REFERENCES

1. Ginhoux F, Greter M, Leboeuf M, Nandi S, See P, et al. Fate mapping analysis reveals that adult microglia derive from primitive macrophages. Science 2010;330:841-5.

2. Schulz C, Gomez Perdiguero E, Chorro L, Szabo-Rogers H, Cagnard N, et al. A lineage of myeloid cells independent of Myb and hematopoietic stem cells. Science 2012;336:86-90.

3. Wolf SA, Boddeke HW, Kettenmann H. Microglia in Physiology and Disease. Annu Rev Physiol 2017;79:619-43.

4. Bennett ML, Bennett FC. The influence of environment and origin on brain resident macrophages and implications for therapy. Nat Neurosci 2020;23:157-66.

5. Prinz M, Priller J. The role of peripheral immune cells in the CNS in steady state and disease. Nat Neurosci 2017;20:136-44.

6. Yamasaki R, Lu H, Butovsky O, Ohno N, Rietsch AM, et al. Differential roles of microglia and monocytes in the inflamed central nervous system. J Exp Med 2014;211:1533-49.

7. Nimmerjahn A, Kirchhoff F, Helmchen F. Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Science 2005;308:1314-8.

8. Sierra A, Tremblay MÈ, Wake H. Never-resting microglia: physiological roles in the healthy brain and pathological implications. Front Cell Neurosci 2014;8:240.

9. Wake H, Moorhouse AJ, Jinno S, Kohsaka S, Nabekura J. Resting microglia directly monitor the functional state of synapses in vivo and determine the fate of ischemic terminals. J Neurosci 2009;29:3974-80.

10. Davalos D, Grutzendler J, Yang G, Kim JV, Zuo Y, et al. ATP mediates rapid microglial response to local brain injury in vivo. Nat Neurosci 2005;8:752-8.

11. von Bernhardi R, Heredia F, Salgado N, Muñoz P. Microglia function in the normal brain. Adv Exp Med Biol 2016;949:67-92.

12. Kettenmann H, Hanisch UK, Noda M, Verkhratsky A. Physiology of microglia. Physiol Rev 2011;91:461-553.

13. Byrnes KR, Loane DJ, Stoica BA, Zhang J, Faden AI. Delayed mGluR5 activation limits neuroinflammation and neurodegeneration after traumatic brain injury. J Neuroinflammation 2012;9:43.

14. Tay TL, Mai D, Dautzenberg J, Fernández-Klett F, Lin G, et al. A new fate mapping system reveals context-dependent random or clonal expansion of microglia. Nat Neurosci 2017;20:793-803.

15. Crotti A, Ransohoff RM. Microglial physiology and pathophysiology: insights from genome-wide transcriptional profiling. Immunity 2016;44:505-15.

16. Chen SH, Oyarzabal EA, Hong JS. Critical role of the Mac1/NOX2 pathway in mediating reactive microgliosis-generated chronic neuroinflammation and progressive neurodegeneration. Curr Opin Pharmacol 2016;26:54-60.

17. Ransohoff RM, Khoury JE. Microglia in health and disease. Cold Spring Harb 2016;8:a020560.

18. Chen Z, Trapp BD. Microglia and neuroprotection. J Neurochem 2016;136 Suppl 1:10-7.

19. Raffo-Romero A, Arab T, Al-Amri IS, Le Marrec-Croq F, Van Camp C, et al. Medicinal leech CNS as a model for exosome studies in the crosstalk between microglia and neurons. Int J Mol Sci 2018;19:4124.

20. Pósfai B, Cserép C, Orsolits B, Dénes Á. New insights into microglia–neuron interactions: a neuron’s perspective. Neuroscience 2019;405:103-17.

21. Kumar A, Barrett JP, Alvarez-Croda DM, Stoica BA, Faden AI, et al. NOX2 drives M1-like microglial/macrophage activation and neurodegeneration following experimental traumatic brain injury. Brain Behav Immun 2016;58:291-309.

22. Hool LC. The L-type Ca(2+) channel as a potential mediator of pathology during alterations in cellular redox state. Heart Lung Circ 2009;18:3-10.

23. Hool LC, Arthur PG. Decreasing cellular hydrogen peroxide with catalase mimics the effects of hypoxia on the sensitivity of the L-type Ca2+ channel to β-adrenergic receptor stimulation in cardiac myocytes. Circ Res 2002;91:601-9.

24. Hudasek K, Brown ST, Fearon IM. H2O2 regulates recombinant Ca2+ channel α1C subunits but does not mediate their sensitivity to acute hypoxia. Biochem Biophys Res Commun 2004;318:135-41.

25. Mossakowski AA, Pohlan J, Bremer D, Lindquist R, Millward JM, et al. Tracking CNS and systemic sources of oxidative stress during the course of chronic neuroinflammation. Acta Neuropathol 2015;130:799-814.

26. Benned-Jensen T, Christensen RK, Denti F, Perrier JF, Rasmussen HB, et al. Live imaging of Kv7.2/7.3 cell surface dynamics at the axon initial segment: high steady-state stability and calpain-dependent excitotoxic downregulation revealed. J Neurosci 2016;36:2261-6.

27. Clark KC, Josephson A, Benusa SD, Hartley RK, Baer M, et al. Compromised axon initial segment integrity in EAE is preceded by microglial reactivity and contact. Glia 2016;64:1190-1209.

28. Benusa SD, George NM, Sword BA, DeVries GH, Dupree JL. Acute neuroinflammation induces AIS structural plasticity in a NOX2-dependent manner. J Neuroinflammation 2017;14:116.

29. Clark K, Sword BA, Dupree JL. Oxidative stress induces disruption of the axon initial segment. ASN Neuro 2017;9:1759091417745426.

30. Del Puerto A, Fronzaroli-Molinieres L, Perez-Alvarez MJ, Giraud P, Carlier E, et al. ATP-P2X7 receptor modulates axon initial segment composition and function in physiological conditions and brain injury. Cereb Cortex 2015;25:2282-94.

31. Evans MD, Sammons RP, Lebron S, Dumitrescu AS, Watkins TB, et al. Calcineurin signaling mediates activity-dependent relocation of the axon initial segment. J Neurosci 2013;33:6950-63.

32. Schafer DP, Jha S, Liu F, Akella T, McCullough LD, et al. Disruption of the axon initial segment cytoskeleton is a new mechanism for neuronal injury. J Neurosci 2009;29:13242-54.

33. Bilimoria PM, Stevens B. Microglia function during brain development: new insights from animal models. Brain Res 2015;1617:7-17.

34. Bordt EA, Ceasrine AM, Bilbo SD. Microglia and sexual differentiation of the developing brain: a focus on ontogeny and intrinsic factors. Glia 2019. Epub ahead of print. doi: 10.1002/glia.23753

35. Kato G, Inada H, Wake H, Akiyoshi R, Miyamoto A, et al. Microglial contact prevents excess depolarization and rescues neurons from excitotoxicity. eNeuro 2016;3.

36. Li Y, Du XF, Liu CS, Wen ZL, Du JL. Reciprocal regulation between resting microglial dynamics and neuronal activity in vivo. Dev Cell 2012;23:1189-202.

37. Cserép C, Pósfai B, Lénárt N, Fekete R, László ZI, et al. Microglia monitor and protect neuronal function through specialized somatic purinergic junctions. Science 2020;367:528-37.

38. Miyamoto A, Wake H, Ishikawa AW, Eto K, Shibata K, et al. Microglia contact induces synapse formation in developing somatosensory cortex. Nat Commun 2016;7:12540.

39. Eyo UB, Murugan M, Wu LJ. Microglia-neuron communication in epilepsy. Glia 2017;65:5-18.

40. Eyo UB, Wu LJ. Bidirectional microglia-neuron communication in the healthy brain. Neural Plast 2013;2013:456857.

41. Kettenmann H, Kirchhoff F, Verkhratsky A. Microglia: new roles for the synaptic stripper. Neuron 2013;77:10-8.

42. Schafer DP, Lehrman EK, Kautzman AG, Koyama R, Mardinly AR, et al. Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner. Neuron 2012;74:691-705.

43. Tremblay MÈ, Lowery RL, Majewska AK. Microglial interactions with synapses are modulated by visual experience. PLoS Biol 2010;8:e1000527.

44. Weinhard L, di Bartolomei G, Bolasco G, Machado P, Schieber NL, et al. Microglia remodel synapses by presynaptic trogocytosis and spine head filopodia induction. Nat Commun 2018;9:1228.

45. Baalman K, Marin MA, Ho TS, Godoy M, Cherian L, et al. Axon initial segment-associated microglia. J Neurosci 2015;35:2283-92.

46. Catale C, Gironda S, Iacono LL, Carola V. Microglial function in the effects of early-life stress on brain and behavioral development. J Clin Med 2020;9:E468.

47. Koellhoffer EC, McCullough LD, Ritzel RM. Old maids: aging and its impact on microglia function. Int J Mol Sci 2017;18:769.

48. Akhmetzyanova E, Kletenkov K, Mukhamedshina Y, Rizvanov A. Different approaches to modulation of microglia phenotypes after spinal cord injury. Front Syst Neurosci 2019;13:37.

49. Gaudet AD, Fonken LK. Glial cells shape pathology and repair after spinal cord injury. Neurotherapeutics 2018;15:554-77.

50. Gorse KM, Lafrenaye AD. The importance of inter-species variation in traumatic brain injury-induced alterations of microglial-axonal interactions. Front Neurol 2018;9:778.

51. Lafrenaye AD. Physical interactions between activated microglia and injured axons: do all contacts lead to phagocytosis? Neural Regen Res 2016;11:538-40.

52. Lafrenaye AD, Todani M, Walker SA, Povlishock JT. Microglia processes associate with diffusely injured axons following mild traumatic brain injury in the micro pig. J Neuroinflammation 2015;12:186.

53. Bitsch A, Schuchardt J, Bunkowski S, Kuhlmann T, Brück W. Acute axonal injury in multiple sclerosis. Correlation with demyelination and inflammation. Brain 2000;123:1174-83.

54. Hemmer B, Kerschensteiner M, Korn T. Role of the innate and adaptive immune responses in the course of multiple sclerosis. Lancet Neurol 2015;14:406-19.

55. Sørensen TL, Ransohoff RM. Etiology and pathogenesis of multiple sclerosis. Semin Neurol 1998;18:287-94.

56. Trebst C, Sørensen TL, Kivisäkk P, Cathcart MK, Hesselgesser J, et al. CCR1+/CCR5+ mononuclear phagocytes accumulate in the central nervous system of patients with multiple sclerosis. Am J Pathol 2001;159:1701-10.

57. Thompson KK, Tsirka SE. The diverse roles of microglia in the neurodegenerative aspects of central nervous system (CNS) autoimmunity. Int J Mol Sci 2017;18:504.

58. Bitsch A, Wegener C, da Costa C, Bunkowski S, Reimers CD, et al. Lesion development in Marburg’s type of acute multiple sclerosis: from inflammation to demyelination. Mult Scler 1999;5:138-46.

59. Ferguson B, Matyszak MK, Esiri MM, Perry VH. Axonal damage in acute multiple sclerosis lesions. Brain 1997;120:393-9.

60. Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mörk S, et al. Axonal transection in the lesions of multiple sclerosis. N Engl J Med 1998;338:278-85.

61. Reich DS, Lucchinetti CF, Calabresi PA. Multiple sclerosis. N Engl J Med 2018;378:169-80.

62. Bjartmar C, Kinkel RP, Kidd G, Rudick RA, Trapp BD. Axonal loss in normal-appearing white matter in a patient with acute MS. Neurology 2001;57:1248-52.

63. Kornek B, Lassmann H. Axonal pathology in multiple sclerosis. A historical note. Brain Pathol 1999;9:651-6.

64. Lassmann H, van Horssen J. The molecular basis of neurodegeneration in multiple sclerosis. FEBS Lett 2011;585:3715-23.

65. Black JA, Newcombe J, Trapp BD, Waxman SG. Sodium channel expression within chronic multiple sclerosis plaques. J Neuropathol Exp Neurol 2007;66:828-37.

66. Dutta R, Trapp BD. Mechanisms of neuronal dysfunction and degeneration in multiple sclerosis. Prog Neurobiol 2011;93:1-12.

67. Howell OW, Rundle JL, Garg A, Komada M, Brophy PJ, et al. Activated microglia mediate axoglial disruption that contributes to axonal injury in multiple sclerosis. J Neuropathol Exp Neurol 2010;69:1017-33.

68. Peterson JW, Bö L, Mörk S, Chang A, Trapp BD. Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions. Ann Neurol 2001;50:389-400.

69. Pomicter AD, Shroff SM, Fuss B, Sato-Bigbee C, Brophy PJ, et al. Novel forms of neurofascin 155 in the central nervous system: alterations in paranodal disruption models and multiple sclerosis. Brain 2010;133:389-405.

70. Waxman SG. Axonal dysfunction in chronic multiple sclerosis: meltdown in the membrane. Ann Neurol 2008;63:411-3.

71. Calabrese M, Reynolds R, Magliozzi R, Castellaro M, Morra A, et al. Regional distribution and evolution of gray matter damage in different populations of multiple sclerosis patients. PloS One 2015;10:e0135428.

72. Ajami B, Bennett JL, Krieger C, McNagny KM, Rossi FM. Infiltrating monocytes trigger EAE progression, but do not contribute to the resident microglia pool. Nat Neurosci 2011;14:1142-9.

73. Huitinga I, van Rooijen N, de Groot CJ, Uitdehaag BM, Dijkstra CD. Suppression of experimental allergic encephalomyelitis in Lewis rats after elimination of macrophages. J Exp Med 1990;172:1025-33.

74. Huitinga I, Damoiseaux JG, Döpp EA, Dijkstra CD. Treatment with anti-CR3 antibodies ED7 and ED8 suppresses experimental allergic encephalomyelitis in Lewis rats. Eur J Immunol 1993;23:709-15.

75. Ransohoff RM. Animal models of multiple sclerosis: the good, the bad and the bottom line. Nat Neurosci 2012;15:1074-7.

76. Denic A, Johnson AJ, Bieber AJ, Warrington AE, Rodriguez M, et al. The relevance of animal models in multiple sclerosis research. Pathophysiology 2011;18:21-9.

77. Dupree JL, Mason JL, Marcus JR, Stull M, Levinson R, et al. Oligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheath. Neuron Glia Biol 2004;1:179-92.

78. Torre-Fuentes L, Moreno-Jiménez L, Pytel V, Matías-Guiu JA, Gómez-Pinedo U, et al. Experimental models of demyelination and remyelination. Neurologia 2017:S0213-4853:30236.

79. Beeton C, Garcia A, Chandy KG. Induction and clinical scoring of chronic-relapsing experimental autoimmune encephalomyelitis. J Vis Exp 2007;224.

80. Kipp M, Nyamoya S, Hochstrasser T, Amor S. Multiple sclerosis animal models: a clinical and histopathological perspective. Brain Pathol 2017;27:123-37.

81. Williams KC, Ulvestad E, Hickey WF. Immunology of multiple sclerosis. Clin Neurosci 1994;2:229-45.

82. Buttermore ED, Thaxton CL, Bhat MA. Organization and maintenance of molecular domains in myelinated axons. J Neurosci Res 2013;91:603-22.

83. Bhat MA, Rios JC, Lu Y, Garcia-Fresco GP, Ching W, et al. Axon-glia interactions and the domain organization of myelinated axons requires neurexin IV/Caspr/Paranodin. Neuron 2001;30:369-83.

84. Dupree JL, Girault JA, Popko B. Axo-glial interactions regulate the localization of axonal paranodal proteins. J Cell Biol 1999;147:1145-52.

85. Ishibashi T, Ikenaka K, Shimizu T, Kagawa T, Baba H. Initiation of sodium channel clustering at the node of Ranvier in the mouse optic nerve. Neurochem Res 2003;28:117-25.

86. Pillai AM, Thaxton C, Pribisko AL, Cheng JG, Dupree JL, et al. Spatiotemporal ablation of myelinating glia-specific neurofascin (Nfasc NF155) in mice reveals gradual loss of paranodal axoglial junctions and concomitant disorganization of axonal domains. J Neurosci Res 2009;87:1773-93.

87. Rasband MN, Peles E, Trimmer JS, Levinson SR, Lux SE, et al. Dependence of nodal sodium channel clustering on paranodal axoglial contact in the developing CNS. J Neurosci 1999;19:7516-28.

88. Rosenbluth J, Dupree JL, Popko B. Nodal sodium channel domain integrity depends on the conformation of the paranodal junction, not on the presence of transverse bands. Glia 2003;41:318-25.

89. Suzuki A, Hoshi T, Ishibashi T, Hayashi A, Yamaguchi Y, et al. Paranodal axoglial junction is required for the maintenance of the Nav1.6-type sodium channel in the node of Ranvier in the optic nerves but not in peripheral nerve fibers in the sulfatide-deficient mice. Glia 2004;46:274-83.

90. Coman I, Aigrot MS, Seilhean D, Reynolds R, Girault JA, et al. Nodal, paranodal and juxtaparanodal axonal proteins during demyelination and remyelination in multiple sclerosis. Brain 2006;129:3186-95.

91. Zoupi L, Markoullis K, Kleopa KA, Karagogeos D. Alterations of juxtaparanodal domains in two rodent models of CNS demyelination. Glia 2013;61:1236-49.

92. Prinz M, Priller J, Sisodia SS, Ransohoff RM. Heterogeneity of CNS myeloid cells and their roles in neurodegeneration. Nat Neurosci 2011;14:1227-35.

93. Steinman L, Martin R, Bernard C, Conlon P, Oksenberg JR. Multiple sclerosis: deeper understanding of its pathogenesis reveals new targets for therapy. Annu Rev Neurosci 2002;25:491-505.

94. Fife BT, Huffnagle GB, Kuziel WA, Karpus WJ. CC chemokine receptor 2 is critical for induction of experimental autoimmune encephalomyelitis. J Exp Med 2000;192:899-905.

95. Izikson L, Klein RS, Charo IF, Weiner HL, Luster AD. Resistance to experimental autoimmune encephalomyelitis in mice lacking the CC chemokine receptor (CCR)2. J Exp Med 2000;192:1075-80.

96. Buffington SA, Rasband MN. The axon initial segment in nervous system disease and injury. Eur J Neurosci 2011;34:1609-19.

97. Hedstrom KL, Ogawa Y, Rasband MN. AnkyrinG is required for maintenance of the axon initial segment and neuronal polarity. J Cell Biol 2008;183:635-40.

98. Jenkins SM, Bennett V. Developing nodes of Ranvier are defined by ankyrin-G clustering and are independent of paranodal axoglial adhesion. Proc Natl Acad Sci U S A 2002;99:2303-8.

99. Hartley RK. Differential reactivity of microglia in two mouse models of multiple sclerosis. Theses Diss 2016.

100. Inayat MS, El-Amouri IS, Bani-Ahmad M, Elford HL, Gallicchio VS, et al. Inhibition of allogeneic inflammatory responses by the Ribonucleotide Reductase Inhibitors, Didox and Trimidox. J Inflamm (Lond) 2010;7:43.

101. Matsebatlela TM, Anderson AL, Gallicchio VS, Elford H, Rice CD. 3,4-Dihydroxy-benzohydroxamic acid (Didox) suppresses pro-inflammatory profiles and oxidative stress in TLR4-activated RAW264.7 murine macrophages. Chem Biol Interact 2015;233:95-105.

102. Turchan J, Pocernich CB, Gairola C, Chauhan A, Schifitto G, et al. Oxidative stress in HIV demented patients and protection ex vivo with novel antioxidants. Neurology 2003;60:307-14.

103. Hamada MS, Kole MH. Myelin loss and axonal ion channel adaptations associated with gray matter neuronal hyperexcitability. J Neurosci 2015;35:7272-86.

104. Evans MD, Dumitrescu AS, Kruijssen DLH, Taylor SE, Grubb MS. Rapid modulation of axon initial segment length influences repetitive spike firing. Cell Rep 2015;13:1233-45.

105. Grubb MS, Burrone J. Activity-dependent relocation of the axon initial segment fine-tunes neuronal excitability. Nature 2010;465:1070-4.

106. Kuba H, Adachi R, Ohmori H. Activity-dependent and activity-independent development of the axon initial segment. J Neurosci 2014;34:3443-53.

107. Paolicelli RC, Bolasco G, Pagani F, Maggi L, Scianni M, et al. Synaptic pruning by microglia is necessary for normal brain development. Science 2011;333:1456-8.

108. Rogers JT, Morganti JM, Bachstetter AD, Hudson CE, Peters MM, et al. CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity. Version 2. J Neurosci 2011;31:16241-50.

109. Zhan Y, Paolicelli RC, Sforazzini F, Weinhard L, Bolasco G, et al. Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior. Nat Neurosci 2014;17:400-6.

110. Coronado VG, McGuire LC, Sarmiento K, Bell J, Lionbarger MR, et al. Trends in traumatic brain injury in the U.S. and the public health response: 1995-2009. J Safety Res 2012;43:299-307.

111. Gardner RC, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Mol Cell Neurosci 2015;66:75-80.

112. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil 2006;21:375-8.

113. Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic brain injury-related emergency department visits, hospitalizations, and deaths - United States, 2007 and 2013. MMWR Surveill Summ 2017;66:1-16.

114. Coughlin JM, Wang Y, Minn I, Bienko N, Ambinder EB, et al. Imaging of glial cell activation and white matter integrity in brains of active and recently retired national football league players. JAMA Neurol 2017;74:67-74.

115. Das M, Mohapatra S, Mohapatra SS. New perspectives on central and peripheral immune responses to acute traumatic brain injury. J Neuroinflammation 2012;9:236.

116. Kelley BJ, Lifshitz J, Povlishock JT. Neuroinflammatory responses after experimental diffuse traumatic brain injury. J Neuropathol Exp Neurol 2007;66:989-1001.

117. Morganti-Kossmann MC, Satgunaseelan L, Bye N, Kossmann T. Modulation of immune response by head injury. Injury 2007;38:1392-400.

118. Nizamutdinov D, Shapiro LA. Overview of traumatic brain injury: an immunological context. Brain Sci 2017;7.

119. Velázquez A, Ortega M, Rojas S, González-Oliván FJ, Rodríguez-Baeza A. Widespread microglial activation in patients deceased from traumatic brain injury. Brain Inj 2015;29:1126-33.

120. Coughlin JM, Wang Y, Munro CA, Ma S, Yue C, et al. Neuroinflammation and brain atrophy in former NFL players: an in vivo multimodal imaging pilot study. Neurobiol Dis 2015;74:58-65.

121. Ramlackhansingh AF, Brooks DJ, Greenwood RJ, Bose SK, Turkheimer FE, et al. Inflammation after trauma: microglial activation and traumatic brain injury. Ann Neurol 2011;70:374-83.

122. Zhou Y, Lui YW, Zuo XN, Milham MP, Reaume J, et al. Characterization of thalamo-cortical association using amplitude and connectivity of functional MRI in mild traumatic brain injury. J Magn Reson Imaging 2014;39:1558-68.

123. Boche D, Perry VH, Nicoll JA. Review: activation patterns of microglia and their identification in the human brain. Neuropathol Appl Neurobiol 2013;39:3-18.

124. Engel S, Schluesener H, Mittelbronn M, Seid K, Adjodah D, et al. Dynamics of microglial activation after human traumatic brain injury are revealed by delayed expression of macrophage-related proteins MRP8 and MRP14. Acta Neuropathol 2000;100:313-22.

125. Johnson VE, Stewart JE, Begbie FD, Trojanowski JQ, Smith DH, et al. Inflammation and white matter degeneration persist for years after a single traumatic brain injury. Brain 2013;136:28-42.

126. Engel S, Isenmann S, Ständer M, Rieger J, Bähr M, et al. Inhibition of experimental rat glioma growth by decorin gene transfer is associated with decreased microglial infiltration. J Neuroimmunol 1999;99:13-8.

127. Marklund N. Rodent models of traumatic brain injury: methods and challenges. Methods Mol Biol 2016;1462:29-46.

128. Xiong Y, Mahmood A, Chopp M. Animal models of traumatic brain injury. Nat Rev Neurosci 2013;14:128-42.

129. Donat CK, Scott G, Gentleman SM, Sastre M. Microglial activation in traumatic brain injury. Front Aging Neurosci 2017;9:208.

130. Gensel JC, Zhang B. Macrophage activation and its role in repair and pathology after spinal cord injury. Brain Res 2015;1619:1-11.

131. Kigerl KA, Gensel JC, Ankeny DP, Alexander JK, Donnelly DJ, et al. Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. J Neurosci 2009;29:13435-44.

132. Loane DJ, Kumar A, Stoica BA, Cabatbat R, Faden AI. Progressive neurodegeneration after experimental brain trauma: association with chronic microglial activation. J Neuropathol Exp Neurol 2014;73:14-29.

133. Jassam YN, Izzy S, Whalen M, McGavern DB, El Khoury J. Neuroimmunology of traumatic brain injury: time for a paradigm shift. Neuron 2017;95:1246-65.

134. Tapp ZM, Godbout JP, Kokiko-Cochran ON. A tilted axis: maladaptive inflammation and HPA axis dysfunction contribute to consequences of TBI. Front Neurol 2019;10:345.

135. Zanier ER, Marchesi F, Ortolano F, Perego C, Arabian M, et al. Fractalkine receptor deficiency is associated with early protection but late worsening of outcome following brain trauma in mice. J Neurotrauma 2016;33:1060-72.

136. Weber MD, McKim DB, Niraula A, Witcher KG, Yin W, et al. The influence of microglial elimination and repopulation on stress sensitization induced by repeated social defeat. Biol Psychiatry 2019;85:667-78.

137. d’Avila JC, Lam TI, Bingham D, Shi J, Won SJ, et al. Microglial activation induced by brain trauma is suppressed by post-injury treatment with a PARP inhibitor. J Neuroinflammation 2012;9:31.

138. Siopi E, Llufriu-Dabén G, Fanucchi F, Plotkine M, Marchand-Leroux C, et al. Evaluation of late cognitive impairment and anxiety states following traumatic brain injury in mice: the effect of minocycline. Neurosci Lett 2012;511:110-5.

139. Eyo UB, Gu N, De S, Dong H, Richardson JR, et al. Modulation of microglial process convergence toward neuronal dendrites by extracellular calcium. J Neurosci 2015;35:2417-22.

140. Garrido-Mesa N, Zarzuelo A, Gálvez J. Minocycline: far beyond an antibiotic. Br J Pharmacol 2013;169:337-52.

141. Homsi S, Federico F, Croci N, Palmier B, Plotkine M, et al. Minocycline effects on cerebral edema: relations with inflammatory and oxidative stress markers following traumatic brain injury in mice. Brain Res 2009;1291:122-32.

142. Sanchez Mejia RO, Ona VO, Li M, Friedlander RM. Minocycline reduces traumatic brain injury-mediated caspase-1 activation, tissue damage, and neurological dysfunction. Neurosurgery 2001;48:1393-9.

143. Stirling DP, Khodarahmi K, Liu J, McPhail LT, McBride CB, et al. Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury. J Neurosci 2004;24:2182-90.

144. Meythaler J, Fath J, Fuerst D, Zokary H, Freese K, et al. Safety and feasibility of minocycline in treatment of acute traumatic brain injury. Brain Inj 2019;33:679-89.

145. Bye N, Habgood MD, Callaway JK, Malakooti N, Potter A, et al. Transient neuroprotection by minocycline following traumatic brain injury is associated with attenuated microglial activation but no changes in cell apoptosis or neutrophil infiltration. Exp Neurol 2007;204:220-33.

146. Hanlon LA, Raghupathi R, Huh JW. Differential effects of minocycline on microglial activation and neurodegeneration following closed head injury in the neonate rat. Exp Neurol 2017;290:1-14.

147. Lopez-Rodriguez AB, Siopi E, Finn DP, Marchand-Leroux C, Garcia-Segura LM, et al. CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cereb Cortex 2015;25:35-45.

148. Simon DW, Aneja RK, Alexander H, Bell MJ, Bayır H, et al. Minocycline attenuates high mobility group box 1 translocation, microglial activation, and thalamic neurodegeneration after traumatic brain injury in post-natal day 17 Rats. J Neurotrauma 2018;35:130-8.

149. Bachstetter AD, Zhou Z, Rowe RK, Xing B, Goulding DS, et al. MW151 inhibited IL-1β levels after traumatic brain injury with no effect on microglia physiological responses. PLoS One 2016;11:e0149451.

150. Witcher KG, Bray CE, Dziabis JE, McKim DB, Benner BN, et al. Traumatic brain injury-induced neuronal damage in the somatosensory cortex causes formation of rod-shaped microglia that promote astrogliosis and persistent neuroinflammation. Glia 2018;66:2719-36.

151. Henry RJ, Ritzel RM, Barrett JP, Doran SJ, Jiao Y, et al. Microglial depletion with CSF1R inhibitor during chronic phase of experimental traumatic brain injury reduces neurodegeneration and neurological deficits. J Neurosci 2020:2402-19.

152. Büki A, Povlishock JT. All roads lead to disconnection?--Traumatic axonal injury revisited. Acta Neurochir (Wien) 2006;148:181-93.

153. Gentleman SM, Nash MJ, Sweeting CJ, Graham DI, Roberts GW. Beta-amyloid precursor protein (beta APP) as a marker for axonal injury after head injury. Neurosci Lett 1993;160:139-44.

154. Johnson VE, Stewart W, Weber MT, Cullen DK, Siman R, et al. SNTF immunostaining reveals previously undetected axonal pathology in traumatic brain injury. Acta Neuropathol 2016;131:115-35.

155. Povlishock JT, Erb DE, Astruc J. Axonal response to traumatic brain injury: reactive axonal change, deafferentation, and neuroplasticity. J Neurotrauma 1992;9:S189-200.

156. Sherriff FE, Bridges LR, Gentleman SM, Sivaloganathan S, Wilson S. Markers of axonal injury in post mortem human brain. Acta Neuropathol 1994;88:433-9.

157. Koliatsos VE, Alexandris AS. Wallerian degeneration as a therapeutic target in traumatic brain injury. Curr Opin Neurol 2019;32:786-95.

158. Stoll G, Müller HW. Nerve injury, axonal degeneration and neural regeneration: basic insights. Brain Pathol 1999;9:313-25.

159. Yin TC, Voorhees JR, Genova RM, Davis KC, Madison AM, et al. Acute axonal degeneration drives development of cognitive, motor, and visual deficits after blast-mediated traumatic brain injury in mice. eNeuro 2016;3.

160. Fu R, Shen Q, Xu P, Luo JJ, Tang Y. Phagocytosis of microglia in the central nervous system diseases. Mol. Neurobiol 2014;49:1422-34.

161. Neumann H, Kotter MR, Franklin RJM. Debris clearance by microglia: an essential link between degeneration and regeneration. Brain J Neurol 2009;132:288-95.

162. Bechmann I, Nitsch R. Astrocytes and microglial cells incorporate degenerating fibers following entorhinal lesion: a light, confocal, and electron microscopical study using a phagocytosis-dependent labeling technique. Glia 1997;20:145-54.

163. Wang J, Fox MA, Povlishock JT. Diffuse traumatic axonal injury in the optic nerve does not elicit retinal ganglion cell loss. J Neuropathol Exp Neurol 2013;72:768-81.

164. Holloway OG, Canty AJ, King AE, Ziebell JM. Rod microglia and their role in neurological diseases. Semin Cell Dev Biol 2019;94:96-103.

165. Graeber MB. Changing face of microglia. Science 2010;330:783-8.

166. Cao T, Thomas TC, Ziebell JM, Pauly JR, Lifshitz J. Morphological and genetic activation of microglia after diffuse traumatic brain injury in the rat. Neuroscience 2012;225:65-75.

167. Thomas TC, Ogle SB, Rumney BM, May HG, Adelson PD, et al. Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus. Behav Brain Res 2018;340:137-46.

168. Ziebell JM, Taylor SE, Cao T, Harrison JL, Lifshitz J. Rod microglia: elongation, alignment, and coupling to form trains across the somatosensory cortex after experimental diffuse brain injury. J Neuroinflammation 2012;9:247.

169. Bachstetter AD, Rowe RK, Kaneko M, Goulding D, Lifshitz J, et al. The p38α MAPK regulates microglial responsiveness to diffuse traumatic brain injury. J Neurosci 2013;33:6143-53.

170. Greer JE, Hånell A, McGinn MJ, Povlishock JT. Mild traumatic brain injury in the mouse induces axotomy primarily within the axon initial segment. Acta Neuropathol 2013;126:59-74.

171. Lifshitz J, Kelley BJ, Povlishock JT. Perisomatic thalamic axotomy after diffuse traumatic brain injury is associated with atrophy rather than cell death. J Neuropathol Exp Neurol 2007;66:218-29.

172. Wofford KL, Harris JP, Browne KD, Brown DP, Grovola MR, et al. Rapid neuroinflammatory response localized to injured neurons after diffuse traumatic brain injury in swine. Exp Neurol 2017;290:85-94.

173. Szalay G, Martinecz B, Lénárt N, Környei Z, Orsolits B, et al. Microglia protect against brain injury and their selective elimination dysregulates neuronal network activity after stroke. Nat Commun 2016;7:11499.

174. Eyo UB, Peng J, Murugan M, Mo M, Lalani A, et al. Regulation of physical microglia-neuron interactions by fractalkine signaling after status epilepticus. eNeuro 2017;3.

175. Eyo UB, Gu N, De S, Dong H, Richardson JR, et al. Modulation of microglial process convergence toward neuronal dendrites by extracellular calcium. J Neurosci 2015;35:2417-22.

176. Swiatkowski P, Murugan M, Eyo UB, Wang Y, Rangaraju S, et al. Activation of microglial P2Y12 receptor is required for outward potassium currents in response to neuronal injury. Neuroscience 2016;318:22-33.

177. Dissing-Olesen L, LeDue JM, Rungta RL, Hefendehl JK, Choi HB, et al. Activation of neuronal NMDA receptors triggers transient ATP-mediated microglial process outgrowth. J Neurosci 2014;34:10511-27.

178. Eyo UB, Peng J, Swiatkowski P, Mukherjee A, Bispo A, et al. Neuronal hyperactivity recruits microglial processes via neuronal NMDA receptors and microglial P2Y12 receptors after status epilepticus. J Neurosci 2014;34:10528-40.

179. Greer JE, Povlishock JT, Jacobs KM. Electrophysiological abnormalities in both axotomized and nonaxotomized pyramidal neurons following mild traumatic brain injury. J Neurosci 2012;32:6682-7.

180. Hånell A, Greer JE, Jacobs KM. Increased network excitability due to altered synaptic inputs to neocortical layer v intact and axotomized pyramidal neurons after mild traumatic brain injury. J Neurotrauma 2015;32:1590-8.

181. Ryu J, Horkayne-Szakaly I, Xu L, Pletnikova O, Leri F, et al. The problem of axonal injury in the brains of veterans with histories of blast exposure. Acta Neuropathol Commun 2014;2:153.

182. Oehmichen M, Theuerkauf I, Meissner C. Is traumatic axonal injury (AI) associated with an early microglial activation? Application of a double-labeling technique for simultaneous detection of microglia and AI. Acta Neuropathol 1999;97:491-4.

183. Schirmer L, Merkler D, König FB, Brück W, Stadelmann C. Neuroaxonal regeneration is more pronounced in early multiple sclerosis than in traumatic brain injury lesions. Brain Pathol Zurich Switz 2013;23:2-12.

184. Christman CW, Grady MS, Walker SA, Holloway KL, Povlishock JT. Ultrastructural studies of diffuse axonal injury in humans. J Neurotrauma 1994;11:173-86.

185. Christman CW, Salvant JB, Walker SA, Povlishock JT. Characterization of a prolonged regenerative attempt by diffusely injured axons following traumatic brain injury in adult cat: a light and electron microscopic immunocytochemical study. Acta Neuropathol 1997;94:329-37.

186. Harris NG, Mironova YA, Hovda DA, Sutton RL. Pericontusion axon sprouting is spatially and temporally consistent with a growth-permissive environment after traumatic brain injury. J Neuropathol Exp Neurol 2010;69:139-54.

187. Venkatesan C, Chrzaszcz M, Cho N, Wainwright MS. Chronic upregulation of activated microglia immunoreactive for galectin-3/Mac-2 and nerve growth factor following diffuse axonal injury. J Neuroinflammation 2010;7:32.

Neuroimmunology and Neuroinflammation
ISSN 2349-6142 (Online) 2347-8659 (Print)

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/