Cited by 1Neuroscience and Neuropharmacology ResearchGenetics and Neurodevelopmental DisordersNeuroinflammation and Neurodegeneration Mechanisms

Pathological Synaptic Plasticity in Neurological Disorders

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Jin, CongYu, Karlstedt, Kaj·2025·Synaptic Plasticity - Neurobiology, Neuroanatomy, and Clinical Neuroscience

Abstract

This chapter will introduce the concept of pathological synaptic plasticity and its pivotal role in the progression of various neurological disorders. Synaptic plasticity, the brain's ability to strengthen or weaken synapses in response to activity, is essential for learning and memory. However, when these mechanisms are disrupted, they can contribute to the pathology of diseases such as Alzheimer’s disease, Parkinson’s disease, epilepsy, schizophrenia, and autism spectrum disorders. This chapter explores the molecular and cellular foundations of synaptic plasticity, identifies how its dysregulation leads to neurological dysfunction, and examines the clinical implications. Additionally, it reviews current and emerging therapeutic strategies aimed at restoring normal synaptic function, offering insights into potential future research directions and treatment modalities.

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Crossref · 10.5772/intechopen.1007753

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  • Structural plasticity is tightly coupled to functional changes: LTP is generally associated with spine enlargement or increased spine density, whereas LTD is linked to spine shrinkage and synaptic weakening.

    “Structural plasticity is tightly coupled to these functional changes, as LTP is generally associated with spine enlargement or increased spine density, whereas LTD is linked to spine shrinkage and synaptic weakening (Jin and Karlstedt, 2025; Rodrigues et al., 2024).”

    From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Jin and Karlstedt, 2025

    Section 2.2 says LTP strengthens synaptic connections and LTD weakens them, supporting the functional-change part of the claim. Section 3.1 says synaptic plasticity can reorganize neuronal structure and function, but our copy does not link LTP to spine enlargement or increased density, or LTD to spine shrinkage. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Activation of NMDA receptors triggers postsynaptic Ca2+ influx, and the magnitude and duration of this signal determine the direction of plasticity.

    “Activation of these receptors triggers postsynaptic Ca2+ influx, and the magnitude and duration of this signal determine the direction of plasticity (Jin and Karlstedt, 2025; Rodrigues et al., 2024).”
  • Exposure to dicofol has been associated with long-lasting cognitive and emotional impairments.

    “Exposure to dicofol has been associated with long-lasting cognitive and emotional impairments, while prenatal exposure to mirex has been linked to neurodevelopmental disorders in children evident as early as preschool age (Jin and Karlstedt, 2025; Puertas et al., 2010).”

    From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Jin and Karlstedt, 2025

    The passages from §§4.3 and 5.4 discuss cognitive deficits in schizophrenia, not effects of dicofol exposure (page numbers unavailable). Searches for dicofol, pesticide exposure, and long-lasting cognitive or emotional impairments found no passage addressing the attributed claim. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 264

  1. Hughes JR. Post-tetanic potentiation. Physiological Reviews. 1958;38(1):91-113. DOI: 10.1152/physrev.1958.38.1.91 · DOI
  2. Malenka RC, Bear MF. LTP and LTD: An embarrassment of riches. Neuron. 2004;44(1):5-21. DOI: 10.1016/j. neuron.2004.09.012 · DOI · Paper page
  3. Kandel ER, Dudai Y, Mayford MR. The molecular and systems biology of memory. Cell. 2014;157(1):163-186. DOI: 10.1016/j.cell.2014.03.001 · DOI · Paper page
  4. Nabavi S, Fox R, Proulx CD, Lin JY, Tsien RY, Malinow R. Engineering a memory with LTD and LTP. Nature. 2014;511(7509):348-352. DOI: 10.1038/ nature13294. Epub 2014 Jun 1 · DOI · Paper page
  5. Bliss TV, Lomo T. Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of Physiology. 1973;232(2):331-356. DOI: 10.1113/jphysiol.1973.sp010273 · DOI · Paper page
  6. Barrionuevo G, Schottler F, Lynch G. The effects of repetitive low frequency stimulation on control and "potentiated" synaptic responses in the hippocampus. Life Sciences. 1980;27(24):2385-2391. DOI: 10.1016/0024-3205(80)90509-3 · DOI · Paper page
  7. Dudek SM, Bear MF. Homosynaptic long-term depression in area CA1 of hippocampus and effects of N-methyl-D- aspartate receptor blockade. Proceedings of the National Academy of Sciences of the United States of America. 1992;89(10):4363-4367. DOI: 10.1073/ pnas.89.10.4363 · DOI · Paper page
  8. Citri A, Malenka RC. Synaptic plasticity: Multiple forms, functions, and mechanisms. Neuropsychopharmacology. 2008;33(1):18-41. DOI: 10.1038/ sj.npp.1301559 · DOI · Paper page
  9. Turrigiano GG, Nelson SB. Homeostatic plasticity in the developing nervous system. Nature Reviews. Neuroscience. 2004;5(2):97-107
  10. Shouval HZ. Models of synaptic plasticity. Scholarpedia. 2007;2:1605
  11. Bear MF, Abraham WC. Long- term depression in hippocampus. Annual Review of Neuroscience. 1996;19:437-462. DOI: 10.1146/annurev. ne.19.030196.002253 · DOI
  12. Nicoll RA, Malenka RC. Contrasting properties of two forms of long-term potentiation in the hippocampus. Nature. 1995;377(6545):115-118. DOI: 10.1038/377115a0 · DOI
  13. Linden DJ, Connor JA. Participation of postsynaptic PKC in cerebellar long-term depression in culture. Science. 1991;254(5038):1656-1659. DOI: 10.1126/ science.1721243 · DOI
  14. De Zeeuw CI, Hansel C, Bian F, Koekkoek SK, van Alphen AM, Linden DJ, et al. Expression of a protein kinase C inhibitor in Purkinje cells blocks cerebellar LTD and adaptation of the vestibulo-ocular reflex. Neuron. 1998;20(3):495-508. DOI: 10.1016/ s0896-6273(00)80990-3 · DOI
  15. Bellone C, Lüscher C. mGluRs induce a long-term depression in the ventral tegmental area that involves a switch of the subunit composition of AMPA receptors. The European Journal of Neuroscience. 2005;21(5):1280-1288. DOI: 10.1111/j.1460-9568.2005.03979.x · DOI
  16. Huang CC, Hsu KS. Sustained activation of metabotropic glutamate receptor 5 and protein tyrosine phosphatases mediate the expression of (S)-3,5-dihydroxyphenylglycine- induced long-term depression in the hippocampal CA1 region. Journal of Neurochemistry. 2006;96(1):179-194. DOI: 10.1111/j.1471-4159.2005.03527.x · DOI
  17. Hou L, Klann E. Activation of the phosphoinositide 3-kinase-Akt- mammalian target of rapamycin signaling pathway is required for metabotropic glutamate receptor- dependent long-term depression. The Journal of Neuroscience. 2004;24(28):6352-6361. DOI: 10.1523/ JNEUROSCI.0995-04.2004 · DOI · Paper page
  18. Huber KM, Kayser MS, Bear MF. Role for rapid dendritic protein synthesis in hippocampal mGluR-dependent long-term depression. Science. 2000;288(5469):1254-1257. DOI: 10.1126/ science.288.5469.1254 · DOI
  19. Huber KM, Roder JC, Bear MF. Chemical induction of mGluR5-and protein synthesis-dependent long- term depression in hippocampal area CA1. Journal of Neurophysiology. 2001;86(1):321-325. DOI: 10.1152/ jn.2001.86.1.321 · DOI
  20. Snyder EM, Philpot BD, Huber KM, Dong X, Fallon JR, Bear MF. Internalization of ionotropic glutamate receptors in response to mGluR activation. Nature Neuroscience. 2001;4(11):1079-1085. DOI: 10.1038/ nn746 · DOI
  21. Ito M. Long-term depression. Annual Review of Neuroscience. 1989;12:85-102. DOI: 10.1146/annurev. ne.12.030189.000505 · DOI
  22. Linden DJ, Connor JA. Long-term synaptic depression. Annual Review of Neuroscience. 1995;18:319-357. DOI: 10.1146/annurev.ne.18.030195.001535 · DOI
  23. Huganir RL, Nicoll RA. AMPARs and synaptic plasticity: The last 25 years. Neuron. 2013;80(3):704-717. DOI: 10.1016/j.neuron.2013.10.025 · DOI · Paper page
  24. Gerdeman GL, Ronesi J, Lovinger DM. Postsynaptic endocannabinoid release is critical to long-term depression in the striatum. Nature Neuroscience. 2002;5(5):446-451. DOI: 10.1038/nn832 · DOI
  25. Robbe D, Alonso G, Chaumont S, Bockaert J, Manzoni OJ. Role of p/q-Ca2+ channels in metabotropic glutamate receptor 2/3-dependent presynaptic long- term depression at nucleus accumbens synapses. The Journal of Neuroscience. 2002;22(11):4346-4356. DOI: 10.1523/ JNEUROSCI.22-11-04346.2002 · DOI
  26. Sjöström PJ, Turrigiano GG, Nelson SB. Neocortical LTD via coincident activation of presynaptic NMDA and cannabinoid receptors. Neuron. 2003;39(4):641-654. DOI: 10.1016/s0896-6273(03)00476-8 · DOI
  27. Safo PK, Regehr WG. Endocannabinoids control the induction of cerebellar LTD. Neuron. 2005;48(4):647-659. DOI: 10.1016/j. neuron.2005.09.020 · DOI
  28. Chevaleyre V, Takahashi KA, Castillo PE. Endocannabinoid-mediated synaptic plasticity in the CNS. Annual Review of Neuroscience. 2006;29:37-76. DOI: 10.1146/annurev. neuro.29.051605.112834 · DOI
  29. Viveros MP, Marco EM, Llorente R, López-Gallardo M. Endocannabinoid system and synaptic plasticity: Implications for emotional responses. Neural Plasticity. 2007;2007:52908. DOI: 10.1155/2007/52908 · DOI
  30. Mulkey RM, Malenka RC. Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus. Neuron. 1992;9(5):967-975. DOI: 10.1016/0896-6273(92)90248-c · DOI · Paper page
  31. Aiba A, Kano M, Chen C, Stanton ME, Fox GD, Herrup K, et al. Deficient cerebellar long-term depression and impaired motor learning in mGluR1 mutant mice. Cell. 1994;79(2):377-388
  32. Shigemoto R, Abe T, Nomura S, Nakanishi S, Hirano T. Antibodies inactivating mGluR1 metabotropic glutamate receptor block long-term depression in cultured Purkinje cells. Neuron. 1994;12(6):1245-1255. DOI: 10.1016/0896-6273(94)90441-3 · DOI
  33. Malenka RC, Nicoll RA. Long-term potentiation-a decade of progress? Science. 1999;285(5435):1870-1874. DOI: 10.1126/science.285.5435.1870 · DOI · Paper page
  34. Bliss TV, Collingridge GL. A synaptic model of memory: Long-term potentiation in the hippocampus. Nature. 1993;361(6407):31-39. DOI: 10.1038/361031a0 · DOI · Paper page
  35. Malenka RC, Kauer JA, Zucker RS, Nicoll RA. Postsynaptic calcium is sufficient for potentiation of hippocampal synaptic transmission. Science. 1988;242(4875):81-84. DOI: 10.1126/science.2845577 · DOI · Paper page
  36. Yang SN, Tang YG, Zucker RS. Selective induction of LTP and LTD by postsynaptic [Ca2+]i elevation. Journal of Neurophysiology. 1999;81(2):781-787. DOI: 10.1152/jn.1999.81.2.781 · DOI · Paper page
  37. Derkach V, Barria A, Soderling TR. Ca 2+ /calmodulin-kinase II enhances channel conductance of alpha-amino-3- hydroxy-5-methyl-4-isoxazolepropionate type glutamate receptors. Proceedings of the National Academy of Sciences of the United States of America. 1999;96:3269-3274
  38. Derkach VA, Oh MC, Guire ES, Soderling TR. Regulatory mechanisms of AMPA receptors in synaptic plasticity. Nature Reviews. Neuroscience. 2007;8(2):101-113. DOI: 10.1038/nrn2055 · DOI · Paper page
  39. Park AJ, Havekes R, Choi JH, Luczak V, Nie T, Huang T, et al. A presynaptic role for PKA in synaptic tagging and memory. Neurobiology of Learning and Memory. 2014;114:101-112. DOI: 10.1016/j.nlm.2014.05.005 · DOI
  40. Abbott LF, Regehr WG. Synaptic computation. Nature. 2004;431(7010):796-803. DOI: 10.1038/ nature03010 · DOI · Paper page
  41. Hennig MH. Theoretical models of synaptic short term plasticity. Frontiers in Computational Neuroscience. 2013;7:45. DOI: 10.3389/ fncom.2013.00045 · DOI
  42. Appelbaum LG, Shenasa MA, Stolz L, Daskalakis Z. Synaptic plasticity and mental health: Methods, challenges and opportunities. Neuropsychopharmacology. 2023;48(1):113-120. DOI: 10.1038/ s41386-022-01370-w · DOI · Paper page
  43. DeKosky ST, Scheff SW. Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity. Annals of Neurology. 1990;27(5):457-464. DOI: 10.1002/ ana.410270502 · DOI · Paper page
  44. Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, et al. Physical basis of cognitive alterations in Alzheimer's disease: Synapse loss is the major correlate of cognitive impairment. Annals of Neurology. 1991;30(4):572- 580. DOI: 10.1002/ana.410300410 · DOI · Paper page
  45. Selkoe DJ. Alzheimer's disease is a synaptic failure. Science. 2002;298(5594):789-791. DOI: 10.1126/ science.1074069 · DOI · Paper page
  46. Honer WG. Pathology of presynaptic proteins in Alzheimer's disease: More than simple loss of terminals. Neurobiology of Aging. 2003;24(8):1047-1062. DOI: 10.1016/j. neurobiolaging.2003.04.005 · DOI · Paper page
  47. Palop JJ, Chin J, Mucke L. A network dysfunction perspective on neurodegenerative diseases. Nature. 2006;443(7113):768-773. DOI: 10.1038/ nature05289 · DOI
  48. Meftah S, Gan J. Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression. Frontiers in Synaptic Neuroscience. 2023;15:1129036. DOI: 10.3389/fnsyn.2023.1129036 · DOI
  49. Shaw P, Lerch JP, Pruessner JC, Taylor KN, Rose AB, Greenstein D, et al. Cortical morphology in children and adolescents with different apolipoprotein E gene polymorphisms: An observational study. Lancet Neurology. 2007;6(6):494-500. DOI: 10.1016/ S1474-4422(07)70106-0 · DOI
  50. Domínguez-Álvaro M, Montero-Crespo M, Blazquez-Llorca L, DeFelipe J, Alonso-Nanclares L. 3D electron microscopy study of synaptic organization of the normal human transentorhinal cortex and its possible alterations in Alzheimer's disease. eNeuro. 2019;6(4):ENE URO.0140-19.2019. DOI: 10.1523/ ENEURO.0140-19.2019 · DOI
  51. Gong Y, Lippa CF, Zhu J, Lin Q, Rosso AL. Disruption of glutamate receptors at shank-postsynaptic platform in Alzheimer's disease. Brain Research. 2009;1292:191-198. DOI: 10.1016/j. brainres.2009.07.056. Epub 2009 Jul 25 · DOI
  52. Marcello E, Epis R, Saraceno C, Gardoni F, Borroni B, Cattabeni F, et al. SAP97-mediated local trafficking is altered in Alzheimer disease patients' hippocampus. Neurobiology of Aging. 2012;33(2):422.e1-422.10. DOI: 10.1016/j. neurobiolaging.2010.09.015 · DOI
  53. Sze C, Bi H, Kleinschmidt- DeMasters BK, Filley CM, Martin LJ. N-methyl-D-aspartate receptor subunit proteins and their phosphorylation status are altered selectively in Alzheimer's disease. Journal of the Neurological Sciences. 2001;182(2):151-159. DOI: 10.1016/s0022-510x(00)00467-6 · DOI
  54. Bi H, Sze CI. N-methyl-D-aspartate receptor subunit NR2A and NR2B messenger RNA levels are altered in the hippocampus and entorhinal cortex in Alzheimer's disease. Journal of the Neurological Sciences. 2002;200(1-2):11-18. DOI: 10.1016/ s0022-510x(02)00087-4 · DOI
  55. Romanelli MF, Morris JC, Ashkin K, Coben LA. Advanced Alzheimer's disease is a risk factor for late-onset seizures. Archives of Neurology. 1990;47(8):847-850. DOI: 10.1001/ archneur.1990.00530080029006 · DOI
  56. Irizarry MC, Jin S, He F, Emond JA, Raman R, Thomas RG, et al. Incidence of new-onset seizures in mild to moderate Alzheimer disease. Archives of Neurology. 2012;69(3):368-372. DOI: 10.1001/archneurol.2011.830 · DOI
  57. Nicastro N, Assal F, Seeck M. From here to epilepsy: The risk of seizure in patients with Alzheimer's disease. Epileptic Disorders. 2016;18(1):1-12. DOI: 10.1684/epd.2016.0808 · DOI
  58. Li S, Selkoe DJ. A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer's brain. Journal of Neurochemistry. 2020;154(6):583-597. DOI: 10.1111/ jnc.15007 · DOI
  59. Schirinzi T, Canevelli M, Suppa A, Bologna M, Marsili L. The continuum between neurodegeneration, brain plasticity, and movement: A critical appraisal. Reviews in the Neurosciences. 2020;31(7):723-742. DOI: 10.1515/ revneuro-2020-0011 · DOI
  60. Kawabata S. Excessive/aberrant and maladaptive synaptic plasticity: A hypothesis for the pathogenesis of Alzheimer's disease. Frontiers in Aging Neuroscience. 2022;14:913693. DOI: 10.3389/fnagi.2022.913693 · DOI · Paper page
  61. Latif-Hernandez A, Sabanov V, Ahmed T, Craessaerts K, Saito T, Saido T, et al. The two faces of synaptic failure in App NL-G-F knock-in mice. Alzheimer's Research & Therapy. 2020;12(1):100. DOI: 10.1186/s13195-020-00667-6 · DOI
  62. Arroyo-García LE, Isla AG, Andrade-Talavera Y, Balleza-Tapia H, Loera-Valencia R, Alvarez-Jimenez L, et al. Impaired spike-gamma coupling of area CA3 fast-spiking interneurons as the earliest functional impairment in the App NL-G-F mouse model of Alzheimer's disease. Molecular Psychiatry. 2021;26(10):5557-5567. DOI: 10.1038/ s41380-021-01257-0 · DOI
  63. Mehak SF, Shivakumar AB, Kumari S, Muralidharan B, Gangadharan G. Theta and gamma oscillatory dynamics in mouse models of Alzheimer's disease: A path to prospective therapeutic intervention. Neuroscience and Biobehavioral Reviews. 2022;136:104628. DOI: 10.1016/j. neubiorev.2022.104628 · DOI
  64. Regan P, Piers T, Yi JH, Kim DH, Huh S, Park SJ, et al. Tau phosphorylation at serine 396 residue is required for hippocampal LTD. The Journal of Neuroscience. 2015;35(12):4804-4812. DOI: 10.1523/JNEUROSCI.2842-14.2015 · DOI · Paper page
  65. Bejanin A, Schonhaut DR, La Joie R, Kramer JH, Baker SL, Sosa N, et al. Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease. Brain. 2017;140(12):3286-3300. DOI: 10.1093/ brain/awx243 · DOI · Paper page
  66. Xia C, Makaretz SJ, Caso C, McGinnis S, Gomperts SN, Sepulcre J, et al. Association of In Vivo [18F]AV-1451 tau PET imaging results with cortical atrophy and symptoms in typical and atypical Alzheimer disease. JAMA Neurology. 2017;74(4):427-436. DOI: 10.1001/jamaneurol.2016.5755 · DOI
  67. Eckermann K, Mocanu MM, Khlistunova I, Biernat J, Nissen A, Hofmann A, et al. The beta-propensity of tau determines aggregation and synaptic loss in inducible mouse models of tauopathy. The Journal of Biological Chemistry. 2007;282(43):31755-31765. DOI: 10.1074/jbc.M705282200 · DOI · Paper page
  68. Sahara N, Murayama M, Higuchi M, Suhara T, Takashima A. Biochemical distribution of tau protein in Synaptosomal fraction of transgenic mice expressing human P301L tau. Frontiers in Neurology. 2014;5:26. DOI: 10.3389/fneur.2014.00026 · DOI
  69. Xia D, Li C, Götz J. Pseudophosphorylation of tau at distinct epitopes or the presence of the P301L mutation targets the microtubule- associated protein tau to dendritic spines. Biochimica et Biophysica Acta. 2015;1852(5):913-924. DOI: 10.1016/j. bbadis.2014.12.017 · DOI
  70. Yoshiyama Y, Higuchi M, Zhang B, Huang SM, Iwata N, Saido TC, et al. Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron. 2007;53(3):337- 351. DOI: 10.1016/j.neuron.2007.01.010. Erratum in: Neuron. 2007;54(2):343-4 · DOI · Paper page
  71. Hill E, Karikari TK, Moffat KG, Richardson MJE, Wall MJ. Introduction of tau oligomers into cortical neurons alters action potential dynamics and disrupts synaptic transmission and plasticity. eNeuro. 2019;6(5):ENE URO.0166-19.2019. DOI: 10.1523/ ENEURO.0166-19.2019 · DOI
  72. Fá M, Puzzo D, Piacentini R, Staniszewski A, Zhang H, Baltrons MA, et al. Extracellular tau oligomers produce an immediate impairment of LTP and memory. Scientific Reports. 2016;6:19393. DOI: 10.1038/srep19393 · DOI
  73. Puzzo D, Piacentini R, Fá M, Gulisano W, Li Puma DD, Staniszewski A, et al. LTP and memory impairment caused by extracellular Aβ and tau oligomers is APP-dependent. eLife. 2017;6:e26991. DOI: 10.7554/ eLife.26991 · DOI · Paper page
  74. Sydow A, Van der Jeugd A, Zheng F, Ahmed T, Balschun D, Petrova O, et al. Tau-induced defects in synaptic plasticity, learning, and memory are reversible in transgenic mice after switching off the toxic tau mutant. The Journal of Neuroscience. 2011;31(7):2511-2525. DOI: 10.1523/ JNEUROSCI.5245-10.2011 · DOI · Paper page
  75. Booth CA, Witton J, Nowacki J, Tsaneva-Atanasova K, Jones MW, Randall AD, et al. Altered intrinsic pyramidal neuron properties and pathway-specific synaptic dysfunction underlie aberrant hippocampal network function in a mouse model of Tauopathy. The Journal of Neuroscience. 2016;36(2):350-363. DOI: 10.1523/ JNEUROSCI.2151-15.2016 · DOI
  76. Taylor HBC, Emptage NJ, Jeans AF. Long-term depression links amyloid-β to the pathological hyperphosphorylation of tau. Cell Reports. 2021;36(9):109638. DOI: 10.1016/j.celrep.2021.109638 · DOI
  77. Sourkes TL, Poirier LJ. Neurochemical bases of tremor and other disorders of movement. Canadian Medical Association Journal. 1966;94(2):53-60
  78. Pearce J, Pearce I. Current concepts of parkinsonism. Postgraduate Medical Journal. 1971;47(554):794-799. DOI: 10.1136/pgmj.47.554.794 · DOI
  79. Albin RL, Young AB, Penney JB. The functional anatomy of basal ganglia disorders. Trends in Neurosciences. 1989;12(10):366-375. DOI: 10.1016/0166-2236(89)90074-x · DOI · Paper page
  80. Kreitzer AC, Malenka RC. Striatal plasticity and basal ganglia circuit function. Neuron. 2008;60(4):543-554. DOI: 10.1016/j.neuron.2008.11.005 · DOI
  81. Pedrosa V, Clopath C. The role of neuromodulators in cortical plasticity. A computational perspective. Frontiers in Synaptic Neuroscience. 2017;8:38. DOI: 10.3389/fnsyn.2016.00038 · DOI
  82. Gerfen CR, Engber TM, Mahan LC, Susel Z, Chase TN, Monsma FJ Jr, et al. D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons. Science. 1990;250(4986):1429-1432. DOI: 10.1126/science.2147780 · DOI · Paper page
  83. Surmeier DJ, Graves SM, Shen W. Dopaminergic modulation of striatal networks in health and Parkinson's disease. Current Opinion in Neurobiology. 2014;29:109-117. DOI: 10.1016/j.conb.2014.07.008 · DOI
  84. Mallet N, Ballion B, Le Moine C, Gonon F. Cortical inputs and GABA interneurons imbalance projection neurons in the striatum of parkinsonian rats. The Journal of Neuroscience. 2006;26(14):3875-3884. DOI: 10.1523/ JNEUROSCI.4439-05.2006 · DOI
  85. Ryan MB, Bair-Marshall C, Nelson AB. Aberrant striatal activity in parkinsonism and levodopa- induced dyskinesia. Cell Reports. 2018;23(12):3438-3446.e5. DOI: 10.1016/j.celrep.2018.05.059 · DOI
  86. Escande MV, Taravini IR, Zold CL, Belforte JE, Murer MG. Loss of homeostasis in the direct pathway in a mouse model of asymptomatic Parkinson's disease. The Journal of Neuroscience. 2016;36(21):5686-5698. DOI: 10.1523/JNEUROSCI.0492-15.2016 · DOI
  87. Parker PR, Lalive AL, Kreitzer AC. Pathway-specific remodeling of thalamostriatal synapses in parkinsonian mice. Neuron. 2016;89(4):734-740. DOI: 10.1016/j.neuron.2015.12.038 · DOI
  88. Suarez LM, Solis O, Sanz-Magro A, Alberquilla S, Moratalla R. Dopamine D1 receptors regulate spines in striatal direct-pathway and indirect-pathway neurons. Movement Disorders. 2020;35(10):1810-1821. DOI: 10.1002/ mds.28174 · DOI
  89. Schwarzschild MA, Agnati L, Fuxe K, Chen JF, Morelli M. Targeting adenosine A2A receptors in Parkinson's disease. Trends in Neurosciences. 2006;29(11):647-654. DOI: 10.1016/j. tins.2006.09.004 · DOI
  90. Shen W, Flajolet M, Greengard P, Surmeier DJ. Dichotomous dopaminergic control of striatal synaptic plasticity. Science. 2008;321(5890):848-851. DOI: 10.1126/science.1160575 · DOI · Paper page
  91. Thiele SL, Chen B, Lo C, Gertler TS, Warre R, Surmeier JD, et al. Selective loss of bi-directional synaptic [98] Chu HY. Synaptic and cellular plasticity in Parkinson's disease. Acta Pharmacologica Sinica. 2020;41(4):447- 452. DOI: 10.1038/s41401-020-0371-0 · DOI
  92. Shahmoradian SH, Lewis AJ, Genoud C, Hench J, Moors TE, Navarro PP, et al. Lewy pathology in Parkinson's disease consists of crowded organelles and lipid membranes. Nature Neuroscience. 2019;22(7):1099-1109. DOI: 10.1038/s41593-019-0423-2 · DOI
  93. Lashuel HA. Do Lewy bodies contain alpha-synuclein fibrils? And does it matter? A brief history and critical analysis of recent reports. Neurobiology of Disease. 2020;141:104876. DOI: 10.1016/j.nbd.2020.104876 · DOI
  94. Simón-Sánchez J, Schulte C, Bras JM, Sharma M, Gibbs JR, Berg D, et al. Genome-wide association study reveals genetic risk underlying Parkinson's disease. Nature Genetics. 2009;41(12):1308-1312. DOI: 10.1038/ ng.487 · DOI
  95. Albarran E, Sun Y, Liu Y, Raju K, Dong A, Li Y, et al. Postsynaptic synucleins mediate endocannabinoid signaling. Nature Neuroscience. 2023;26(6):997-1007. DOI: 10.1038/ s41593-023-01345-0 · DOI
  96. Lewis DA, Sweet RA. Schizophrenia from a neural circuitry perspective: Advancing toward rational pharmacological therapies. The Journal of Clinical Investigation. 2009;119(4):706- 716. DOI: 10.1172/JCI37335 · DOI
  97. Garey LJ, Ong WY, Patel TS, Kanani M, Davis A, Mortimer AM, et al. Reduced dendritic spine density on cerebral cortical pyramidal neurons in schizophrenia. Journal of Neurology, Neurosurgery, and Psychiatry. 1998;65(4):446-453. DOI: 10.1136/ jnnp.65.4.446 · DOI
  98. Glantz LA, Lewis DA. Decreased dendritic spine density on prefrontal cortical pyramidal neurons in schizophrenia. Archives of General Psychiatry. 2000;57(1):65-73. DOI: 10.1001/archpsyc.57.1.65 · DOI · Paper page
  99. Kolluri N, Sun Z, Sampson AR, Lewis DA. Lamina-specific reductions in dendritic spine density in the prefrontal cortex of subjects with schizophrenia. The American Journal of Psychiatry. 2005;162(6):1200-1202. DOI: 10.1176/ appi.ajp.162.6.1200 [108] · DOI
  100. Jones EG. Cortical development and thalamic pathology in schizophrenia. Schizophrenia Bulletin. 1997;23(3):483- 501. DOI: 10.1093/schbul/23.3.483 · DOI
  101. Moghaddam B. Targeting metabotropic glutamate receptors for treatment of the cognitive symptoms of schizophrenia. Psychopharmacology. 2004;174(1):39-44. DOI: 10.1007/ s00213-004-1792-z · DOI
  102. Patil ST, Zhang L, Martenyi F, Lowe SL, Jackson KA, Andreev BV, et al. Activation of mGlu2/3 receptors as a new approach to treat schizophrenia: A randomized phase 2 clinical trial. Nature Medicine. 2007;13(9):1102- 1107. DOI: 10.1038/nm1632. Epub 2007 Sep 2. Erratum in: Nat Med. 2007 Oct;13(10):1264 · DOI · Paper page
  103. Crabtree GW, Gogos JA. Synaptic plasticity, neural circuits, and the emerging role of altered short-term information processing in schizophrenia. Frontiers in Synaptic Neuroscience. 2014;6:28. DOI: 10.3389/ fnsyn.2014.00028 · DOI
  104. Javitt DC, Zukin SR. Recent advances in the phencyclidine model of schizophrenia. The American Journal of Psychiatry. 1991;148(10):1301-1308. DOI: 10.1176/ajp.148.10.1301 · DOI · Paper page
  105. Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner JD, et al. Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Archives of General Psychiatry. 1994;51(3):199-214. DOI: 10.1001/ archpsyc.1994.03950030035004 · DOI · Paper page
  106. Coyle JT. Glutamate and schizophrenia: Beyond the dopamine hypothesis. Cellular and Molecular Neurobiology. 2006;26(4-6):365-384. DOI: 10.1007/s10571-006-9062-8 · DOI · Paper page
  107. Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurology. 2011;10(1):63-74. DOI: 10.1016/S1474-4422(10)70253-2 · DOI
  108. Al-Diwani A, Handel A, Townsend L, Pollak T, Leite MI, Harrison PJ, et al. The psychopathology of NMDAR-antibody encephalitis in adults: A systematic review and phenotypic analysis of individual patient data. Lancet Psychiatry. 2019;6(3):235-246. DOI: 10.1016/ S2215-0366(19)30001-X · DOI
  109. Weickert CS, Fung SJ, Catts VS, Schofield PR, Allen KM, Moore LT, et al. Molecular evidence of N-methyl- D-aspartate receptor hypofunction in schizophrenia. Molecular Psychiatry. 2013;18(11):1185-1192. DOI: 10.1038/ mp.2012.137 · DOI
  110. Catts VS, Lai YL, Weickert CS, Weickert TW, Catts SV. A quantitative review of the postmortem evidence for decreased cortical N-methyl-D- aspartate receptor expression levels in schizophrenia: How can we link molecular abnormalities to mismatch negativity deficits? Biological Psychology. 2016;116:57-67. DOI: 10.1016/j.biopsycho.2015.10.013 · DOI
  111. Banerjee A, Wang HY, Borgmann-Winter KE, MacDonald ML, Kaprielian H, Stucky A, et al. Src kinase as a mediator of convergent molecular abnormalities leading to NMDAR hypoactivity in schizophrenia. Molecular Psychiatry. 2015;20(9):1091-1100. DOI: 10.1038/mp.2014.115 · DOI
  112. Gerber DJ, Hall D, Miyakawa T, Demars S, Gogos JA, Karayiorgou M, et al. Evidence for association of schizophrenia with genetic variation in the 8p21.3 gene, PPP3CC, encoding the calcineurin gamma subunit. Proceedings of the National Academy of Sciences of the United States of America. 2003;100(15):8993-8998. DOI: 10.1073/ pnas.1432927100 · DOI
  113. Miyakawa T, Leiter LM, Gerber DJ, Gainetdinov RR, Sotnikova TD, Zeng H, et al. Conditional calcineurin knockout mice exhibit multiple abnormal behaviors related to schizophrenia. Proceedings of the National Academy of Sciences of the United States of America. 2003;100(15):8987-8992. DOI: 10.1073/ pnas.1432926100 · DOI · Paper page
  114. Du J, Gray NA, Falke CA, Chen W, Yuan P, Szabo ST, et al. Modulation of synaptic plasticity by antimanic agents: The role of AMPA glutamate receptor subunit 1 synaptic expression. The Journal of Neuroscience. 2004;24(29):6578-6589. DOI: 10.1523/ JNEUROSCI.1258-04.2004 · DOI · Paper page
  115. Du J, Suzuki K, Wei Y, Wang Y, Blumenthal R, Chen Z, et al. The anticonvulsants lamotrigine, riluzole, and valproate differentially regulate AMPA receptor membrane localization: Relationship to clinical effects in mood disorders. Neuropsychopharmacology. 2007;32(4):793-802. DOI: 10.1038/ sj.npp.1301178 · DOI
  116. Compte A, Brunel N, Goldman-Rakic PS, Wang XJ. Synaptic mechanisms and network dynamics underlying spatial working memory in a cortical network model. Cerebral Cortex. 2000;10(9):910-923. DOI: 10.1093/ cercor/10.9.910 · DOI · Paper page
  117. Mongillo G, Barak O, Tsodyks M. Synaptic theory of working memory. Science. 2008;319(5869):1543-1546. DOI: 10.1126/science.1150769 · DOI · Paper page
  118. Frankle WG, Lerma J, Laruelle M. The synaptic hypothesis of schizophrenia. Neuron. 2003;39(2):205-216. DOI: 10.1016/ s0896-6273(03)00423-9 · DOI
  119. Paterlini M, Zakharenko SS, Lai WS, Qin J, Zhang H, Mukai J, et al. Transcriptional and behavioral interaction between 22q11.2 orthologs modulates schizophrenia- related phenotypes in mice. Nature Neuroscience. 2005;8(11):1586-1594. DOI: 10.1038/nn1562 · DOI
  120. Millar JK, Wilson-Annan JC, Anderson S, Christie S, Taylor MS, Semple CA, et al. Disruption of two novel genes by a translocation co-segregating with schizophrenia. Human Molecular Genetics. 2000;9(9):1415-1423. DOI: 10.1093/hmg/9.9.1415 · DOI · Paper page
  121. Blackwood DH, Fordyce A, Walker MT, St. Clair DM, Porteous DJ, Muir WJ. Schizophrenia and affective disorders-cosegregation with a translocation at chromosome 1q42 that directly disrupts brain-expressed genes: Clinical and P300 findings in a family. American Journal of Human Genetics. 2001;69(2):428-433. DOI: 10.1086/321969 · DOI
  122. Bradshaw NJ, Trossbach SV, Köber S, Walter S, Prikulis I, Weggen S, et al. Disrupted in schizophrenia 1 regulates the processing of reelin in the perinatal cortex. Schizophrenia Research. 2020;215:506-513. DOI: 10.1016/j. schres.2017.04.012 · DOI
  123. Lakatosova S, Ostatnikova D. Reelin and its complex involvement in brain development and function. The International Journal of Biochemistry & Cell Biology. 2012;44(9):1501-1504. DOI: 10.1016/j.biocel.2012.06.002 · DOI
  124. Pantazopoulos H, Berretta S. In sickness and in health: Perineuronal nets and synaptic plasticity in psychiatric disorders. Neural Plasticity. 2016;2016:9847696. DOI: 10.1155/2016/9847696 · DOI
  125. Dityatev A, Seidenbecher CI, Schachner M. Compartmentalization from the outside: The extracellular matrix and functional microdomains in the brain. Trends in Neurosciences. 2010;33(11):503-512. DOI: 10.1016/j. tins.2010.08.003 · DOI
  126. Schell MJ, Molliver ME, Snyder SH. D-serine, an endogenous synaptic modulator: Localization to astrocytes and glutamate-stimulated release. Proceedings of the National Academy of Sciences of the United States of America. 1995;92(9):3948-3952. DOI: 10.1073/ pnas.92.9.3948 · DOI · Paper page
  127. Lepeta K, Lourenco MV, Schweitzer BC, Martino Adami PV, Banerjee P, Catuara-Solarz S, et al. Synaptopathies: Synaptic dysfunction in neurological disorders -A review from students to students. Journal of Neurochemistry. 2016;138(6):785-805. DOI: 10.1111/jnc.13713 · DOI · Paper page
  128. Qiu S, Zhao LF, Korwek KM, Weeber EJ. Differential reelin- induced enhancement of NMDA and AMPA receptor activity in the adult hippocampus. The Journal of Neuroscience. 2006;26(50):12943-12955. DOI: 10.1523/JNEUROSCI.2561-06.2006 · DOI · Paper page
  129. Dityatev A, Schachner M, Sonderegger P. The dual role of the extracellular matrix in synaptic plasticity and homeostasis. Nature Reviews. Neuroscience. 2010;11(11):735-746. DOI: 10.1038/nrn2898 · DOI · Paper page
  130. Pozo K, Goda Y. Unraveling mechanisms of homeostatic synaptic plasticity. Neuron. 2010;66(3):337-351. DOI: 10.1016/j.neuron.2010.04.028 · DOI · Paper page
  131. Frischknecht R, Heine M, Perrais D, Seidenbecher CI, Choquet D, Gundelfinger ED. Brain extracellular matrix affects AMPA receptor lateral mobility and short-term synaptic plasticity. Nature Neuroscience. 2009;12(7):897-904. DOI: 10.1038/ nn.2338 · DOI · Paper page
  132. Earls LR, Zakharenko SS. A synaptic function approach to investigating complex psychiatric diseases. The Neuroscientist. 2014;20(3):257-271. DOI: 10.1177/1073858413498307 · DOI
  133. Bitanihirwe BK, Mauney SA, Woo TU. Weaving a net of neurobiological mechanisms in schizophrenia and Unraveling the underlying pathophysiology. Biological Psychiatry. 2016;80(8):589-598. DOI: 10.1016/j.biopsych.2016.03.1047 · DOI
  134. Levy AD, Omar MH, Koleske AJ. Extracellular matrix control of dendritic spine and synapse structure and plasticity in adulthood. Frontiers in Neuroanatomy. 2014;8:116. DOI: 10.3389/ fnana.2014.00116 · DOI
  135. Mundy P. Annotation: The neural basis of social impairments in autism: The role of the dorsal medial-frontal cortex and anterior cingulate system. Journal of Child Psychology and Psychiatry. 2003;44(6):793-809. DOI: 10.1111/1469-7610.00165 · DOI
  136. Belmonte MK, Allen G, Beckel-Mitchener A, Boulanger LM, Carper RA, Webb SJ. Autism and abnormal development of brain connectivity. The Journal of Neuroscience. 2004;24(42):9228-9231. DOI: 10.1523/JNEUROSCI.3340-04.2004 · DOI · Paper page
  137. Rinaldi T, Kulangara K, Antoniello K, Markram H. Elevated NMDA receptor levels and enhanced postsynaptic long-term potentiation induced by prenatal exposure to valproic acid. Proceedings of the National Academy of Sciences of the United States of America. 2007;104(33):13501-13506. DOI: 10.1073/pnas.0704391104 · DOI · Paper page
  138. Rinaldi T, Perrodin C, Markram H. Hyper-connectivity and hyper-plasticity in the medial prefrontal cortex in the valproic acid animal model of autism. Frontiers in Neural Circuits. 2008;2:4. DOI: 10.3389/neuro.04.004.2008 · DOI · Paper page
  139. Markram K, Markram H. The intense world theory -A unifying theory of the neurobiology of autism. Frontiers in Human Neuroscience. 2010;4:224. DOI: 10.3389/fnhum.2010.00224 · DOI
  140. Ecker C, Murphy D. Neuroimaging in autism-from basic science to translational research. Nature Reviews. Neurology. 2014;10(2):82-91. DOI: 10.1038/nrneurol.2013.276 · DOI
  141. Mansour Y, Ahmed SN, Kulesza R. Abnormal morphology and subcortical projections to the medial geniculate in an animal model of autism. Experimental Brain Research. 2021;239(2):381-400. DOI: 10.1007/s00221-020-05982-w · DOI
  142. Park BY, Hong SJ, Valk SL, Paquola C, Benkarim O, Bethlehem RAI, et al. Differences in subcortico-cortical interactions identified from connectome and microcircuit models in autism. Nature Communications. 2021;12(1):2225. DOI: 10.1038/ s41467-021-21732-0 · DOI
  143. Arguello PA, Gogos JA. Genetic and cognitive windows into circuit mechanisms of psychiatric disease. Trends in Neurosciences. 2012;35(1):3- 13. DOI: 10.1016/j.tins.2011.11.007 · DOI
  144. Fu YH, Kuhl DP, Pizzuti A, Pieretti M, Sutcliffe JS, Richards S, et al. Variation of the CGG repeat at the fragile X site results in genetic instability: Resolution of the Sherman paradox. Cell. 1991;67(6):1047-1058. DOI: 10.1016/0092-8674(91)90283-5 · DOI · Paper page
  145. Verkerk AJ, Pieretti M, Sutcliffe JS, Fu YH, Kuhl DP, Pizzuti A, et al. Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome. Cell. 1991;65(5):905-914. DOI: 10.1016/0092-8674(91)90397-h · DOI · Paper page
  146. Amir RE, Van den Veyver IB, Wan M, Tran CQ, Francke U, Zoghbi HY. Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2. Nature Genetics. 1999;23(2):185-188. DOI: 10.1038/13810 · DOI · Paper page
  147. Bonaglia MC, Giorda R, Borgatti R, Felisari G, Gagliardi C, Selicorni A, et al. Disruption of the ProSAP2 gene in a t(12;22)(q24.1;q13.3) is associated with the 22q13.3 deletion syndrome. American Journal of Human Genetics. 2001;69(2):261-268. DOI: 10.1086/321293. Epub 2001 Jun 18 · DOI · Paper page
  148. O'Donnell WT, Warren ST. A decade of molecular studies of fragile X syndrome. Annual Review of Neuroscience. 2002;25:315-338. DOI: 10.1146/annurev.neuro.25.112701.142909 · DOI
  149. Qin M, Kang J, Burlin TV, Jiang C, Smith CB. Postadolescent changes in regional cerebral protein synthesis: An in vivo study in the FMR1 null mouse. The Journal of Neuroscience. 2005;25(20):5087-5095. DOI: 10.1523/ JNEUROSCI.0093-05.2005 · DOI · Paper page
  150. Huber KM, Gallagher SM, Warren ST, Bear MF. Altered synaptic plasticity in a mouse model of fragile X mental retardation. Proceedings of the National Academy of Sciences of the United States of America. 2002;99(11):7746-7750. DOI: 10.1073/ pnas.122205699 · DOI · Paper page
  151. Greenough WT, Klintsova AY, Irwin SA, Galvez R, Bates KE, Weiler IJ. Synaptic regulation of protein synthesis and the fragile X protein. Proceedings of the National Academy of Sciences of the United States of America. 2001;98(13):7101-7106. DOI: 10.1073/ pnas.141145998 · DOI · Paper page
  152. Bear MF, Huber KM, Warren ST. The mGluR theory of fragile X mental retardation. Trends in Neurosciences. 2004;27(7):370-377. DOI: 10.1016/j. tins.2004.04.009 · DOI · Paper page
  153. Fyke W, Velinov M. FMR1 and autism, an intriguing connection revisited. Genes (Basel). 2021;12(8):1218. DOI: 10.3390/genes12081218 · DOI
  154. Lewis JD, Meehan RR, Henzel WJ, Maurer-Fogy I, Jeppesen P, Klein F, et al. Purification, sequence, and cellular localization of a novel chromosomal protein that binds to methylated DNA. Cell. 1992;69(6):905-914. DOI: 10.1016/0092-8674(92)90610-o · DOI · Paper page
  155. Jones PL, Veenstra GJ, Wade PA, Vermaak D, Kass SU, Landsberger N, et al. Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription. Nature Genetics. 1998;19(2):187-191. DOI: 10.1038/561 · DOI
  156. Nan X, Ng HH, Johnson CA, Laherty CD, Turner BM, Eisenman RN, et al. Transcriptional repression by the methyl-CpG-binding protein MeCP2 involves a histone deacetylase complex. Nature. 1998;393(6683):386-389. DOI: 10.1038/30764 · DOI · Paper page
  157. Chen WG, Chang Q, Lin Y, Meissner A, West AE, Griffith EC, et al. Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2. Science. 2003;302(5646):885-889. DOI: 10.1126/ science.1086446 · DOI · Paper page
  158. Martinowich K, Hattori D, Wu H, Fouse S, He F, Hu Y, et al. DNA methylation-related chromatin remodeling in activity-dependent BDNF gene regulation. Science. 2003;302(5646):890-893. DOI: 10.1126/ science.1090842 · DOI · Paper page
  159. Yasui DH, Peddada S, Bieda MC, Vallero RO, Hogart A, Nagarajan RP, et al. Integrated epigenomic analyses of neuronal MeCP2 reveal a role for long-range interaction with active genes. Proceedings of the National Academy of Sciences of the United States of America. 2007;104(49):19416-19421. DOI: 10.1073/ pnas.0707442104 · DOI
  160. Chahrour M, Jung SY, Shaw C, Zhou X, Wong ST, Qin J, et al. MeCP2, a key contributor to neurological disease, activates and represses transcription. Science. 2008;320(5880):1224-1229. DOI: 10.1126/science.1153252 · DOI · Paper page
  161. Shahbazian MD, Antalffy B, Armstrong DL, Zoghbi HY. Insight into Rett syndrome: MeCP2 levels display tissue-and cell-specific differences and correlate with neuronal maturation. Human Molecular Genetics. 2002;11(2):115-124. DOI: 10.1093/ hmg/11.2.115 · DOI
  162. Maezawa I, Swanberg S, Harvey D, LaSalle JM, Jin LW. Rett syndrome astrocytes are abnormal and spread MeCP2 deficiency through gap junctions. The Journal of Neuroscience. 2009;29(16):5051-5061. DOI: 10.1523/ JNEUROSCI.0324-09.2009 · DOI
  163. Maezawa I, Jin LW. Rett syndrome microglia damage dendrites and synapses by the elevated release of glutamate. The Journal of Neuroscience. 2010;30(15):5346-5356. DOI: 10.1523/ JNEUROSCI.5966-09.2010 · DOI
  164. Kifayathullah LA, Arunachalam JP, Bodda C, Agbemenyah HY, Laccone FA, Mannan AU. MeCP2 mutant protein is expressed in astrocytes as well as in neurons and localizes in the nucleus. Cytogenetic and Genome Research. 2010;129(4):290-297. DOI: 10.1159/000315906 · DOI
  165. Asaka Y, Jugloff DG, Zhang L, Eubanks JH, Fitzsimonds RM. Hippocampal synaptic plasticity is impaired in the Mecp2-null mouse model of Rett syndrome. Neurobiology of Disease. 2006;21(1):217-227. DOI: 10.1016/j.nbd.2005.07.005 · DOI
  166. Moretti P, Levenson JM, Battaglia F, Atkinson R, Teague R, Antalffy B, et al. Learning and memory and synaptic plasticity are impaired in a mouse model of Rett syndrome. The Journal of Neuroscience. 2006;26(1):319-327. DOI: 10.1523/JNEUROSCI.2623-05.2006 · DOI · Paper page
  167. Collins AL, Levenson JM, Vilaythong AP, Richman R, Armstrong DL, Noebels JL, et al. Mild overexpression of MeCP2 causes a progressive neurological disorder in mice. Human Molecular Genetics. 2004;13(21):2679-2689. DOI: 10.1093/ hmg/ddh282 · DOI · Paper page
  168. Ballas N, Lioy DT, Grunseich C, Mandel G. Non-cell autonomous influence of MeCP2- deficient glia on neuronal dendritic morphology. Nature Neuroscience. 2009;12(3):311-317. DOI: 10.1038/nn.2275 · DOI · Paper page
  169. Anderlid BM, Schoumans J, Annerén G, Tapia-Paez I, Dumanski J, Blennow E, et al. FISH-mapping of a 100-kb terminal 22q13 deletion. Human Genetics. 2002;110(5):439-443. DOI: 10.1007/s00439-002-0713-7 · DOI
  170. Dhar SU, del Gaudio D, German JR, Peters SU, Ou Z, Bader PI, et al. 22q13.3 deletion syndrome: Clinical and molecular analysis using array CGH. American Journal of Medical Genetics. Part A. 2010;152A(3):573-581. DOI: 10.1002/ajmg.a.33253 · DOI · Paper page
  171. Durand CM, Betancur C, Boeckers TM, Bockmann J, Chaste P, Fauchereau F, et al. Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders. Nature Genetics. 2007;39(1):25-27. DOI: 10.1038/ng1933 · DOI · Paper page
  172. Okamoto N, Kubota T, Nakamura Y, Murakami R, Nishikubo T, Tanaka I, et al. 22q13 microduplication in two patients with common clinical manifestations: A recognizable syndrome? American Journal of Medical Genetics. Part A. 2007;143A(23):2804- 2809. DOI: 10.1002/ajmg.a.31771 · DOI · Paper page
  173. Roussignol G, Ango F, Romorini S, Tu JC, Sala C, Worley PF, et al. Shank expression is sufficient to induce functional dendritic spine synapses in aspiny neurons. The Journal of Neuroscience. 2005;25(14): 3560-3570. DOI: 10.1523/ JNEUROSCI.4354-04.2005 · DOI · Paper page
  174. Bozdagi O, Sakurai T, Papapetrou D, Wang X, Dickstein DL, Takahashi N, et al. Haploinsufficiency of the autism- associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication. Molecular Autism. 2010;1(1):15. DOI: 10.1186/2040-2392-1-15 · DOI · Paper page
  175. Arons MH, Thynne CJ, Grabrucker AM, Li D, Schoen M, Cheyne JE, et al. Autism-associated mutations in ProSAP2/Shank3 impair synaptic transmission and neurexin- neuroligin-mediated transsynaptic signaling. The Journal of Neuroscience. 2012;32(43):14966-14978. DOI: 10.1523/ JNEUROSCI.2215-12.2012 · DOI
  176. 193Autism Genome Project Consortium, Szatmari P, Paterson AD, Zwaigenbaum L, Roberts W, Brian J, et al. Mapping autism risk loci using genetic linkage and chromosomal rearrangements. Nature Genetics. 2007;39(3):319-328. DOI: 10.1038/ng1985 · DOI · Paper page
  177. Kim HG, Kishikawa S, Higgins AW, Seong IS, Donovan DJ, Shen Y, et al. Disruption of neurexin 1 associated with autism spectrum disorder. American Journal of Human Genetics. 2008;82(1):199-207. DOI: 10.1016/j. ajhg.2007.09.011 · DOI · Paper page
  178. Gauthier J, Siddiqui TJ, Huashan P, Yokomaku D, Hamdan FF, Champagne N, et al. Truncating mutations in NRXN2 and NRXN1 in autism spectrum disorders and schizophrenia. Human Genetics. 2011;130(4):563-573. DOI: 10.1007/s00439-011-0975-z · DOI · Paper page
  179. Konopka G, Wexler E, Rosen E, Mukamel Z, Osborn GE, Chen L, et al. Modeling the functional genomics of autism using human neurons. Molecular Psychiatry. 2012;17(2):202-214. DOI: 10.1038/mp.2011.60 · DOI
  180. Jamain S, Quach H, Betancur C, Råstam M, Colineaux C, Gillberg IC, et al. Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism. Nature Genetics. 2003;34(1):27-29. DOI: 10.1038/ng1136 · DOI · Paper page
  181. Südhof TC. Neuroligins and neurexins link synaptic function to cognitive disease. Nature. 2008;455(7215):903-911. DOI: 10.1038/ nature07456 · DOI · Paper page
  182. Tabuchi K, Blundell J, Etherton MR, Hammer RE, Liu X, Powell CM, et al. A neuroligin-3 mutation implicated in autism increases inhibitory synaptic transmission in mice. Science. 2007;318(5847):71-76. DOI: 10.1126/ science.1146221 · DOI · Paper page
  183. Radyushkin K, Hammerschmidt K, Boretius S, Varoqueaux F, El-Kordi A, Ronnenberg A, et al. Neuroligin-3- deficient mice: Model of a monogenic heritable form of autism with an olfactory deficit. Genes, Brain, and Behavior. 2009;8(4):416-425. DOI: 10.1111/j.1601-183X.2009.00487.x · DOI
  184. Jamain S, Radyushkin K, Hammerschmidt K, Granon S, Boretius S, Varoqueaux F, et al. Reduced social interaction and ultrasonic communication in a mouse model of monogenic heritable autism. Proceedings of the National Academy of Sciences of the United States of America. 2008;105(5):1710-1715. DOI: 10.1073/ pnas.0711555105 · DOI · Paper page
  185. Cavazos JE, Cross DJ. The role of synaptic reorganization in mesial temporal lobe epilepsy. Epilepsy & Behavior. 2006;8(3):483-493. DOI: 10.1016/j.yebeh.2006.01.011 · DOI
  186. Engel J Jr. Update on surgical treatment of the epilepsies. Clinical and Experimental Neurology. 1992;29:32-48
  187. Babb TL, Lieb JP, Brown WJ, Pretorius J, Crandall PH. Distribution of pyramidal cell density and hyperexcitability in the epileptic human hippocampal formation. Epilepsia. 1984;25(6):721-728. DOI: 10.1111/j.1528- 1157.1984.tb03483.x · DOI
  188. Wuarin JP, Dudek FE. Excitatory synaptic input to granule cells increases with time after kainate treatment. Journal of Neurophysiology. 2001;85(3):1067-1077. DOI: 10.1152/ jn.2001.85.3.1067 · DOI
  189. Okazaki MM, Molnár P, Nadler JV. Recurrent mossy fiber pathway in rat dentate gyrus: Synaptic currents evoked in presence and absence of seizure-induced growth. Journal of Neurophysiology. 1999;81(4):1645-1660. DOI: 10.1152/jn.1999.81.4.1645 · DOI
  190. Scharfman HE, Sollas AL, Berger RE, Goodman JH. Electrophysiological evidence of monosynaptic excitatory transmission between granule cells after seizure-induced mossy fiber sprouting. Journal of Neurophysiology. 2003;90(4):2536-2547. DOI: 10.1152/ jn.00251.2003 · DOI
  191. Santhakumar V, Aradi I, Soltesz I. Role of mossy fiber sprouting and mossy cell loss in hyperexcitability: A network model of the dentate gyrus incorporating cell types and axonal topography. Journal of Neurophysiology. 2005;93(1):437-453. DOI: 10.1152/jn.00777.2004 · DOI · Paper page
  192. Kullmann DM, Asztely F, Walker MC. The role of mammalian ionotropic receptors in synaptic plasticity: LTP, LTD and epilepsy. Cellular and Molecular Life Sciences. 2000;57(11):1551-1561. DOI: 10.1007/ pl00000640 · DOI
  193. Mody I, Heinemann U. NMDA receptors of dentate gyrus granule cells participate in synaptic transmission following kindling. Nature. 1987;326(6114):701-704. DOI: 10.1038/326701a0 · DOI
  194. Pratt GD, Kokaia M, Bengzon J, Kokaia Z, Fritschy JM, Möhler H, et al. Differential regulation of N-methyl- D-aspartate receptor subunit messenger RNAs in kindling-induced epileptogenesis. Neuroscience. 1993;57(2):307-318. DOI: 10.1016/0306-4522(93)90064-m · DOI
  195. Pollard H, Héron A, Moreau J, Ben-Ari Y, Khrestchatisky M. Alterations of the GluR-B AMPA receptor subunit flip/flop expression in kainate- induced epilepsy and ischemia. Neuroscience. 1993;57(3):545-554. DOI: 10.1016/0306-4522(93)90004-y · DOI
  196. Friedman LK, Pellegrini-Giampietro DE, Sperber EF, Bennett MV, Moshé SL, Zukin RS. Kainate-induced status epilepticus alters glutamate and GABAA receptor gene expression in adult rat hippocampus: An in situ hybridization study. The Journal of Neuroscience. 1994;14(5 Pt. 1):2697-2707. DOI: 10.1523/ JNEUROSCI.14-05-02697.1994 · DOI
  197. Kamphuis W, De Rijk TC, Talamini LM, Lopes da Silva FH. Rat hippocampal kindling induces changes in the glutamate receptor mRNA expression patterns in dentate granule neurons. The European Journal of Neuroscience. 1994;6(7):1119-1127. DOI: 10.1111/ j.1460-9568.1994.tb00609.x · DOI
  198. Kamphuis W, Hendriksen H, Diegenbach PC, Lopes da Silva FH. N-methyl-D-aspartate and kainate receptor gene expression in hippocampal pyramidal and granular neurons in the kindling model of epileptogenesis. Neuroscience. 1995;67(3):551-559. DOI: 10.1016/0306-4522(95)00070-y · DOI
  199. de Lanerolle NC, Eid T, von Campe G, Kovacs I, Spencer DD, Brines M. Glutamate receptor subunits GluR1 and GluR2/3 distribution shows reorganization in the human epileptogenic hippocampus. The European Journal of Neuroscience. 1998;10(5):1687-1703. DOI: 10.1046/j.1460-9568.1998.00171.x · DOI
  200. Köhr G, De Koninck Y, Mody I. Properties of NMDA receptor channels in neurons acutely isolated from epileptic (kindled) rats. The Journal of Neuroscience. 1993;13(8):3612-3627. DOI: 10.1523/ JNEUROSCI.13-08-03612.1993 · DOI

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Sorted by citations

Authors
Jin, C., & Karlstedt, K.
Corresponding author
Jin, CongYu
Venue
Synaptic Plasticity - Neurobiology, Neuroanatomy, and Clinical Neuroscience
Publisher
IntechOpen
Published
2025-04-28
OpenAlex
W4410567151
Cited by
1
References
23
Citations by year
2025: 1
FWCI
3.34
Type
book chapter
Language
en
Open access
Locations
IntechOpen eBooks (publishedVersion, cc-by)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
synaptic plasticity, neurological disorders, Alzheimer's disease, Parkinson's disease, epilepsy, schizophrenia, autism spectrum disorder, synaptic dysfunction

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