CA2+ CALMODULIN-DEPENDENT KINASE-II MEDIATES SIMULTANEOUS ENHANCEMENTOF GAP-JUNCTIONAL CONDUCTANCE AND GLUTAMATERGIC TRANSMISSION/

While chemical synapses are very plastic and modifiable by defined act ivity patterns, gap junctions, which mediate electrical transmission, have been classically perceived as passive intercellular channels. Exc itatory transmission between auditory afferents and the goldfish Mauth ner cell is mediated by coexisting gap junctions and glutamatergic syn apses. Although an increased intracellular Ca2+ concentration is expec ted to reduce gap junctional conductance, both components of the synap tic response were instead enhanced by postsynaptic increases in Ca2+-c oncentration, produced by patterned synaptic activity or intradendriti c Ca2+ injections, The synaptically induced potentiations were blocked by intradendritic injection of KN-93, a Ca2+/calmodulin-dependent kin ase (CaM-K) inhibitor, or CaM-KIINtide, a potent and specific peptide inhibitor of CaM-KII, whereas the responses were potentiated by inject ion of an activated form of CaM-KII, The striking similarities of the mechanisms reported here with those proposed for long-term potentiatio n of mammalian glutamatergic synapses suggest that gap junctions are a lso similarly regulated and indicate a primary role for CaM-KII in sha ping and regulating interneuronal communication, regardless of its mod ality.