Acetylcholine release from the rabbit retina mediated by kainate receptors
The cholinergic amacrine cells of the rabbit retina may be labeled with 3H-choline (3H-Ch), and the activity of the cholinergic population may be monitored by following the release of 3H-ACh. Glutamate analogs caused massive ACh release, up to 50 times the basal efflux, with the following rank order...
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| Veröffentlicht in: | The Journal of neuroscience 1991-01, Vol.11 (1), p.111-122 |
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| creator | Linn, DM Blazynski, C Redburn, DA Massey, SC |
| description | The cholinergic amacrine cells of the rabbit retina may be labeled with 3H-choline (3H-Ch), and the activity of the cholinergic population may be monitored by following the release of 3H-ACh. Glutamate analogs caused massive ACh release, up to 50 times the basal efflux, with the following rank order of potency: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) greater than quisqualate (QQ) = kainate (KA) much greater than NMDA (in magnesium-free medium) much greater than glutamate greater than aspartate. In contrast, the release of 3H-Ch was unchanged. Submaximal doses of each agonist were used to establish the specifity of glutamate antagonists. Kynurenic acid was selective for KA much greater than QQ, and 6,7-dinitroquinoxaline-2,3-dione (DNQX) was selective for KA greater than QQ much greater than NMDA. At low doses, which selectively blocked the response to KA, both antagonists blocked the light-evoked release of ACh. These results suggest that ACh release may be produced via several glutamate receptors, but the physiological input to the cholinergic amacrine cells is mediated by KA receptors. Because these cells receive direct input from cone bipolar cells, this work supports previous evidence that the bipolar cell transmitter is glutamate. |
| doi_str_mv | 10.1523/JNEUROSCI.11-01-00111.1991 |
| format | Article |
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Glutamate analogs caused massive ACh release, up to 50 times the basal efflux, with the following rank order of potency: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) greater than quisqualate (QQ) = kainate (KA) much greater than NMDA (in magnesium-free medium) much greater than glutamate greater than aspartate. In contrast, the release of 3H-Ch was unchanged. Submaximal doses of each agonist were used to establish the specifity of glutamate antagonists. Kynurenic acid was selective for KA much greater than QQ, and 6,7-dinitroquinoxaline-2,3-dione (DNQX) was selective for KA greater than QQ much greater than NMDA. At low doses, which selectively blocked the response to KA, both antagonists blocked the light-evoked release of ACh. These results suggest that ACh release may be produced via several glutamate receptors, but the physiological input to the cholinergic amacrine cells is mediated by KA receptors. Because these cells receive direct input from cone bipolar cells, this work supports previous evidence that the bipolar cell transmitter is glutamate.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.11-01-00111.1991</identifier><identifier>PMID: 1670781</identifier><identifier>CODEN: JNRSDS</identifier><language>eng</language><publisher>Washington, DC: Soc Neuroscience</publisher><subject>Acetylcholine - metabolism ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid ; Animals ; Aspartic Acid - pharmacology ; Biological and medical sciences ; Choline - metabolism ; Eye and associated structures. Visual pathways and centers. Vision ; Fundamental and applied biological sciences. Psychology ; Glutamates - pharmacology ; Glutamic Acid ; Ibotenic Acid - analogs & derivatives ; Ibotenic Acid - pharmacology ; In Vitro Techniques ; Kainic Acid - metabolism ; Kainic Acid - pharmacology ; N-Methylaspartate - pharmacology ; Quisqualic Acid - pharmacology ; Rabbits ; Receptors, Kainic Acid ; Receptors, Neurotransmitter - drug effects ; Receptors, Neurotransmitter - physiology ; Retina - drug effects ; Retina - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>The Journal of neuroscience, 1991-01, Vol.11 (1), p.111-122</ispartof><rights>1991 INIST-CNRS</rights><rights>1991 by Society for Neuroscience 1991</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-25ff835f6476f67cde55858585fb0a0287ce25a5f08d2dc075f04e6908ab8cbe3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6575200/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6575200/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,4025,27925,27926,27927,53793,53795</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19813694$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1670781$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Linn, DM</creatorcontrib><creatorcontrib>Blazynski, C</creatorcontrib><creatorcontrib>Redburn, DA</creatorcontrib><creatorcontrib>Massey, SC</creatorcontrib><title>Acetylcholine release from the rabbit retina mediated by kainate receptors</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>The cholinergic amacrine cells of the rabbit retina may be labeled with 3H-choline (3H-Ch), and the activity of the cholinergic population may be monitored by following the release of 3H-ACh. Glutamate analogs caused massive ACh release, up to 50 times the basal efflux, with the following rank order of potency: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) greater than quisqualate (QQ) = kainate (KA) much greater than NMDA (in magnesium-free medium) much greater than glutamate greater than aspartate. In contrast, the release of 3H-Ch was unchanged. Submaximal doses of each agonist were used to establish the specifity of glutamate antagonists. Kynurenic acid was selective for KA much greater than QQ, and 6,7-dinitroquinoxaline-2,3-dione (DNQX) was selective for KA greater than QQ much greater than NMDA. At low doses, which selectively blocked the response to KA, both antagonists blocked the light-evoked release of ACh. These results suggest that ACh release may be produced via several glutamate receptors, but the physiological input to the cholinergic amacrine cells is mediated by KA receptors. Because these cells receive direct input from cone bipolar cells, this work supports previous evidence that the bipolar cell transmitter is glutamate.</description><subject>Acetylcholine - metabolism</subject><subject>alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid</subject><subject>Animals</subject><subject>Aspartic Acid - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Choline - metabolism</subject><subject>Eye and associated structures. Visual pathways and centers. Vision</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glutamates - pharmacology</subject><subject>Glutamic Acid</subject><subject>Ibotenic Acid - analogs & derivatives</subject><subject>Ibotenic Acid - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Kainic Acid - metabolism</subject><subject>Kainic Acid - pharmacology</subject><subject>N-Methylaspartate - pharmacology</subject><subject>Quisqualic Acid - pharmacology</subject><subject>Rabbits</subject><subject>Receptors, Kainic Acid</subject><subject>Receptors, Neurotransmitter - drug effects</subject><subject>Receptors, Neurotransmitter - physiology</subject><subject>Retina - drug effects</subject><subject>Retina - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVFv0zAQxy0EGmXwEZAiJHhLd-fEccID0lRtbNPEJGDPluPYi8FJiu2u6rfHodUKT8gn2br73f_O-hPyDmGJjBZnN18u7r_efVtdLxFzSAGIuMSmwWdkkYgmpyXgc7IAyiGvSl6-JK9C-AEAHJCfkBOsOPAaF-TmXOm4c6qfnB115rXTMujM-GnIYp8Ssm1tTPloR5kNurMy6i5rd9lPmTJxblF6HScfXpMXRrqg3xzuU3J_efF9dZXf3n2-Xp3f5oohjTllxtQFM2mtylRcdZqx-s8xLUigNVeaMskM1B3tFPD0KnXVQC3bWrW6OCWf9rrrTZsWUnqMXjqx9naQficmacW_ldH24mF6FBXjjAIkgQ8HAT_92ugQxWCD0s7JUU-bIGooONCy_C-IrIamaDCBH_eg8lMIXpunbRDEbJl4skwgCkgxWyZmy1Lz27__c2zde5Tq7w91GZR0xstR2XDEmsRUTXnkevvQb63XIgzSuaSKYrvdzuPScCx-A5DlrqY</recordid><startdate>19910101</startdate><enddate>19910101</enddate><creator>Linn, DM</creator><creator>Blazynski, C</creator><creator>Redburn, DA</creator><creator>Massey, SC</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</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><scope>5PM</scope></search><sort><creationdate>19910101</creationdate><title>Acetylcholine release from the rabbit retina mediated by kainate receptors</title><author>Linn, DM ; Blazynski, C ; Redburn, DA ; Massey, SC</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-25ff835f6476f67cde55858585fb0a0287ce25a5f08d2dc075f04e6908ab8cbe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Acetylcholine - metabolism</topic><topic>alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid</topic><topic>Animals</topic><topic>Aspartic Acid - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Choline - metabolism</topic><topic>Eye and associated structures. Visual pathways and centers. Vision</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glutamates - pharmacology</topic><topic>Glutamic Acid</topic><topic>Ibotenic Acid - analogs & derivatives</topic><topic>Ibotenic Acid - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Kainic Acid - metabolism</topic><topic>Kainic Acid - pharmacology</topic><topic>N-Methylaspartate - pharmacology</topic><topic>Quisqualic Acid - pharmacology</topic><topic>Rabbits</topic><topic>Receptors, Kainic Acid</topic><topic>Receptors, Neurotransmitter - drug effects</topic><topic>Receptors, Neurotransmitter - physiology</topic><topic>Retina - drug effects</topic><topic>Retina - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Linn, DM</creatorcontrib><creatorcontrib>Blazynski, C</creatorcontrib><creatorcontrib>Redburn, DA</creatorcontrib><creatorcontrib>Massey, SC</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Linn, DM</au><au>Blazynski, C</au><au>Redburn, DA</au><au>Massey, SC</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acetylcholine release from the rabbit retina mediated by kainate receptors</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>1991-01-01</date><risdate>1991</risdate><volume>11</volume><issue>1</issue><spage>111</spage><epage>122</epage><pages>111-122</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><coden>JNRSDS</coden><abstract>The cholinergic amacrine cells of the rabbit retina may be labeled with 3H-choline (3H-Ch), and the activity of the cholinergic population may be monitored by following the release of 3H-ACh. Glutamate analogs caused massive ACh release, up to 50 times the basal efflux, with the following rank order of potency: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) greater than quisqualate (QQ) = kainate (KA) much greater than NMDA (in magnesium-free medium) much greater than glutamate greater than aspartate. In contrast, the release of 3H-Ch was unchanged. Submaximal doses of each agonist were used to establish the specifity of glutamate antagonists. Kynurenic acid was selective for KA much greater than QQ, and 6,7-dinitroquinoxaline-2,3-dione (DNQX) was selective for KA greater than QQ much greater than NMDA. At low doses, which selectively blocked the response to KA, both antagonists blocked the light-evoked release of ACh. These results suggest that ACh release may be produced via several glutamate receptors, but the physiological input to the cholinergic amacrine cells is mediated by KA receptors. Because these cells receive direct input from cone bipolar cells, this work supports previous evidence that the bipolar cell transmitter is glutamate.</abstract><cop>Washington, DC</cop><pub>Soc Neuroscience</pub><pmid>1670781</pmid><doi>10.1523/JNEUROSCI.11-01-00111.1991</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Acetylcholine - metabolism alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Animals Aspartic Acid - pharmacology Biological and medical sciences Choline - metabolism Eye and associated structures. Visual pathways and centers. Vision Fundamental and applied biological sciences. Psychology Glutamates - pharmacology Glutamic Acid Ibotenic Acid - analogs & derivatives Ibotenic Acid - pharmacology In Vitro Techniques Kainic Acid - metabolism Kainic Acid - pharmacology N-Methylaspartate - pharmacology Quisqualic Acid - pharmacology Rabbits Receptors, Kainic Acid Receptors, Neurotransmitter - drug effects Receptors, Neurotransmitter - physiology Retina - drug effects Retina - physiology Vertebrates: nervous system and sense organs |
| title | Acetylcholine release from the rabbit retina mediated by kainate receptors |
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