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Calcium stores regulate the polarity and input specificity of synaptic modification

Author

Listed:
  • Makoto Nishiyama

    (University of California at San Diego
    New York University School of Medicine)

  • Kyonsoo Hong

    (University of California at San Diego
    New York University School of Medicine)

  • Katsuhiko Mikoshiba

    (Mikoshiba Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST))

  • Mu-ming Poo

    (University of California at San Diego
    Mikoshiba Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST))

  • Kunio Kato

    (Mikoshiba Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST))

Abstract

Activity-induced synaptic modification is essential for the development and plasticity of the nervous system1,2,3. Repetitive correlated activation of pre- and postsynaptic neurons can induce persistent enhancement or decrement of synaptic efficacy, commonly referred to as long-term potentiation or depression2,3(LTP or LTD). An important unresolved issue is whether and to what extent LTP and LTD are restricted to the activated synapses4,5,6,7,8. Here we show that, in the CA1 region of the hippocampus, reduction of postsynaptic calcium influx by partial blockade of NMDA (N-methyl-d-aspartate) receptors results in a conversion of LTP to LTD and a loss of input specificity normally associated with LTP, with LTD appearing at heterosynaptic inputs. The induction of LTD at homo- and heterosynaptic sites requires functional ryanodine receptors and inositol triphosphate (InsP3) receptors, respectively. Functional blockade or genetic deletion of type 1 InsP3 receptors led to a conversion of LTD to LTP and elimination of heterosynaptic LTD, whereas blocking ryanodine receptors eliminated only homosynaptic LTD. Thus, postsynaptic Ca2+, deriving from Ca2+ influx and differential release of Ca2+ from internal stores through ryanodine and InsP3 receptors, regulates both the polarity and input specificity of activity-induced synaptic modification.

Suggested Citation

  • Makoto Nishiyama & Kyonsoo Hong & Katsuhiko Mikoshiba & Mu-ming Poo & Kunio Kato, 2000. "Calcium stores regulate the polarity and input specificity of synaptic modification," Nature, Nature, vol. 408(6812), pages 584-588, November.
    • Handle: RePEc:nat:nature:v:408:y:2000:i:6812:d:10.1038_35046067
    DOI: 10.1038/35046067
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    Cited by:

    1. Yu, Haitao & Guo, Xinmeng & Wang, Jiang & Deng, Bin & Wei, Xile, 2015. "Vibrational resonance in adaptive small-world neuronal networks with spike-timing-dependent plasticity," Physica A: Statistical Mechanics and its Applications, Elsevier, vol. 436(C), pages 170-179.
    2. Dariusz Świetlik, 2018. "Simulations of Learning, Memory, and Forgetting Processes with Model of CA1 Region of the Hippocampus," Complexity, Hindawi, vol. 2018, pages 1-13, December.
    3. Thomas E. Chater & Maximilian F. Eggl & Yukiko Goda & Tatjana Tchumatchenko, 2024. "Competitive processes shape multi-synapse plasticity along dendritic segments," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    4. Pierre Yger & Kenneth D Harris, 2013. "The Convallis Rule for Unsupervised Learning in Cortical Networks," PLOS Computational Biology, Public Library of Science, vol. 9(10), pages 1-16, October.

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