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http://purl.uniprot.org/citations/30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30833508http://www.w3.org/2000/01/rdf-schema#comment"Repetitive action potentials (APs) in hippocampal CA3 pyramidal cells (CA3-PCs) backpropagate to distal apical dendrites, and induce calcium and protein tyrosine kinase (PTK)-dependent downregulation of Kv1.2, resulting in long-term potentiation of direct cortical inputs and intrinsic excitability (LTP-IE). When APs were elicited by direct somatic stimulation of CA3-PCs from rodents of either sex, only a narrow window of distal dendritic [Ca2+] allowed LTP-IE because of Ca2+-dependent coactivation of PTK and protein tyrosine phosphatase (PTP), which renders non-mossy fiber (MF) inputs incompetent in LTP-IE induction. High-frequency MF inputs, however, could induce LTP-IE at high dendritic [Ca2+] of the window. We show that MF input-induced Zn2+ signaling inhibits postsynaptic PTP, and thus enables MF inputs to induce LTP-IE at a wide range of [Ca2+]i values. Extracellular chelation of Zn2+ or genetic deletion of vesicular zinc transporter abrogated the privilege of MF inputs for LTP-IE induction. Moreover, the incompetence of somatic stimulation was rescued by the inhibition of PTP or a supplement of extracellular zinc, indicating that MF input-induced increase in dendritic [Zn2+] facilitates the induction of LTP-IE by inhibiting PTP. Consistently, high-frequency MF stimulation induced immediate and delayed elevations of [Zn2+] at proximal and distal dendrites, respectively. These results indicate that MF inputs are uniquely linked to the regulation of direct cortical inputs owing to synaptic Zn2+ signaling.SIGNIFICANCE STATEMENT Zn2+ has been mostly implicated in pathological processes, and the physiological roles of synaptically released Zn2+ in intracellular signaling are little known. We show here that Zn2+ released from hippocampal mossy fiber (MF) terminals enters postsynaptic CA3 pyramidal cells, and plays a facilitating role in MF input-induced heterosynaptic potentiation of perforant path (PP) synaptic inputs through long-term potentiation of intrinsic excitability (LTP-IE). We show that the window of cytosolic [Ca2+] that induces LTP-IE is normally very narrow because of the Ca2+-dependent coactivation of antagonistic signaling pairs, whereby non-MF inputs become ineffective in inducing excitability change. The MF-induced Zn2+ signaling, however, biases toward facilitating the induction of LTP-IE. The present study elucidates why MF inputs are more privileged for the regulation of PP synapses."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.org/dc/terms/identifier"doi:10.1523/jneurosci.2130-18.2019"xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Kim S."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Jeong H.J."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Lee D.G."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Lee S.H."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Kang J.S."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Hyun J.H."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Eom K."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/author"Ho W.K."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/name"J Neurosci"xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/pages"3812-3831"xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/title"Intracellular Zn2+ Signaling Facilitates Mossy Fiber Input-Induced Heterosynaptic Potentiation of Direct Cortical Inputs in Hippocampal CA3 Pyramidal Cells."xsd:string
http://purl.uniprot.org/citations/30833508http://purl.uniprot.org/core/volume"39"xsd:string
http://purl.uniprot.org/citations/30833508http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30833508
http://purl.uniprot.org/citations/30833508http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30833508
http://purl.uniprot.org/uniprot/#_P97441-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
http://purl.uniprot.org/uniprot/#_Q3UN07-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
http://purl.uniprot.org/uniprot/#_Q3TMQ7-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
http://purl.uniprot.org/uniprot/#_Q6NZC3-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
http://purl.uniprot.org/uniprot/#_S4R2M0-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
http://purl.uniprot.org/uniprot/#_S4R2S4-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
http://purl.uniprot.org/uniprot/#_S4R166-mappedCitation-30833508http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30833508
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