Neuroplastin in Ca2+ signal regulationand plasticity of glutamatergic synapses
Ayse Malci1
Xiao Lin2
Yun Stone Shi2
Rodrigo Herrera-Molina3
1.Center for Neuroscience Research,Children'sNational Medical Center,Washington,DC,USA2.Guangdong Institute of Intelligence Science and Technology,Zhuhai,Guangdong Province,China3.Combinatorial Combinatorial NeuroImaging,Leibniz Institute for Neurobiology,Magdeburg,Germany;Centro Integrativo de Biología y Química Aplicada,Universidad Bernardo O'Higgins,Santiago,Chile
摘要：The main function of neurons is informationtransmission in the form of action potentials. Tofulfill this duty, neurons are connected functionallywith each other via synapses, the microscopicstructures where specialized molecular machineryis strategically placed to release and receiveneurotransmitters and to generate and extinguishcalcium (Ca2+) signals. These synaptic molecularcomponents are highly dynamic and they influenceeach other to confer structural and functionaladaptability (plasticity) to neuronal communication(Biederer et al., 2017). Recently, neuroplastin(Np), a cell recognition molecule, has emergedto play diverse neuronal functions includingsynapse formation, spine structure, Ca2+ signalregulation, excitatory/inhibitory balance, andsynaptic plasticity. Evidence from different labs hasconverged to form a coherent picture; however,the uncovered mechanisms may represent onlythe tip of Np's iceberg. Many questions remain tobe answered. For example, why do neurons needtwo Np isoforms? How do Np isoforms contributeto Ca2+ signal regulation and synaptic plasticity?
机标关键词：neuroplastinsignalglutamatergicplasticityregulationandsynapses
论文发表日期：2023-08-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1705-1706 )