Analysis of rapid calcium signals in synaptosomes
A combination of the stopped-flow technology with dual channel spectrofluorometry of Ca 2+-indicators was utilized for the measurement of rapid Ca 2+-signals in rat cerebral cortical synaptosomes evoked by K +-depolarization. There was no observable contribution of Ca 2+-ions from intracellular stor...
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| Veröffentlicht in: | Neurochemistry international 1993-10, Vol.23 (4), p.331-341 |
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| creator | Tareilus, Erwin Schoch, Juergen Adams, Michael Breer, Heinz |
| description | A combination of the stopped-flow technology with dual channel spectrofluorometry of Ca
2+-indicators was utilized for the measurement of rapid Ca
2+-signals in rat cerebral cortical synaptosomes evoked by K
+-depolarization. There was no observable contribution of Ca
2+-ions from intracellular stores to the rise in [Ca
2+]
i. The kinetics of the fast increase in intracellular Ca
2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca
2+]
i and the time course of Ca
2+-channel inactivation were determined for depolarizations obtained by different extracellular K
+-concentrations ([K
+]
o). An apparent threshold was observed at about 18 mM [K
+]
o; a maximal Ca
2+-signal amplitude was estimated at about 40 mM [K
+]
o. Pharmacological properties of the involved Ca
2+-channels were determined using selective Ca
2+-channel blockers (Dihydropyridines, ω-Conotoxin, ω-Agatoxins); the results suggest that a P-type voltage-dependent Ca
2+-channel is the relevant channel type, generating the evoked Ca
2+-signals in rat cerebral cortical synaptosomes. |
| doi_str_mv | 10.1016/0197-0186(93)90077-I |
| format | Article |
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2+-indicators was utilized for the measurement of rapid Ca
2+-signals in rat cerebral cortical synaptosomes evoked by K
+-depolarization. There was no observable contribution of Ca
2+-ions from intracellular stores to the rise in [Ca
2+]
i. The kinetics of the fast increase in intracellular Ca
2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca
2+]
i and the time course of Ca
2+-channel inactivation were determined for depolarizations obtained by different extracellular K
+-concentrations ([K
+]
o). An apparent threshold was observed at about 18 mM [K
+]
o; a maximal Ca
2+-signal amplitude was estimated at about 40 mM [K
+]
o. Pharmacological properties of the involved Ca
2+-channels were determined using selective Ca
2+-channel blockers (Dihydropyridines, ω-Conotoxin, ω-Agatoxins); the results suggest that a P-type voltage-dependent Ca
2+-channel is the relevant channel type, generating the evoked Ca
2+-signals in rat cerebral cortical synaptosomes.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/0197-0186(93)90077-I</identifier><identifier>PMID: 8220175</identifier><identifier>CODEN: NEUIDS</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Biochemistry and metabolism ; Biological and medical sciences ; Cadmium - pharmacology ; Cadmium Chloride ; Calcium - metabolism ; Central nervous system ; Cerebral Cortex - metabolism ; Chlorides - pharmacology ; Cobalt - pharmacology ; Fundamental and applied biological sciences. Psychology ; Kinetics ; Membrane Potentials - drug effects ; Potassium Chloride - pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction - drug effects ; Synaptosomes - drug effects ; Synaptosomes - metabolism ; Synaptosomes - physiology ; Time Factors ; Vertebrates: nervous system and sense organs</subject><ispartof>Neurochemistry international, 1993-10, Vol.23 (4), p.331-341</ispartof><rights>1993</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-8e1642c1917cab76ae1099526197a3b779b53bd2958c719af3aa88bbf558f0873</citedby><cites>FETCH-LOGICAL-c481t-8e1642c1917cab76ae1099526197a3b779b53bd2958c719af3aa88bbf558f0873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/019701869390077I$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3749177$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8220175$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tareilus, Erwin</creatorcontrib><creatorcontrib>Schoch, Juergen</creatorcontrib><creatorcontrib>Adams, Michael</creatorcontrib><creatorcontrib>Breer, Heinz</creatorcontrib><title>Analysis of rapid calcium signals in synaptosomes</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>A combination of the stopped-flow technology with dual channel spectrofluorometry of Ca
2+-indicators was utilized for the measurement of rapid Ca
2+-signals in rat cerebral cortical synaptosomes evoked by K
+-depolarization. There was no observable contribution of Ca
2+-ions from intracellular stores to the rise in [Ca
2+]
i. The kinetics of the fast increase in intracellular Ca
2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca
2+]
i and the time course of Ca
2+-channel inactivation were determined for depolarizations obtained by different extracellular K
+-concentrations ([K
+]
o). An apparent threshold was observed at about 18 mM [K
+]
o; a maximal Ca
2+-signal amplitude was estimated at about 40 mM [K
+]
o. Pharmacological properties of the involved Ca
2+-channels were determined using selective Ca
2+-channel blockers (Dihydropyridines, ω-Conotoxin, ω-Agatoxins); the results suggest that a P-type voltage-dependent Ca
2+-channel is the relevant channel type, generating the evoked Ca
2+-signals in rat cerebral cortical synaptosomes.</description><subject>Animals</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Cadmium - pharmacology</subject><subject>Cadmium Chloride</subject><subject>Calcium - metabolism</subject><subject>Central nervous system</subject><subject>Cerebral Cortex - metabolism</subject><subject>Chlorides - pharmacology</subject><subject>Cobalt - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Kinetics</subject><subject>Membrane Potentials - drug effects</subject><subject>Potassium Chloride - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction - drug effects</subject><subject>Synaptosomes - drug effects</subject><subject>Synaptosomes - metabolism</subject><subject>Synaptosomes - physiology</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LxDAQhoMo67r6DxR6ENFDNdM2TXIRlsWPhQUveg5pmkqkX2a6wv57U7fs0VMg7zPDOw8hl0DvgUL-QEHymILIb2V6JynlPF4fkTkInsSSs-yYzA_IKTlD_KIBkpTNyEwkCQXO5gSWra536DDqqsjr3pWR0bVx2yZC9xkyjFwb4a7V_dBh11g8JydV-LYX07sgH89P76vXePP2sl4tN7HJBAyxsJBniQEJ3OiC59oClZIleaik04JzWbC0KBPJhOEgdZVqLURRVIyJigqeLsjNfm_vu--txUE1Do2ta93abouK5zRjjIoAZnvQ-A7R20r13jXa7xRQNZpSowY1alAyVX-m1DqMXU37t0Vjy8PQpCbk11OuMSipvG6NwwOW8iycNtZ83GM2uPhx1is0zrbGls5bM6iyc__3-AVag4Mm</recordid><startdate>19931001</startdate><enddate>19931001</enddate><creator>Tareilus, Erwin</creator><creator>Schoch, Juergen</creator><creator>Adams, Michael</creator><creator>Breer, Heinz</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>7X8</scope></search><sort><creationdate>19931001</creationdate><title>Analysis of rapid calcium signals in synaptosomes</title><author>Tareilus, Erwin ; Schoch, Juergen ; Adams, Michael ; Breer, Heinz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-8e1642c1917cab76ae1099526197a3b779b53bd2958c719af3aa88bbf558f0873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Biochemistry and metabolism</topic><topic>Biological and medical sciences</topic><topic>Cadmium - pharmacology</topic><topic>Cadmium Chloride</topic><topic>Calcium - metabolism</topic><topic>Central nervous system</topic><topic>Cerebral Cortex - metabolism</topic><topic>Chlorides - pharmacology</topic><topic>Cobalt - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Kinetics</topic><topic>Membrane Potentials - drug effects</topic><topic>Potassium Chloride - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction - drug effects</topic><topic>Synaptosomes - drug effects</topic><topic>Synaptosomes - metabolism</topic><topic>Synaptosomes - physiology</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tareilus, Erwin</creatorcontrib><creatorcontrib>Schoch, Juergen</creatorcontrib><creatorcontrib>Adams, Michael</creatorcontrib><creatorcontrib>Breer, Heinz</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>MEDLINE - Academic</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tareilus, Erwin</au><au>Schoch, Juergen</au><au>Adams, Michael</au><au>Breer, Heinz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of rapid calcium signals in synaptosomes</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>1993-10-01</date><risdate>1993</risdate><volume>23</volume><issue>4</issue><spage>331</spage><epage>341</epage><pages>331-341</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><coden>NEUIDS</coden><abstract>A combination of the stopped-flow technology with dual channel spectrofluorometry of Ca
2+-indicators was utilized for the measurement of rapid Ca
2+-signals in rat cerebral cortical synaptosomes evoked by K
+-depolarization. There was no observable contribution of Ca
2+-ions from intracellular stores to the rise in [Ca
2+]
i. The kinetics of the fast increase in intracellular Ca
2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca
2+]
i and the time course of Ca
2+-channel inactivation were determined for depolarizations obtained by different extracellular K
+-concentrations ([K
+]
o). An apparent threshold was observed at about 18 mM [K
+]
o; a maximal Ca
2+-signal amplitude was estimated at about 40 mM [K
+]
o. Pharmacological properties of the involved Ca
2+-channels were determined using selective Ca
2+-channel blockers (Dihydropyridines, ω-Conotoxin, ω-Agatoxins); the results suggest that a P-type voltage-dependent Ca
2+-channel is the relevant channel type, generating the evoked Ca
2+-signals in rat cerebral cortical synaptosomes.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>8220175</pmid><doi>10.1016/0197-0186(93)90077-I</doi><tpages>11</tpages></addata></record> |
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| ispartof | Neurochemistry international, 1993-10, Vol.23 (4), p.331-341 |
| issn | 0197-0186 1872-9754 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Biochemistry and metabolism Biological and medical sciences Cadmium - pharmacology Cadmium Chloride Calcium - metabolism Central nervous system Cerebral Cortex - metabolism Chlorides - pharmacology Cobalt - pharmacology Fundamental and applied biological sciences. Psychology Kinetics Membrane Potentials - drug effects Potassium Chloride - pharmacology Rats Rats, Sprague-Dawley Signal Transduction - drug effects Synaptosomes - drug effects Synaptosomes - metabolism Synaptosomes - physiology Time Factors Vertebrates: nervous system and sense organs |
| title | Analysis of rapid calcium signals in synaptosomes |
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