Presynaptic Disruption of Transmitter Release by Lead
Low concentrations of inorganic lead ions (Pb 2+) disrupt transmitter release by causing aberrant augmentation of spontaneous and suppression of evoked release. These effects result from high affinity interactions of Pb 2+ with the voltage-gated calcium channels (VGCC) as well as Ca 2+ binding prote...
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| Veröffentlicht in: | Neurotoxicology (Park Forest South) 2004-06, Vol.25 (4), p.599-604 |
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| creator | Suszkiw, Janusz B. |
| description | Low concentrations of inorganic lead ions (Pb
2+) disrupt transmitter release by causing aberrant augmentation of spontaneous and suppression of evoked release. These effects result from high affinity interactions of Pb
2+ with the voltage-gated calcium channels (VGCC) as well as Ca
2+ binding proteins which regulate the synaptic vesicle mobilization, docking, and exocytosis processes. Augmentation of spontaneous release may involve stimulation of vesicle mobilization consequent to Pb
2+ activation of CaMKII-dependent phosphorylation of synapsin I and/or stimulation of asynchronous exocytosis via direct Pb
2+ activation of the putative exocytotic Ca
2+-sensor protein synaptotagmin I. In addition, synergistic stimulation of PLC and DAG/Pb
2+-dependent activation of PKC may enhance the secretagogue effects of Pb
2+ by increasing metal sensitivity of exocytosis and/or modulating calcium channel activity. In contrast to intracellularly-mediated actions of Pb
2+ resulting in augmentation of spontaneous release, the inhibition of evoked transmitter release by Pb
2+ is largely attributable to extracellular block of the voltage-gated calcium channels. |
| doi_str_mv | 10.1016/j.neuro.2003.09.009 |
| format | Article |
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2+) disrupt transmitter release by causing aberrant augmentation of spontaneous and suppression of evoked release. These effects result from high affinity interactions of Pb
2+ with the voltage-gated calcium channels (VGCC) as well as Ca
2+ binding proteins which regulate the synaptic vesicle mobilization, docking, and exocytosis processes. Augmentation of spontaneous release may involve stimulation of vesicle mobilization consequent to Pb
2+ activation of CaMKII-dependent phosphorylation of synapsin I and/or stimulation of asynchronous exocytosis via direct Pb
2+ activation of the putative exocytotic Ca
2+-sensor protein synaptotagmin I. In addition, synergistic stimulation of PLC and DAG/Pb
2+-dependent activation of PKC may enhance the secretagogue effects of Pb
2+ by increasing metal sensitivity of exocytosis and/or modulating calcium channel activity. In contrast to intracellularly-mediated actions of Pb
2+ resulting in augmentation of spontaneous release, the inhibition of evoked transmitter release by Pb
2+ is largely attributable to extracellular block of the voltage-gated calcium channels.</description><identifier>ISSN: 0161-813X</identifier><identifier>EISSN: 1872-9711</identifier><identifier>DOI: 10.1016/j.neuro.2003.09.009</identifier><identifier>PMID: 15183013</identifier><language>eng</language><publisher>Orlando, FL: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Calcium channels ; Calcium Channels - metabolism ; Calcium Channels - secretion ; Calmodulin ; Chemical and industrial products toxicology. Toxic occupational diseases ; Exocytosis ; Humans ; Lead ; Lead - toxicity ; Medical sciences ; Metals and various inorganic compounds ; Neurotransmitter Agents - antagonists & inhibitors ; Neurotransmitter Agents - metabolism ; Neurotransmitter Agents - secretion ; PKC ; PLC ; Presynaptic Terminals - drug effects ; Presynaptic Terminals - metabolism ; Presynaptic Terminals - secretion ; Synaptotagmin ; Toxicology</subject><ispartof>Neurotoxicology (Park Forest South), 2004-06, Vol.25 (4), p.599-604</ispartof><rights>2003 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-7763c5b29500125df1d921eead45b8ede255232d41e03a3ca781792f3afcbad43</citedby><cites>FETCH-LOGICAL-c416t-7763c5b29500125df1d921eead45b8ede255232d41e03a3ca781792f3afcbad43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuro.2003.09.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15858492$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15183013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suszkiw, Janusz B.</creatorcontrib><title>Presynaptic Disruption of Transmitter Release by Lead</title><title>Neurotoxicology (Park Forest South)</title><addtitle>Neurotoxicology</addtitle><description>Low concentrations of inorganic lead ions (Pb
2+) disrupt transmitter release by causing aberrant augmentation of spontaneous and suppression of evoked release. These effects result from high affinity interactions of Pb
2+ with the voltage-gated calcium channels (VGCC) as well as Ca
2+ binding proteins which regulate the synaptic vesicle mobilization, docking, and exocytosis processes. Augmentation of spontaneous release may involve stimulation of vesicle mobilization consequent to Pb
2+ activation of CaMKII-dependent phosphorylation of synapsin I and/or stimulation of asynchronous exocytosis via direct Pb
2+ activation of the putative exocytotic Ca
2+-sensor protein synaptotagmin I. In addition, synergistic stimulation of PLC and DAG/Pb
2+-dependent activation of PKC may enhance the secretagogue effects of Pb
2+ by increasing metal sensitivity of exocytosis and/or modulating calcium channel activity. In contrast to intracellularly-mediated actions of Pb
2+ resulting in augmentation of spontaneous release, the inhibition of evoked transmitter release by Pb
2+ is largely attributable to extracellular block of the voltage-gated calcium channels.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium channels</subject><subject>Calcium Channels - metabolism</subject><subject>Calcium Channels - secretion</subject><subject>Calmodulin</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Exocytosis</subject><subject>Humans</subject><subject>Lead</subject><subject>Lead - toxicity</subject><subject>Medical sciences</subject><subject>Metals and various inorganic compounds</subject><subject>Neurotransmitter Agents - antagonists & inhibitors</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Neurotransmitter Agents - secretion</subject><subject>PKC</subject><subject>PLC</subject><subject>Presynaptic Terminals - drug effects</subject><subject>Presynaptic Terminals - metabolism</subject><subject>Presynaptic Terminals - secretion</subject><subject>Synaptotagmin</subject><subject>Toxicology</subject><issn>0161-813X</issn><issn>1872-9711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90M9LwzAUwPEgipvTv0CQXvTWmpc0bXPwIPMnDBSZ4C2k6StkdO1MWmH_vZkr6MlTcvi8l_Al5BxoAhSy61XS4uC6hFHKEyoTSuUBmUKRs1jmAIdkGhTEBfCPCTnxfkUpiDyTx2QCAgpOgU-JeHXot63e9NZEd9a7Idy6NurqaOl069e279FFb9ig9hiV22iBujolR7VuPJ6N54y8P9wv50_x4uXxeX67iE0KWR_necaNKJkU4WkmqhoqyQDDglSUBVbIhGCcVSkg5ZobnReQS1ZzXZsyID4jV_u9G9d9Duh7tbbeYNPoFrvBq6Alz1MRIN9D4zrvHdZq4-xau60Cqna11Er91FK7WopKFWqFqYtx_VCusfqdGfMEcDkC7Y1u6lDEWP_HFaJIJQvuZu8wxPiy6JQ3FluDlXVoelV19t-PfANVToi3</recordid><startdate>20040601</startdate><enddate>20040601</enddate><creator>Suszkiw, Janusz B.</creator><general>Elsevier B.V</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20040601</creationdate><title>Presynaptic Disruption of Transmitter Release by Lead</title><author>Suszkiw, Janusz B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-7763c5b29500125df1d921eead45b8ede255232d41e03a3ca781792f3afcbad43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium channels</topic><topic>Calcium Channels - metabolism</topic><topic>Calcium Channels - secretion</topic><topic>Calmodulin</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Exocytosis</topic><topic>Humans</topic><topic>Lead</topic><topic>Lead - toxicity</topic><topic>Medical sciences</topic><topic>Metals and various inorganic compounds</topic><topic>Neurotransmitter Agents - antagonists & inhibitors</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>Neurotransmitter Agents - secretion</topic><topic>PKC</topic><topic>PLC</topic><topic>Presynaptic Terminals - drug effects</topic><topic>Presynaptic Terminals - metabolism</topic><topic>Presynaptic Terminals - secretion</topic><topic>Synaptotagmin</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Suszkiw, Janusz B.</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicology (Park Forest South)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suszkiw, Janusz B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Presynaptic Disruption of Transmitter Release by Lead</atitle><jtitle>Neurotoxicology (Park Forest South)</jtitle><addtitle>Neurotoxicology</addtitle><date>2004-06-01</date><risdate>2004</risdate><volume>25</volume><issue>4</issue><spage>599</spage><epage>604</epage><pages>599-604</pages><issn>0161-813X</issn><eissn>1872-9711</eissn><abstract>Low concentrations of inorganic lead ions (Pb
2+) disrupt transmitter release by causing aberrant augmentation of spontaneous and suppression of evoked release. These effects result from high affinity interactions of Pb
2+ with the voltage-gated calcium channels (VGCC) as well as Ca
2+ binding proteins which regulate the synaptic vesicle mobilization, docking, and exocytosis processes. Augmentation of spontaneous release may involve stimulation of vesicle mobilization consequent to Pb
2+ activation of CaMKII-dependent phosphorylation of synapsin I and/or stimulation of asynchronous exocytosis via direct Pb
2+ activation of the putative exocytotic Ca
2+-sensor protein synaptotagmin I. In addition, synergistic stimulation of PLC and DAG/Pb
2+-dependent activation of PKC may enhance the secretagogue effects of Pb
2+ by increasing metal sensitivity of exocytosis and/or modulating calcium channel activity. In contrast to intracellularly-mediated actions of Pb
2+ resulting in augmentation of spontaneous release, the inhibition of evoked transmitter release by Pb
2+ is largely attributable to extracellular block of the voltage-gated calcium channels.</abstract><cop>Orlando, FL</cop><pub>Elsevier B.V</pub><pmid>15183013</pmid><doi>10.1016/j.neuro.2003.09.009</doi><tpages>6</tpages></addata></record> |
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| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Biological and medical sciences Calcium channels Calcium Channels - metabolism Calcium Channels - secretion Calmodulin Chemical and industrial products toxicology. Toxic occupational diseases Exocytosis Humans Lead Lead - toxicity Medical sciences Metals and various inorganic compounds Neurotransmitter Agents - antagonists & inhibitors Neurotransmitter Agents - metabolism Neurotransmitter Agents - secretion PKC PLC Presynaptic Terminals - drug effects Presynaptic Terminals - metabolism Presynaptic Terminals - secretion Synaptotagmin Toxicology |
| title | Presynaptic Disruption of Transmitter Release by Lead |
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