Ca2+/calmodulin-Dependent Kinase II Mediates Simultaneous Enhancement of Gap-Junctional Conductance and Glutamatergic Transmission
While chemical synapses are very plastic and modifiable by defined activity patterns, gap junctions, which mediate electrical transmission, have been classically perceived as passive intercellular channels. Excitatory transmission between auditory afferents and the goldfish Mauthner cell is mediated...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1998-10, Vol.95 (22), p.13272-13277 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Pereda, Alberto E. Bell, Theodore D. Chang, Bill H. Czernik, Andrew J. Nairn, Angus C. Soderling, Thomas R. Faber, Donald S. |
| description | While chemical synapses are very plastic and modifiable by defined activity patterns, gap junctions, which mediate electrical transmission, have been classically perceived as passive intercellular channels. Excitatory transmission between auditory afferents and the goldfish Mauthner cell is mediated by coexisting gap junctions and glutamatergic synapses. Although an increased intracellular Ca2+concentration is expected to reduce gap junctional conductance, both components of the synaptic response were instead enhanced by postsynaptic increases in Ca2+concentration, produced by patterned synaptic activity or intradendritic Ca2+injections. The synaptically induced potentiations were blocked by intradendritic injection of KN-93, a Ca2+/calmodulin-dependent kinase (CaM-K) inhibitor, or CaM-KIINtide, a potent and specific peptide inhibitor of CaM-KII, whereas the responses were potentiated by injection of an activated form of CaM-KII. The striking similarities of the mechanisms reported here with those proposed for long-term potentiation of mammalian glutamatergic synapses suggest that gap junctions are also similarly regulated and indicate a primary role for CaM-KII in shaping and regulating interneuronal communication, regardless of its modality. |
| doi_str_mv | 10.1073/pnas.95.22.13272 |
| format | Article |
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Excitatory transmission between auditory afferents and the goldfish Mauthner cell is mediated by coexisting gap junctions and glutamatergic synapses. Although an increased intracellular Ca2+concentration is expected to reduce gap junctional conductance, both components of the synaptic response were instead enhanced by postsynaptic increases in Ca2+concentration, produced by patterned synaptic activity or intradendritic Ca2+injections. The synaptically induced potentiations were blocked by intradendritic injection of KN-93, a Ca2+/calmodulin-dependent kinase (CaM-K) inhibitor, or CaM-KIINtide, a potent and specific peptide inhibitor of CaM-KII, whereas the responses were potentiated by injection of an activated form of CaM-KII. The striking similarities of the mechanisms reported here with those proposed for long-term potentiation of mammalian glutamatergic synapses suggest that gap junctions are also similarly regulated and indicate a primary role for CaM-KII in shaping and regulating interneuronal communication, regardless of its modality.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.95.22.13272</identifier><identifier>PMID: 9789078</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Animals ; Antibodies ; Benzylamines - pharmacology ; Biological Sciences ; Biology ; Brain ; Calcium - metabolism ; Calcium Chloride - pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Cell Communication ; Dendrites ; Dendrites - physiology ; Egtazic Acid - pharmacology ; Electric Conductivity ; Electric Stimulation ; Electrodes ; Enzyme Activation ; Enzyme Inhibitors - pharmacology ; Evoked Potentials - drug effects ; Evoked Potentials - physiology ; Excitatory Postsynaptic Potentials - drug effects ; Excitatory Postsynaptic Potentials - physiology ; Gap junctions ; Gap Junctions - physiology ; Glutamic Acid - physiology ; Goldfish ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Nerves ; Neurology ; Neurons - drug effects ; Neurons - physiology ; Neuroscience ; Spinal Cord - physiology ; Sulfonamides - pharmacology ; Synapses ; Synapses - drug effects ; Synapses - physiology ; Synaptic Transmission - physiology ; Tetanus ; Vestibulocochlear Nerve - physiology</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1998-10, Vol.95 (22), p.13272-13277</ispartof><rights>Copyright 1993-1998 National Academy of Sciences</rights><rights>Copyright National Academy of Sciences Oct 27, 1998</rights><rights>Copyright © 1998, The National Academy of Sciences 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/95/22.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/46232$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/46232$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9789078$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pereda, Alberto E.</creatorcontrib><creatorcontrib>Bell, Theodore D.</creatorcontrib><creatorcontrib>Chang, Bill H.</creatorcontrib><creatorcontrib>Czernik, Andrew J.</creatorcontrib><creatorcontrib>Nairn, Angus C.</creatorcontrib><creatorcontrib>Soderling, Thomas R.</creatorcontrib><creatorcontrib>Faber, Donald S.</creatorcontrib><title>Ca2+/calmodulin-Dependent Kinase II Mediates Simultaneous Enhancement of Gap-Junctional Conductance and Glutamatergic Transmission</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>While chemical synapses are very plastic and modifiable by defined activity patterns, gap junctions, which mediate electrical transmission, have been classically perceived as passive intercellular channels. Excitatory transmission between auditory afferents and the goldfish Mauthner cell is mediated by coexisting gap junctions and glutamatergic synapses. Although an increased intracellular Ca2+concentration is expected to reduce gap junctional conductance, both components of the synaptic response were instead enhanced by postsynaptic increases in Ca2+concentration, produced by patterned synaptic activity or intradendritic Ca2+injections. The synaptically induced potentiations were blocked by intradendritic injection of KN-93, a Ca2+/calmodulin-dependent kinase (CaM-K) inhibitor, or CaM-KIINtide, a potent and specific peptide inhibitor of CaM-KII, whereas the responses were potentiated by injection of an activated form of CaM-KII. The striking similarities of the mechanisms reported here with those proposed for long-term potentiation of mammalian glutamatergic synapses suggest that gap junctions are also similarly regulated and indicate a primary role for CaM-KII in shaping and regulating interneuronal communication, regardless of its modality.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Benzylamines - pharmacology</subject><subject>Biological Sciences</subject><subject>Biology</subject><subject>Brain</subject><subject>Calcium - metabolism</subject><subject>Calcium Chloride - pharmacology</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Cell Communication</subject><subject>Dendrites</subject><subject>Dendrites - physiology</subject><subject>Egtazic Acid - pharmacology</subject><subject>Electric Conductivity</subject><subject>Electric Stimulation</subject><subject>Electrodes</subject><subject>Enzyme Activation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Evoked Potentials - drug effects</subject><subject>Evoked Potentials - physiology</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Gap junctions</subject><subject>Gap Junctions - physiology</subject><subject>Glutamic Acid - physiology</subject><subject>Goldfish</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Nerves</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Neuroscience</subject><subject>Spinal Cord - physiology</subject><subject>Sulfonamides - pharmacology</subject><subject>Synapses</subject><subject>Synapses - drug effects</subject><subject>Synapses - physiology</subject><subject>Synaptic Transmission - physiology</subject><subject>Tetanus</subject><subject>Vestibulocochlear Nerve - physiology</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2LFDEUxIMo67h6F0EMHkSQns1Hp7sDXmRcx9EVD67nkE6_3s2QTsZOInr1LzfjDOvHwdM71O8VRRVCDylZUtLys53XcSnFkrEl5axlt9CCEkmrppbkNloQwtqqq1l9F92LcUsIkaIjJ-hEtp0kbbdAP1aavTgz2k1hyM766jXswA_gE35vizngzQZ_gMHqBBF_slN2SXsIOeJzf629gWnPhhGv9a56l71JNnjt8Cr4IZu0J7D2A167nPRUXOYra_DlrH2cbIwFvo_ujNpFeHC8p-jzm_PL1dvq4uN6s3p1UW15Q1I1AgwtND1pKNemqWlPxnasG9Ci74RmPaubYWRMGJA9EDqKzhjRiYHLXhIN_BS9PPjucj_BYEruWTu1m-2k5-8qaKv-Vry9Vlfhq2K87Uh5f3Z8n8OXDDGpkt-Ac4c6VFva5V0jC_j0H3Ab8lw6iYoRygXv6N7t8Z9hblIchyn6k6NeRvitCsWY-rV0IZ7_n1Bjdi7Bt1TQRwd0G1OYb9i6YZzxn1GatQM</recordid><startdate>19981027</startdate><enddate>19981027</enddate><creator>Pereda, Alberto E.</creator><creator>Bell, Theodore D.</creator><creator>Chang, Bill H.</creator><creator>Czernik, Andrew J.</creator><creator>Nairn, Angus C.</creator><creator>Soderling, Thomas R.</creator><creator>Faber, Donald S.</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><general>The National Academy of Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19981027</creationdate><title>Ca2+/calmodulin-Dependent Kinase II Mediates Simultaneous Enhancement of Gap-Junctional Conductance and Glutamatergic Transmission</title><author>Pereda, Alberto E. ; 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Excitatory transmission between auditory afferents and the goldfish Mauthner cell is mediated by coexisting gap junctions and glutamatergic synapses. Although an increased intracellular Ca2+concentration is expected to reduce gap junctional conductance, both components of the synaptic response were instead enhanced by postsynaptic increases in Ca2+concentration, produced by patterned synaptic activity or intradendritic Ca2+injections. The synaptically induced potentiations were blocked by intradendritic injection of KN-93, a Ca2+/calmodulin-dependent kinase (CaM-K) inhibitor, or CaM-KIINtide, a potent and specific peptide inhibitor of CaM-KII, whereas the responses were potentiated by injection of an activated form of CaM-KII. The striking similarities of the mechanisms reported here with those proposed for long-term potentiation of mammalian glutamatergic synapses suggest that gap junctions are also similarly regulated and indicate a primary role for CaM-KII in shaping and regulating interneuronal communication, regardless of its modality.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>9789078</pmid><doi>10.1073/pnas.95.22.13272</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 1998-10, Vol.95 (22), p.13272-13277 |
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| subjects | Animals Antibodies Benzylamines - pharmacology Biological Sciences Biology Brain Calcium - metabolism Calcium Chloride - pharmacology Calcium-Calmodulin-Dependent Protein Kinase Type 2 Calcium-Calmodulin-Dependent Protein Kinases - metabolism Cell Communication Dendrites Dendrites - physiology Egtazic Acid - pharmacology Electric Conductivity Electric Stimulation Electrodes Enzyme Activation Enzyme Inhibitors - pharmacology Evoked Potentials - drug effects Evoked Potentials - physiology Excitatory Postsynaptic Potentials - drug effects Excitatory Postsynaptic Potentials - physiology Gap junctions Gap Junctions - physiology Glutamic Acid - physiology Goldfish Membrane Potentials - drug effects Membrane Potentials - physiology Nerves Neurology Neurons - drug effects Neurons - physiology Neuroscience Spinal Cord - physiology Sulfonamides - pharmacology Synapses Synapses - drug effects Synapses - physiology Synaptic Transmission - physiology Tetanus Vestibulocochlear Nerve - physiology |
| title | Ca2+/calmodulin-Dependent Kinase II Mediates Simultaneous Enhancement of Gap-Junctional Conductance and Glutamatergic Transmission |
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