Store‐Operated Ca2+ Influx and Voltage‐Gated Ca2+ Channels Coupled to Exocytosis in Pheochromocytoma (PC12) Cells

: Microamperometry was used to monitor quantal catecholamine release from individual PC12 cells in response to raised extracellular K+ and caffeine. K+‐evoked exocytosis was entirely dependent on Ca2+ influx through voltage‐gated Ca2+ channels, and of the subtypes of such channels present in these c...

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Veröffentlicht in:Journal of neurochemistry 1999-08, Vol.73 (2), p.874-880
Hauptverfasser: Taylor, S. C., Peers, C.
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Peers, C.
description : Microamperometry was used to monitor quantal catecholamine release from individual PC12 cells in response to raised extracellular K+ and caffeine. K+‐evoked exocytosis was entirely dependent on Ca2+ influx through voltage‐gated Ca2+ channels, and of the subtypes of such channels present in these cells, influx through N‐type was primarily responsible for triggering exocytosis. L‐type channels played a minor role in mediating K+‐evoked secretion, whereas P/Q‐type channels did not appear to be involved in secretion at all. Caffeine also evoked catecholamine release from PC12 cells, but only in the presence of extracellular Ca2+. Application of caffeine in Ca2+‐free solutions evoked large, transient rises of [Ca2+]i, but did not trigger exocytosis. When Ca2+ was restored to the extracellular solution (in the absence of caffeine), store‐operated Ca2+ influx was observed, which evoked exocytosis. The amount of secretion evoked by this influx pathway was far greater than release triggered by influx through L‐type Ca2+ channels, but less than that caused by Ca2+ influx through N‐type channels. Our results indicate that exocytosis may be regulated even in excitable cells by Ca2+ influx through pathways other than voltage‐gated Ca2+ channels.
doi_str_mv 10.1046/j.1471-4159.1999.0730874.x
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C. ; Peers, C.</creator><creatorcontrib>Taylor, S. C. ; Peers, C.</creatorcontrib><description>: Microamperometry was used to monitor quantal catecholamine release from individual PC12 cells in response to raised extracellular K+ and caffeine. K+‐evoked exocytosis was entirely dependent on Ca2+ influx through voltage‐gated Ca2+ channels, and of the subtypes of such channels present in these cells, influx through N‐type was primarily responsible for triggering exocytosis. L‐type channels played a minor role in mediating K+‐evoked secretion, whereas P/Q‐type channels did not appear to be involved in secretion at all. Caffeine also evoked catecholamine release from PC12 cells, but only in the presence of extracellular Ca2+. Application of caffeine in Ca2+‐free solutions evoked large, transient rises of [Ca2+]i, but did not trigger exocytosis. When Ca2+ was restored to the extracellular solution (in the absence of caffeine), store‐operated Ca2+ influx was observed, which evoked exocytosis. The amount of secretion evoked by this influx pathway was far greater than release triggered by influx through L‐type Ca2+ channels, but less than that caused by Ca2+ influx through N‐type channels. Our results indicate that exocytosis may be regulated even in excitable cells by Ca2+ influx through pathways other than voltage‐gated Ca2+ channels.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.1999.0730874.x</identifier><identifier>PMID: 10428087</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford UK: Blackwell Science Ltd</publisher><subject>Animals ; Biological and medical sciences ; Biological Transport - drug effects ; Biological Transport - physiology ; Ca2+ channels ; Ca2+ stores ; Caffeine - pharmacology ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Calcium Channels - metabolism ; Calcium Channels, L-Type ; Calcium Channels, N-Type ; Catecholamines ; Catecholamines - metabolism ; Cell physiology ; Central Nervous System Stimulants - pharmacology ; Electrophysiology ; Exocytosis ; Exocytosis - physiology ; Fundamental and applied biological sciences. Psychology ; Molecular and cellular biology ; Neurons - chemistry ; Neurons - cytology ; Neurons - metabolism ; Nifedipine - pharmacology ; omega-Agatoxin IVA ; omega-Conotoxin GVIA ; PC12 Cells ; Peptides - pharmacology ; Potassium - pharmacology ; Rats ; Secretion. 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C.</creatorcontrib><creatorcontrib>Peers, C.</creatorcontrib><title>Store‐Operated Ca2+ Influx and Voltage‐Gated Ca2+ Channels Coupled to Exocytosis in Pheochromocytoma (PC12) Cells</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>: Microamperometry was used to monitor quantal catecholamine release from individual PC12 cells in response to raised extracellular K+ and caffeine. K+‐evoked exocytosis was entirely dependent on Ca2+ influx through voltage‐gated Ca2+ channels, and of the subtypes of such channels present in these cells, influx through N‐type was primarily responsible for triggering exocytosis. L‐type channels played a minor role in mediating K+‐evoked secretion, whereas P/Q‐type channels did not appear to be involved in secretion at all. Caffeine also evoked catecholamine release from PC12 cells, but only in the presence of extracellular Ca2+. Application of caffeine in Ca2+‐free solutions evoked large, transient rises of [Ca2+]i, but did not trigger exocytosis. When Ca2+ was restored to the extracellular solution (in the absence of caffeine), store‐operated Ca2+ influx was observed, which evoked exocytosis. The amount of secretion evoked by this influx pathway was far greater than release triggered by influx through L‐type Ca2+ channels, but less than that caused by Ca2+ influx through N‐type channels. Our results indicate that exocytosis may be regulated even in excitable cells by Ca2+ influx through pathways other than voltage‐gated Ca2+ channels.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Transport - drug effects</subject><subject>Biological Transport - physiology</subject><subject>Ca2+ channels</subject><subject>Ca2+ stores</subject><subject>Caffeine - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels - metabolism</subject><subject>Calcium Channels, L-Type</subject><subject>Calcium Channels, N-Type</subject><subject>Catecholamines</subject><subject>Catecholamines - metabolism</subject><subject>Cell physiology</subject><subject>Central Nervous System Stimulants - pharmacology</subject><subject>Electrophysiology</subject><subject>Exocytosis</subject><subject>Exocytosis - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Molecular and cellular biology</subject><subject>Neurons - chemistry</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Nifedipine - pharmacology</subject><subject>omega-Agatoxin IVA</subject><subject>omega-Conotoxin GVIA</subject><subject>PC12 Cells</subject><subject>Peptides - pharmacology</subject><subject>Potassium - pharmacology</subject><subject>Rats</subject><subject>Secretion. Exocytosis</subject><subject>Spider Venoms - pharmacology</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkU1OwzAQhS0EoqVwBWQhFiCUYMduHC8hKqWoopX42VpO7NBEblLFqUh3HIEzchISGiir0cz75knzBoAzjFyMqH-duZgy7FA85C7mnLuIERQw6tZ7oP8n7YM-Qp7nEES9HjiyNkMI-9THh6DX2HhBs9IH66eqKPXXx-dspUtZaQVD6V3BSZ6YdQ1lruBrYSr51iLjnR4uZJ5rY2FYrFemmVYFHNVFvKkKm1qY5nC-0EW8KIvlz3Ap4cU8xN4lDLUx9hgcJNJYfdLVAXi5Gz2H9850Np6EN1MnI3RIHcIU5hEJJKMx4j7xdBwHKlJKEkYj3_cCqViTQIQ4jSKmAkYw0lgmVPl8iBMyAKdb39U6WmolVmW6lOVG_N7fAOcdIG0sTVLKPE7tjuMENYk32O0We0-N3vyzaZ18kYk2ddGmLtqHiO4hohYPj2HXkG8ht3_g</recordid><startdate>199908</startdate><enddate>199908</enddate><creator>Taylor, S. C.</creator><creator>Peers, C.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>199908</creationdate><title>Store‐Operated Ca2+ Influx and Voltage‐Gated Ca2+ Channels Coupled to Exocytosis in Pheochromocytoma (PC12) Cells</title><author>Taylor, S. C. ; Peers, C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j3454-37d19b38a74c09632ecc8dbdda374b6628ad7199b094bb7d87310e1af4d6951f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological Transport - drug effects</topic><topic>Biological Transport - physiology</topic><topic>Ca2+ channels</topic><topic>Ca2+ stores</topic><topic>Caffeine - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels - metabolism</topic><topic>Calcium Channels, L-Type</topic><topic>Calcium Channels, N-Type</topic><topic>Catecholamines</topic><topic>Catecholamines - metabolism</topic><topic>Cell physiology</topic><topic>Central Nervous System Stimulants - pharmacology</topic><topic>Electrophysiology</topic><topic>Exocytosis</topic><topic>Exocytosis - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Molecular and cellular biology</topic><topic>Neurons - chemistry</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Nifedipine - pharmacology</topic><topic>omega-Agatoxin IVA</topic><topic>omega-Conotoxin GVIA</topic><topic>PC12 Cells</topic><topic>Peptides - pharmacology</topic><topic>Potassium - pharmacology</topic><topic>Rats</topic><topic>Secretion. Exocytosis</topic><topic>Spider Venoms - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Taylor, S. C.</creatorcontrib><creatorcontrib>Peers, C.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Taylor, S. C.</au><au>Peers, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Store‐Operated Ca2+ Influx and Voltage‐Gated Ca2+ Channels Coupled to Exocytosis in Pheochromocytoma (PC12) Cells</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>1999-08</date><risdate>1999</risdate><volume>73</volume><issue>2</issue><spage>874</spage><epage>880</epage><pages>874-880</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>: Microamperometry was used to monitor quantal catecholamine release from individual PC12 cells in response to raised extracellular K+ and caffeine. K+‐evoked exocytosis was entirely dependent on Ca2+ influx through voltage‐gated Ca2+ channels, and of the subtypes of such channels present in these cells, influx through N‐type was primarily responsible for triggering exocytosis. L‐type channels played a minor role in mediating K+‐evoked secretion, whereas P/Q‐type channels did not appear to be involved in secretion at all. Caffeine also evoked catecholamine release from PC12 cells, but only in the presence of extracellular Ca2+. Application of caffeine in Ca2+‐free solutions evoked large, transient rises of [Ca2+]i, but did not trigger exocytosis. When Ca2+ was restored to the extracellular solution (in the absence of caffeine), store‐operated Ca2+ influx was observed, which evoked exocytosis. The amount of secretion evoked by this influx pathway was far greater than release triggered by influx through L‐type Ca2+ channels, but less than that caused by Ca2+ influx through N‐type channels. Our results indicate that exocytosis may be regulated even in excitable cells by Ca2+ influx through pathways other than voltage‐gated Ca2+ channels.</abstract><cop>Oxford UK</cop><pub>Blackwell Science Ltd</pub><pmid>10428087</pmid><doi>10.1046/j.1471-4159.1999.0730874.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Biological and medical sciences
Biological Transport - drug effects
Biological Transport - physiology
Ca2+ channels
Ca2+ stores
Caffeine - pharmacology
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Calcium Channels - metabolism
Calcium Channels, L-Type
Calcium Channels, N-Type
Catecholamines
Catecholamines - metabolism
Cell physiology
Central Nervous System Stimulants - pharmacology
Electrophysiology
Exocytosis
Exocytosis - physiology
Fundamental and applied biological sciences. Psychology
Molecular and cellular biology
Neurons - chemistry
Neurons - cytology
Neurons - metabolism
Nifedipine - pharmacology
omega-Agatoxin IVA
omega-Conotoxin GVIA
PC12 Cells
Peptides - pharmacology
Potassium - pharmacology
Rats
Secretion. Exocytosis
Spider Venoms - pharmacology
title Store‐Operated Ca2+ Influx and Voltage‐Gated Ca2+ Channels Coupled to Exocytosis in Pheochromocytoma (PC12) Cells
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