Enhancement of postsynaptic serotonin-activated Cl- currents by depolarization-induced Ca2+ entry into leech neurons.
Postsynaptic Ca2+ signals are a precondition for many types of synapse modification, including long-term potentiation. Here we describe a postsynaptic mechanism that augments synaptic currents at the serotonergic Retzius-P cell synapse of the leech. Depolarizations large enough to elicit Ca2+ currents evoked an increase in the amplitude of serotonin-activated Cl- currents in isolated embryonic neurons as well as at the Retzius-P cell synapse. The effect on embryonic whole cell currents lasted for up to one hour and was abolished in solutions containing Cd2+ as a Ca2+ channel blocker. Hence, Ca2+ influx into the postsynaptic neuron may be a common step regulating the plasticity of various vertebrate as well as invertebrate synapses.
Lessmann
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Lehrstuhl für Molekulare Neurobiochemie, Ruhr-Universität Bochum, F.R.G.
Dietzel
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ID
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D018118:Chloride Channels / Q000187:drug effects* / Q000502:physiology*; D007865:Leeches; D017774:Long-Term Potentiation / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D017729:Presynaptic Terminals / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects
D018118:Chloride Channels; D012701:Serotonin; D002118:Calcium