title: Ca2+/calmodulin-dependent kinase II mediates simultaneous enhancement of gap-junctional conductance and glutamatergic transmission.
abstract: 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.
authors.affiliation: Allegheny University of the Health Sciences, Philadelphia, PA 19129, USA. Pereda@auhs.edu
authors.forename: A E
authors.initials: AE
authors.lastname: Pereda
authors.forename: T D
authors.initials: TD
authors.lastname: Bell
authors.forename: B H
authors.initials: BH
authors.lastname: Chang
authors.forename: A J
authors.initials: AJ
authors.lastname: Czernik
authors.forename: A C
authors.initials: AC
authors.lastname: Nairn
authors.forename: T R
authors.initials: TR
authors.lastname: Soderling
authors.forename: D S
authors.initials: DS
authors.lastname: Faber
mesh_terms: D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002122:Calcium Chloride / Q000494:pharmacology; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D002450:Cell Communication; D003712:Dendrites / Q000502:physiology; D004533:Egtazic Acid / Q000494:pharmacology; D004553:Electric Conductivity; D004558:Electric Stimulation; D004789:Enzyme Activation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology*; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D017629:Gap Junctions / Q000502:physiology*; D018698:Glutamic Acid / Q000502:physiology*; D006054:Goldfish; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D013116:Spinal Cord / Q000502:physiology*; D013449:Sulfonamides / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*; D000159:Vestibulocochlear Nerve / Q000502:physiology*; D000096926:Benzenesulfonamides
chemical_list: D001596:Benzylamines; D002118:Calcium; D002122:Calcium Chloride; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D004533:Egtazic Acid; D004791:Enzyme Inhibitors; D018698:Glutamic Acid; D013449:Sulfonamides; C072105:KN 93; D000096926:Benzenesulfonamides