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CaMKII regulates the density of central glutamatergic synapses in vivo

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  • Christopher Rongo

    (LSA 361, University of California)

  • Joshua M. Kaplan

    (LSA 361, University of California)

Abstract

Synaptic connections undergo a dynamic process of stabilization or elimination during development, and this process is thought to be critical in memory and learning and in establishing the specificity of synaptic connections1. The type II calcium- and calmodulin-dependent protein kinase (CaMKII) has been proposed to be pivotal in regulating synaptic strength2,3,4 and in maturation of synapses during development5. Here we describe how CaMKII regulates the formation of central glutamatergic synapses in Caenorhabditis elegans. During larval development, the density of ventral nerve cord synapses containing the GLR-1 glutamate receptor is held constant despite marked changes in neurite length. The coupling of synapse number to neurite length requires both CaMKII and voltage-gated calcium channels. CaMKII regulates GLR-1 by at least two distinct mechanisms: regulating transport of GLR-1 from cell bodies to neurites; and regulating the addition or maintenance of GLR-1 to postsynaptic elements.

Suggested Citation

  • Christopher Rongo & Joshua M. Kaplan, 1999. "CaMKII regulates the density of central glutamatergic synapses in vivo," Nature, Nature, vol. 402(6758), pages 195-199, November.
    • Handle: RePEc:nat:nature:v:402:y:1999:i:6758:d:10.1038_46065
    DOI: 10.1038/46065
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    Cited by:

    1. Yue Hao & Haowen Liu & Xian-Ting Zeng & Ya Wang & Wan-Xin Zeng & Kang-Ying Qian & Lei Li & Ming-Xuan Chi & Shangbang Gao & Zhitao Hu & Xia-Jing Tong, 2023. "UNC-43/CaMKII-triggered anterograde signals recruit GABAARs to mediate inhibitory synaptic transmission and plasticity at C. elegans NMJs," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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