[1]Chistiakova M, Bannon NM, Bazhenov M, et al. Heterosynaptic plasticity: multiple mechanisms and multiple roles[J]. Neuroscientist, 2014,20(5):483-498. DOI: 10.1177/1073858414529829.
[2]Park JM, Jung SC, Eun SY. Long-term synaptic plasticity: circuit perturbation and stabilization[J]. Korean J Physiol Pharmacol, 2014,18(6):457-460. DOI: 10.4196/kjpp.2014.18.6.457.
[3]Honkura N, Matsuzaki M, Noguchi J, et al. The subspine organization of actin fibers regulates the structure and plasticity of dendritic spines[J]. Neuron, 2008,57(5):719-729. DOI: 10.1016/j.neuron.2008.01.013.
[4]Kapitein LC, Yau KW, Gouveia SM, et al. NMDA receptor activation suppresses microtubule growth and spine entry[J]. J Neurosci, 2011,31(22):8194-8209. DOI: 10.1523/JNEUROSCI.6215-10.2011.
[5]Hu X, Ballo L, Pietila L, et al. BDNF-induced increase of PSD-95 in dendritic spines requires dynamic microtubule invasions[J]. J Neurosci, 2011,31(43):15597-15603. DOI: 10.1523/JNEUROSCI.2445-11.2011.
[6]Liu YJ, Spangenberg EE, Tang B, et al. Microglia elimination increases neural circuit connectivity and activity in adult mouse cortex[J]. J Neurosci, 2021,41(6):1274-1287. DOI: 10.1523/JNEUROSCI.2140-20.2020.
[7]Stevens B, Allen NJ, Vazquez LE, et al. The classical complement cascade mediates CNS synapse elimination[J]. Cell, 2007,131(6):1164-1178. DOI: 10.1016/j.cell.2007.10.036.
[8]Vainchtein ID, Chin G, Cho FS, et al. Astrocyte-derived interleukin-33 promotes microglial synapse engulfment and neural circuit development[J]. Science, 2018,359(6381):1269-1273. DOI: 10.1126/science.aal3589.
[9]Rauti R, Cellot G, D'Andrea P, et al. BDNF impact on synaptic dynamics: extra or intracellular long-term release differently regulates cultured hippocampal synapses[J]. Mol Brain, 2020,13(1):43. DOI: 10.1186/s13041-020-00582-9.
[10]Tang Y, Le W. Differential roles of M1 and M2 microglia in neurodegenerative diseases[J]. Mol Neurobiol, 2016,53(2):1181-1194. DOI: 10.1007/s12035-014-9070-5.
[11]Wang CS, Kavalali ET, Monteggia LM. BDNF signaling in context: from synaptic regulation to psychiatric disorders[J]. Cell, 2022,185(1):62-76. DOI: 10.1016/j.cell.2021.12.003.
[12]Saw G, Krishna K, Gupta N, et al. Epigenetic regulation of microglial phosphatidylinositol 3-kinase pathway involved in long-term potentiation and synaptic plasticity in rats[J]. Glia, 2020,68(3):656-669. DOI: 10.1002/glia.23748.
[13]Cheng Q, Song SH, Augustine GJ. Calcium-dependent and synapsin-dependent pathways for the presynaptic actions of BDNF[J]. Front Cell Neurosci, 2017,11:75. DOI: 10.3389/fncel.2017.00075.
[14]Gideons ES, Lin PY, Mahgoub M, et al. Chronic lithium treatment elicits its antimanic effects via BDNF-TrkB dependent synaptic downscaling[J]. Elife, 2017,6:e25480. DOI: 10.7554/eLife.25480.
[15]Lalo U, Bogdanov A, Moss GW, et al. Astroglia-derived BDNF and MSK-1 mediate experience- and diet-dependent synaptic plasticity[J]. Brain Sci, 2020,10(7):462. DOI: 10.3390/brainsci10070462.
[16]Horvath PM, Chanaday NL, Alten B, et al. A subthreshold synaptic mechanism regulating BDNF expression and resting synaptic strength[J].Cell Rep, 2021, 36(5):109467.DOI:10.1016/j.celrep.2021.109467.
[17]Gurevich EV, Gainetdinov RR, Gurevich VV. G protein-coupled receptor kinases as regulators of dopamine receptor functions[J]. Pharmacol Res, 2016,111:1-16. DOI: 10.1016/j.phrs.2016.05.010.
[18]Zhou Y, Danbolt NC. Glutamate as a neurotransmitter in the healthy brain[J]. J Neural Transm (Vienna), 2014,121(8):799-817. DOI: 10.1007/s00702-014-1180-8.
[19]Larsen RS, Rao D, Manis PB, et al. STDP in the developing sensory neocortex[J]. Front Synaptic Neurosci, 2010,2:9. DOI: 10.3389/fnsyn.2010.00009.
[20]Czarnecki A, Birtoli B, Ulrich D. Cellular mechanisms of burst firing-mediated long-term depression in rat neocortical pyramidal cells[J]. J Physiol, 2007,578(Pt 2):471-479. DOI: 10.1113/jphysiol.2006.123588.
[21]Larsen RS, Sjöström PJ. Synapse-type-specific plasticity in local circuits[J]. Curr Opin Neurobiol, 2015,35:127-135. DOI: 10.1016/j.conb.2015.08.001.
[22]Davies DA, Adlimoghaddam A, Albensi BC. Role of Nrf2 in synaptic plasticity and memory in Alzheimer's disease[J]. Cells, 2021,10(8):1884. DOI: 10.3390/cells10081884.
[23]Le Douce J, Maugard M, Veran J, et al. Impairment of glycolysis-derived l-serine production in astrocytes contributes to cognitive deficits in Alzheimer's disease[J]. Cell Metab, 2020,31(3):503-517.e8. DOI: 10.1016/j.cmet.2020.02.004.
[24]Wang Y, Fu WY, Cheung K, et al. Astrocyte-secreted IL-33 mediates homeostatic synaptic plasticity in the adult hippocampus[J]. Proc Natl Acad Sci U S A, 2021,118(1):e2020810118. DOI: 10.1073/pnas.2020810118.
[25]Thiele SL, Chen B, Lo C, et al. Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models[J]. Neurobiol Dis, 2014,71:334-344. DOI: 10.1016/j.nbd.2014.08.006.
[26]University of California, San Francisco MS-EPIC Team. Long-term evolution of multiple sclerosis disability in the treatment era[J]. Ann Neurol, 2016,80(4):499-510. DOI: 10.1002/ana.24747.
[27]Di Filippo M, Mancini A, Bellingacci L, et al. Interleukin-17 affects synaptic plasticity and cognition in an experimental model of multiple sclerosis[J]. Cell Rep, 2021,37(10):110094. DOI: 10.1016/j.celrep.2021.110094.
[28]Lassmann H, van Horssen J. Oxidative stress and its impact on neurons and glia in multiple sclerosis lesions[J]. Biochim Biophys Acta, 2016,1862(3):506-510. DOI: 10.1016/j.bbadis.2015.09.018.
[29]Palma FR, He C, Danes JM, et al. Mitochondrial superoxide dismutase: what the established, the intriguing, and the novel reveal about a key cellular redox switch[J]. Antioxid Redox Signal, 2020,32(10):701-714. DOI: 10.1089/ars.2019.7962.
[30]de Curtis M, Garbelli R, Uva L. A hypothesis for the role of axon demyelination in seizure generation[J]. Epilepsia, 2021,62(3):583-595. DOI: 10.1111/epi.16824.
[31]Wang P, Ma K, Yang L, et al. Predicting signaling pathways regulating demyelination in a rat model of lithium-pilocarpine-induced acute epilepsy: a proteomics study[J]. Int J Biol Macromol, 2021,193(Pt B):1457-1470. DOI: 10.1016/j.ijbiomac.2021.10.209.
[32]Vinet J, Vainchtein ID, Spano C, et al. Microglia are less pro-inflammatory than myeloid infiltrates in the hippocampus of mice exposed to status epilepticus[J]. Glia, 2016,64(8):1350-1362. DOI: 10.1002/glia.23008.
[33]Cho K. Emerging roles of complement protein C1q in neurodegeneration[J]. Aging Dis, 2019,10(3):652-663. DOI: 10.14336/AD.2019.0118.
[34]Sellgren CM, Gracias J, Watmuff B, et al. Increased synapse elimination by microglia in schizophrenia patient-derived models of synaptic pruning[J]. Nat Neurosci, 2019,22(3):374-385. DOI: 10.1038/s41593-018-0334-7.
[35]Lepeta K, Kaczmarek L. Matrix metalloproteinase-9 as a novel player in synaptic plasticity and schizophrenia[J]. Schizophr Bull, 2015,41(5):1003-1009. DOI: 10.1093/schbul/sbv036.
[36]Bartsch JC, Schott BH, Behr J. Hippocampal dysfunction in schizophrenia and aberrant hippocampal synaptic plasticity in rodent model psychosis: a selective review[J]. Pharmacopsychiatry, 2023,56(2):57-63. DOI: 10.1055/a-0960-9846.
[37]Mould AW, Hall NA, Milosevic I, et al. Targeting synaptic plasticity in schizophrenia: insights from genomic studies[J]. Trends Mol Med, 2021,27(11):1022-1032. DOI: 10.1016/j.molmed.2021.07.014.
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