101. Ca2+/calmodulin-dependent kinase II mediates simultaneous enhancement of gap-junctional conductance and glutamatergic transmission.
- Author
-
Pereda AE, Bell TD, Chang BH, Czernik AJ, Nairn AC, Soderling TR, and Faber DS
- Subjects
- Animals, Benzylamines pharmacology, Calcium metabolism, Calcium Chloride pharmacology, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Cell Communication, Dendrites physiology, Egtazic Acid pharmacology, Electric Conductivity, Electric Stimulation, Enzyme Activation, Enzyme Inhibitors pharmacology, Evoked Potentials drug effects, Excitatory Postsynaptic Potentials drug effects, Excitatory Postsynaptic Potentials physiology, Goldfish, Membrane Potentials drug effects, Membrane Potentials physiology, Neurons drug effects, Sulfonamides pharmacology, Synapses drug effects, Calcium-Calmodulin-Dependent Protein Kinases metabolism, Evoked Potentials physiology, Gap Junctions physiology, Glutamic Acid physiology, Neurons physiology, Spinal Cord physiology, Synapses physiology, Synaptic Transmission physiology, Vestibulocochlear Nerve physiology
- 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.
- Published
- 1998
- Full Text
- View/download PDF