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Multiple Calcium Channels Mediate Neurotransmitter Release from Peripheral Neurons
We examined the effects of dihydropyridine drugs on evoked neurotransmitter release from cultured neonatal rat sensory and sympathetic neurons. Depolarization with K+-rich solutions increased the release of substance P from cultured sensory neurons. This release was enhanced by BAY K8644 and (+)-202...
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Published in: | Proceedings of the National Academy of Sciences - PNAS 1986-09, Vol.83 (17), p.6656-6659 |
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creator | Perney, Teresa M. Hirning, Lane D. Leeman, Susan E. Miller, Richard J. |
description | We examined the effects of dihydropyridine drugs on evoked neurotransmitter release from cultured neonatal rat sensory and sympathetic neurons. Depolarization with K+-rich solutions increased the release of substance P from cultured sensory neurons. This release was enhanced by BAY K8644 and (+)-202791 and was blocked by a variety of other dihydropyridines including (-)-202791, by Co2+, or in Ca2+-free solutions. K+-rich solutions also stimulated the release of [3H]norepinephrine from cultured sympathetic neurons. This release was also completely blocked by Co2+ or in Ca2+-free solution. In contrast to the situation in sensory neurons, however, the evoked release of [3H]norepinephrine was completely resistant to the blocking effects of dihydropyridine such as nimodipine. However, BAY K8644 was able to enhance the evoked release of [3H]norepinephrine, and this enhancement was blocked by nimodipine. These results are discussed in relation to the possible participation of multiple types of calcium channels in the release of neurotransmitters. |
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Depolarization with K+-rich solutions increased the release of substance P from cultured sensory neurons. This release was enhanced by BAY K8644 and (+)-202791 and was blocked by a variety of other dihydropyridines including (-)-202791, by Co2+, or in Ca2+-free solutions. K+-rich solutions also stimulated the release of [3H]norepinephrine from cultured sympathetic neurons. This release was also completely blocked by Co2+ or in Ca2+-free solution. In contrast to the situation in sensory neurons, however, the evoked release of [3H]norepinephrine was completely resistant to the blocking effects of dihydropyridine such as nimodipine. However, BAY K8644 was able to enhance the evoked release of [3H]norepinephrine, and this enhancement was blocked by nimodipine. These results are discussed in relation to the possible participation of multiple types of calcium channels in the release of neurotransmitters.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.83.17.6656</identifier><identifier>PMID: 2428039</identifier><identifier>CODEN: PNASA6</identifier><language>eng</language><publisher>Washington, DC: National Academy of Sciences of the United States of America</publisher><subject>Agonists ; Animals ; Biological and medical sciences ; Calcium - physiology ; Calcium Channel Blockers - pharmacology ; Calcium channels ; Cell physiology ; Culture Techniques ; Cultured cells ; Dihydropyridines ; Fundamental and applied biological sciences. Psychology ; Ganglia, Spinal - physiology ; Ganglia, Sympathetic - physiology ; Ion Channels - physiology ; Molecular and cellular biology ; Nerves ; Neurons ; Neuroscience ; Neurotransmission ; Neurotransmitter Agents - metabolism ; Neurotransmitters ; Norepinephrine - metabolism ; Peripheral Nerves - physiology ; Potassium - physiology ; Rats ; Sensory neurons ; Substance P - metabolism ; Transmitters</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1986-09, Vol.83 (17), p.6656-6659</ispartof><rights>1987 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c556t-b17c1178770dc28d2c982353cd8cf76aacb089456cbad15a37218e21467d886e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/83/17.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/28417$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/28417$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793,58238,58471</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7878831$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2428039$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Perney, Teresa M.</creatorcontrib><creatorcontrib>Hirning, Lane D.</creatorcontrib><creatorcontrib>Leeman, Susan E.</creatorcontrib><creatorcontrib>Miller, Richard J.</creatorcontrib><title>Multiple Calcium Channels Mediate Neurotransmitter Release from Peripheral Neurons</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>We examined the effects of dihydropyridine drugs on evoked neurotransmitter release from cultured neonatal rat sensory and sympathetic neurons. Depolarization with K+-rich solutions increased the release of substance P from cultured sensory neurons. This release was enhanced by BAY K8644 and (+)-202791 and was blocked by a variety of other dihydropyridines including (-)-202791, by Co2+, or in Ca2+-free solutions. K+-rich solutions also stimulated the release of [3H]norepinephrine from cultured sympathetic neurons. This release was also completely blocked by Co2+ or in Ca2+-free solution. In contrast to the situation in sensory neurons, however, the evoked release of [3H]norepinephrine was completely resistant to the blocking effects of dihydropyridine such as nimodipine. However, BAY K8644 was able to enhance the evoked release of [3H]norepinephrine, and this enhancement was blocked by nimodipine. These results are discussed in relation to the possible participation of multiple types of calcium channels in the release of neurotransmitters.</description><subject>Agonists</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - physiology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium channels</subject><subject>Cell physiology</subject><subject>Culture Techniques</subject><subject>Cultured cells</subject><subject>Dihydropyridines</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ganglia, Spinal - physiology</subject><subject>Ganglia, Sympathetic - physiology</subject><subject>Ion Channels - physiology</subject><subject>Molecular and cellular biology</subject><subject>Nerves</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>Neurotransmission</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Neurotransmitters</subject><subject>Norepinephrine - metabolism</subject><subject>Peripheral Nerves - physiology</subject><subject>Potassium - physiology</subject><subject>Rats</subject><subject>Sensory neurons</subject><subject>Substance P - metabolism</subject><subject>Transmitters</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><recordid>eNp9kc1v1DAQxS0EKkvhjIQEygHRU7b-SOzJgQNa8SW1BVVwtrzOhHXlfGA7CP77erVhoZee5vB-b-bpDSHPGV0zqsT5NJi4BrFmai1lLR-QFaMNK2XV0IdkRSlXJVS8ekyexHhDKW1qoCfkhFccqGhW5Ppy9slNHouN8dbNfbHZmWFAH4tLbJ1JWFzhHMYUzBB7lxKG4ho9mohFF8a--IrBTTsMxh_AIT4ljzrjIz5b5in5_uH9t82n8uLLx8-bdxelrWuZyi1TljEFStHWcmi5bYCLWtgWbKekMXZLoalqabemZbURijNAziqpWgCJ4pS8Peyd5m2PrcUhh_R6Cq434Y8ejdN3lcHt9I_xlxaQmxLZ_2bxh_HnjDHp3kWL3psBxzlqVoHksqkyeH4AbRhjDNgdbzCq91_Q-y9oEJopvf9Cdrz8P9qRX2rP-utFN9Ea3-VyrYtHLJcCIFjGXi3Yfv9f9c6ds3sB3c3eJ_ydMvniQN7ENIZ_gaBiStwCDKOy5g</recordid><startdate>19860901</startdate><enddate>19860901</enddate><creator>Perney, Teresa M.</creator><creator>Hirning, Lane D.</creator><creator>Leeman, Susan E.</creator><creator>Miller, Richard J.</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</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>7QP</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>19860901</creationdate><title>Multiple Calcium Channels Mediate Neurotransmitter Release from Peripheral Neurons</title><author>Perney, Teresa M. ; Hirning, Lane D. ; Leeman, Susan E. ; Miller, Richard J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c556t-b17c1178770dc28d2c982353cd8cf76aacb089456cbad15a37218e21467d886e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Agonists</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - physiology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium channels</topic><topic>Cell physiology</topic><topic>Culture Techniques</topic><topic>Cultured cells</topic><topic>Dihydropyridines</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ganglia, Spinal - physiology</topic><topic>Ganglia, Sympathetic - physiology</topic><topic>Ion Channels - physiology</topic><topic>Molecular and cellular biology</topic><topic>Nerves</topic><topic>Neurons</topic><topic>Neuroscience</topic><topic>Neurotransmission</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>Neurotransmitters</topic><topic>Norepinephrine - metabolism</topic><topic>Peripheral Nerves - physiology</topic><topic>Potassium - physiology</topic><topic>Rats</topic><topic>Sensory neurons</topic><topic>Substance P - metabolism</topic><topic>Transmitters</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Perney, Teresa M.</creatorcontrib><creatorcontrib>Hirning, Lane D.</creatorcontrib><creatorcontrib>Leeman, Susan E.</creatorcontrib><creatorcontrib>Miller, Richard 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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Perney, Teresa M.</au><au>Hirning, Lane D.</au><au>Leeman, Susan E.</au><au>Miller, Richard J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Multiple Calcium Channels Mediate Neurotransmitter Release from Peripheral Neurons</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1986-09-01</date><risdate>1986</risdate><volume>83</volume><issue>17</issue><spage>6656</spage><epage>6659</epage><pages>6656-6659</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><coden>PNASA6</coden><abstract>We examined the effects of dihydropyridine drugs on evoked neurotransmitter release from cultured neonatal rat sensory and sympathetic neurons. Depolarization with K+-rich solutions increased the release of substance P from cultured sensory neurons. This release was enhanced by BAY K8644 and (+)-202791 and was blocked by a variety of other dihydropyridines including (-)-202791, by Co2+, or in Ca2+-free solutions. K+-rich solutions also stimulated the release of [3H]norepinephrine from cultured sympathetic neurons. This release was also completely blocked by Co2+ or in Ca2+-free solution. In contrast to the situation in sensory neurons, however, the evoked release of [3H]norepinephrine was completely resistant to the blocking effects of dihydropyridine such as nimodipine. However, BAY K8644 was able to enhance the evoked release of [3H]norepinephrine, and this enhancement was blocked by nimodipine. These results are discussed in relation to the possible participation of multiple types of calcium channels in the release of neurotransmitters.</abstract><cop>Washington, DC</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>2428039</pmid><doi>10.1073/pnas.83.17.6656</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Agonists Animals Biological and medical sciences Calcium - physiology Calcium Channel Blockers - pharmacology Calcium channels Cell physiology Culture Techniques Cultured cells Dihydropyridines Fundamental and applied biological sciences. Psychology Ganglia, Spinal - physiology Ganglia, Sympathetic - physiology Ion Channels - physiology Molecular and cellular biology Nerves Neurons Neuroscience Neurotransmission Neurotransmitter Agents - metabolism Neurotransmitters Norepinephrine - metabolism Peripheral Nerves - physiology Potassium - physiology Rats Sensory neurons Substance P - metabolism Transmitters |
title | Multiple Calcium Channels Mediate Neurotransmitter Release from Peripheral Neurons |
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