Abstract
Habituation of a behavioral response to a repetitive stimulus enables animals to ignore irrelevant stimuli and focus on behaviorally important events. In Aplysia, habituation is mediated by rapid depression of sensory synapses, which could leave an animal unresponsive to important repetitive stimuli, making it vulnerable to injury. We identified a form of plasticity that prevents synaptic depression depending on the precise stimulus strength. Burst-dependent protection from depression is initiated by trains of 2–4 action potentials and is distinct from previously described forms of synaptic enhancement. The blockade of depression is mediated by presynaptic Ca2+ influx and protein kinase C (PKC) and requires localization of PKC via a PDZ domain interaction with Aplysia PICK1. During protection from depression, PKC acts as a highly sensitive detector of the precise pattern of sensory neuron firing. Behaviorally, burst-dependent protection reduces habituation, enabling animals to maintain responsiveness to stimuli that are functionally important.
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Acknowledgements
We thank W. Sossin, S. Thompson and E. Walters for commenting on an earlier version of this manuscript. We thank P. Shrestha for performing the co-immunoprecipitation and immunoblot experiments. We thank I. Antonov and R. Hawkins for introducing us to their behavioral preparation. This work was supported by US National Institutes of Health grant R01 MH-55880 to T.W.A.
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X.-Y.J. and T.W.A. discovered the BDP phenomenon. Q.W., K.S.M. and T.W.A. designed the experiments. Q.W., X.-Y.J., A.M.N. and S.-G.L. carried out the experiments analyzing the mechanism of BDP. K.S.M. performed the behavioral experiments. T.W.A., K.S.M. and Q.W. wrote the paper.
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Wan, Q., Jiang, XY., Negroiu, A. et al. Protein kinase C acts as a molecular detector of firing patterns to mediate sensory gating in Aplysia. Nat Neurosci 15, 1144–1152 (2012). https://doi.org/10.1038/nn.3158
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DOI: https://doi.org/10.1038/nn.3158
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