule cells. Aspartate-evoked release was Ca
2+-dependent and was abolished by the glutamate receptor inhibitors: Mg
2+ ions and 2-amino-5-phosphonovalerate. The inhibitors of phospholipase A
2, quinacrine and p-bromophenacyi bromide, decreased the release of [
3H]arachidonate in a dose-related manner.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/0028-3908(88)90088-3</identifier><identifier>PMID: 2843786</identifier><identifier>CODEN: NEPHBW</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Arachidonic Acid ; Arachidonic Acids - metabolism ; Aspartate ; Aspartic Acid - analogs & derivatives ; Aspartic Acid - pharmacology ; Biological and medical sciences ; Ca 2 ; Cells, Cultured ; Cerebellum - cytology ; Cerebellum - drug effects ; Cerebellum - metabolism ; Glutamate ; Glutamates - metabolism ; Medical sciences ; Mg 2 ; Miscellaneous ; N-Methylaspartate ; Neuropharmacology ; Neurotransmitters. Neurotransmission. Receptors ; NMDA ; Pharmacology. Drug treatments ; Phencyclidine ; Phospholipase A 2 ; Rats ; Receptors, Glutamate ; Receptors, Neurotransmitter - drug effects</subject><ispartof>Neuropharmacology, 1988-07, Vol.27 (7), p.765-769</ispartof><rights>1988</rights><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-899a339c33348d8f628901d9490970837cb66fd26d82360ff3de5700f4afb27c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0028390888900883$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7121677$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2843786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lazarewicz, J.W.</creatorcontrib><creatorcontrib>Wroblewski, J.T.</creatorcontrib><creatorcontrib>Palmer, M.E.</creatorcontrib><creatorcontrib>Costa, E.</creatorcontrib><title>Activation of N-methyl-D-aspartate-sensitive glutamate receptors stimulates arachidonic acid release in primary cultures of cerebellar granule cells</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>In cultured granule cells prelabeled with [
3H]arachidonate the activation of excitatory amino acid receptors by various agonists results in a dose-dependent stimulation of [
3H]arachidonic acid release. Glutamate and aspartate were the most potent agonists, whereas N-methyl-D-aspartate, kainate and quisqualate were less potent. Other neurotransmitter receptor agonists — GABA, baclofen and norepinephrine — were inactive, while carbachol induced only a slight effect. Since the transmitter-mediated release of [
3H]arachidonate was blocked by phencyclidine, a selective inhibitor of NMDA-sensitive glutamate receptors, it can be inferred that the effects of all other receptor agonists were indirectly mediated via the release of glutamate from granule cells. Aspartate-evoked release was Ca
2+-dependent and was abolished by the glutamate receptor inhibitors: Mg
2+ ions and 2-amino-5-phosphonovalerate. The inhibitors of phospholipase A
2, quinacrine and p-bromophenacyi bromide, decreased the release of [
3H]arachidonate in a dose-related manner.</description><subject>Animals</subject><subject>Arachidonic Acid</subject><subject>Arachidonic Acids - metabolism</subject><subject>Aspartate</subject><subject>Aspartic Acid - analogs & derivatives</subject><subject>Aspartic Acid - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Ca 2</subject><subject>Cells, Cultured</subject><subject>Cerebellum - cytology</subject><subject>Cerebellum - drug effects</subject><subject>Cerebellum - metabolism</subject><subject>Glutamate</subject><subject>Glutamates - metabolism</subject><subject>Medical sciences</subject><subject>Mg 2</subject><subject>Miscellaneous</subject><subject>N-Methylaspartate</subject><subject>Neuropharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>NMDA</subject><subject>Pharmacology. Drug treatments</subject><subject>Phencyclidine</subject><subject>Phospholipase A 2</subject><subject>Rats</subject><subject>Receptors, Glutamate</subject><subject>Receptors, Neurotransmitter - drug effects</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2OFCEUhYnRjO3oG2jCwhhdlF6Kan42k0zG32SiG10TGi4zGKqqBWqSeQ8fWNqu9FJXhHO_e7mcQ8hzBm8ZMPEOoFcd16BeK_VGA6h2e0A2TEneSRDDQ7I5IY_Jk1J-AsCgmDojZ70auFRiQ35fuhrvbI3zROdAv3Yj1tv71L3vbNnbXG3FruBUYqOQ3qSl2rFpNKPDfZ1zoaXGcUlNK9Rm626jn6foqHXRNyqhLUjjRPc5jjbfU7ekuuQGt9ccZtxhSjbTm2ynJWGTUipPyaNgU8Fn63lOfnz88P3qc3f97dOXq8vrzg1M1k5pbTnXjnM-KK-C6JUG5vWgQUtQXLqdEMH3wqueCwiBe9xKgDDYsOul4-fk1XHuPs-_FizVjLEcNrATzksxsrkkttD_F2SD1gK2rIHDEXR5LiVjMOu_DQNzSM0cIjGHSIxS5m9qhre2F-v8ZTeiPzWtMbX6y7Vui7MpNLNcLCdMsp4JKRt2ccSwmXYXMZviIk4OfWx5VePn-O89_gBvnrXY</recordid><startdate>19880701</startdate><enddate>19880701</enddate><creator>Lazarewicz, J.W.</creator><creator>Wroblewski, J.T.</creator><creator>Palmer, M.E.</creator><creator>Costa, E.</creator><general>Elsevier 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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19880701</creationdate><title>Activation of N-methyl-D-aspartate-sensitive glutamate receptors stimulates arachidonic acid release in primary cultures of cerebellar granule cells</title><author>Lazarewicz, J.W. ; Wroblewski, J.T. ; Palmer, M.E. ; Costa, E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-899a339c33348d8f628901d9490970837cb66fd26d82360ff3de5700f4afb27c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Animals</topic><topic>Arachidonic Acid</topic><topic>Arachidonic Acids - metabolism</topic><topic>Aspartate</topic><topic>Aspartic Acid - analogs & derivatives</topic><topic>Aspartic Acid - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Ca 2</topic><topic>Cells, Cultured</topic><topic>Cerebellum - cytology</topic><topic>Cerebellum - drug effects</topic><topic>Cerebellum - metabolism</topic><topic>Glutamate</topic><topic>Glutamates - metabolism</topic><topic>Medical sciences</topic><topic>Mg 2</topic><topic>Miscellaneous</topic><topic>N-Methylaspartate</topic><topic>Neuropharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>NMDA</topic><topic>Pharmacology. Drug treatments</topic><topic>Phencyclidine</topic><topic>Phospholipase A 2</topic><topic>Rats</topic><topic>Receptors, Glutamate</topic><topic>Receptors, Neurotransmitter - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lazarewicz, J.W.</creatorcontrib><creatorcontrib>Wroblewski, J.T.</creatorcontrib><creatorcontrib>Palmer, M.E.</creatorcontrib><creatorcontrib>Costa, E.</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>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lazarewicz, J.W.</au><au>Wroblewski, J.T.</au><au>Palmer, M.E.</au><au>Costa, E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of N-methyl-D-aspartate-sensitive glutamate receptors stimulates arachidonic acid release in primary cultures of cerebellar granule cells</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>1988-07-01</date><risdate>1988</risdate><volume>27</volume><issue>7</issue><spage>765</spage><epage>769</epage><pages>765-769</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>In cultured granule cells prelabeled with [
3H]arachidonate the activation of excitatory amino acid receptors by various agonists results in a dose-dependent stimulation of [
3H]arachidonic acid release. Glutamate and aspartate were the most potent agonists, whereas N-methyl-D-aspartate, kainate and quisqualate were less potent. Other neurotransmitter receptor agonists — GABA, baclofen and norepinephrine — were inactive, while carbachol induced only a slight effect. Since the transmitter-mediated release of [
3H]arachidonate was blocked by phencyclidine, a selective inhibitor of NMDA-sensitive glutamate receptors, it can be inferred that the effects of all other receptor agonists were indirectly mediated via the release of glutamate from granule cells. Aspartate-evoked release was Ca
2+-dependent and was abolished by the glutamate receptor inhibitors: Mg
2+ ions and 2-amino-5-phosphonovalerate. The inhibitors of phospholipase A
2, quinacrine and p-bromophenacyi bromide, decreased the release of [
3H]arachidonate in a dose-related manner.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>2843786</pmid><doi>10.1016/0028-3908(88)90088-3</doi><tpages>5</tpages></addata></record> |
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| ispartof | Neuropharmacology, 1988-07, Vol.27 (7), p.765-769 |
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| source | MEDLINE; ScienceDirect Freedom Collection (Elsevier) |
| subjects | Animals Arachidonic Acid Arachidonic Acids - metabolism Aspartate Aspartic Acid - analogs & derivatives Aspartic Acid - pharmacology Biological and medical sciences Ca 2 Cells, Cultured Cerebellum - cytology Cerebellum - drug effects Cerebellum - metabolism Glutamate Glutamates - metabolism Medical sciences Mg 2 Miscellaneous N-Methylaspartate Neuropharmacology Neurotransmitters. Neurotransmission. Receptors NMDA Pharmacology. Drug treatments Phencyclidine Phospholipase A 2 Rats Receptors, Glutamate Receptors, Neurotransmitter - drug effects |
| title | Activation of N-methyl-D-aspartate-sensitive glutamate receptors stimulates arachidonic acid release in primary cultures of cerebellar granule cells |
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