Activity-dependent short-term enhancement of intercellular coupling.
It was reported previously that repeated brief tetanization of the posterior eight nerve can produce long-term homosynaptic potentiations of the electrotonic and chemical components of the mixed EPSP evoked in the Mauthner cell lateral dendrite by a single stimulus to the nerve. We show here that the same stimulus paradigm can lead, alternatively, to short-term enhancements of both excitatory responses. These transient modifications last for approximately 3 min, with a time course similar to post-tetanic potentiation at chemical synapses. However, a different stimulus pattern that transiently increases the presynaptic calcium concentration, paired-nerve stimuli, does not have any significant effect on electrotonic transmission, whereas it facilitates the chemically mediated EPSP. On the other hand, induction of the short-lasting potentiation of coupling, which depended on the discontinuous or burst-like property of the tetanizing paradigm, required NMDA-receptor activation and was blocked by postsynaptic intradendritic injections of the calcium chelator bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid. The ineffectiveness of presynaptic calcium in potentiating electrotonic coupling likely reflects the involvement of a calcium-dependent regulatory protein in the postsynaptic cell and suggests that hemichannels on the two sides of a gap junction plaque can be modified independently. NMDA-mediated modulation of gap junctions could be widespread, because both types of channels coexist during development and in several mammalian adult central nervous system structures such as hippocampus.
Pereda
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AE
Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia, USA.
Faber
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D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002712:Chlorides / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004558:Electric Stimulation; D017629:Gap Junctions / Q000502:physiology*; D018698:Glutamic Acid / Q000494:pharmacology; D006054:Goldfish / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D013216:Reflex, Startle / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D000159:Vestibulocochlear Nerve / Q000502:physiology*
D002712:Chlorides; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D004533:Egtazic Acid; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium