1 PandyanA D, GregoricM, BarnesM P, et al. Spasticity: clinical perceptions, neurological realities and meaningful measurement [J]. Disabil Rehabil, 2005, 27(1-2): 2-6.
2 McKayW B, SweatmanW M, FieldfoteE C. The experience of spasticity after spinal cord injury: perceived characteristics and impact on daily life [J]. Spinal Cord, 2018, 56(5): 478-486.
3 LuiJ, SaraiM, MillsP B. Chemodenervation for treatment of limb spasticity following spinal cord injury: a systematic review [J]. Spinal Cord, 2015, 53(4): 252-264.
4 AdamsM M, HicksA L. Spasticity after spinal cord injury [J]. Spinal Cord, 2005, 43(10): 577-586.
5 BoulenguezP, LiabeufS, BosR, et al. Down-regulation of the potassium-chloride cotransporter KCC2 contributes to spasticity after spinal cord injury [J]. Nat Med, 2010, 16(3): 302-307.
6 MurrayK C, StephensM J, BallouE W, et al. Motoneuron excitability and muscle spasms are regulated by 5-HT2B and 5-HT2C receptor activity [J]. J Neurophysiol, 2011, 105(2): 731-748.
7 D'AmicoJ M, CondliffeE G, MartinsK J, et al. Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity [J]. Front Integr Neurosci, 2014, 8: 49.
8 BrocardC, PlantierV, BoulenguezP, et al. Cleavage of Na(+) channels by calpain increases persistent Na(+) current and promotes spasticity after spinal cord injury [J]. Nat Med, 2016, 22(4): 404-411.
9 KingwellK. Spinal cord injury: clamping down on calpains to treat injury-induced spasticity [J]. Nat Rev Drug Discov, 2016, 15(5): 310.
10 BallionB, BranchereauP, ChapronJ, et al. Ontogeny of descending serotonergic innervation and evidence for intraspinal 5-HT neurons in the mouse spinal cord [J]. Brain Res Dev Brain Res, 2002, 137(1): 81-88.
11 PerrierJ F, RasmussenH B, ChristensenR K, et al. Modulation of the intrinsic properties of motoneurons by serotonin [J]. Curr Pharm Des, 2013, 19(24): 4371-4384.
12 GhoshM, PearseD D. The role of the serotonergic system in locomotor recovery after spinal cord injury [J]. Front Neural Circuits, 2014, 8: 151.
13 KongX Y, WieneckeJ, HultbornH, et al. Robust upregulation of serotonin 2A receptors after chronic spinal transection of rats: an immunohistochemical study [J]. Brain Res, 2010, 1320: 60-68.
14 RyuY, OgataT, NagaoM, et al. The swimming test is effective for evaluating spasticity after contusive spinal cord injury [J]. PLoS One, 2017, 12(2): e0171937.
15 HalberstadtA L, HeijdenI V D, RudermanM A, et al. 5-HT2A and 5-HT2C receptors exert opposing effects on locomotor activity in mice [J]. Neuropsychopharmacology, 2009, 34(8):1958-1967.
16 RenL Q, WieneckeJ, ChenM, et al. The time course of serotonin 2C receptor expression after spinal transection of rats: an immunohistochemical study [J]. Neuroscience, 2013, 236: 31-46.
17 NavarrettS, CollierL, CardozoC, et al. Alterations of serotonin 2C and 2A receptors in response to T10 spinal cord transection in rats [J]. Neurosci Lett, 2012, 506(1): 74-78.
18 HuschA, PattenG N V, HongD N, et al. Spinal cord injury induces serotonin supersensitivity without increasing intrinsic excitability of mouse V2a interneurons [J]. J Neurosci, 2012, 32(38): 13145-13154.
19 MurrayK C, NakaeA, StephensM J, et al. Recovery of motoneuron and locomotor function after spinal cord injury depends on constitutive activity in 5-HT2C receptors [J]. Nat Med, 2010, 16(6): 694-700.
20 NarzoA F D, KozlenkovA, GeY, et al. Decrease of mRNA editing after spinal cord injury is caused by down-regulation of ADAR2 that is triggered by inflammatory response [J]. Sci Rep, 2015, 5: 12615.
21 BardoniR, TakazawaT, TongC K, et al. Pre- and postsynaptic inhibitory control in the spinal cord dorsal horn [J]. Ann N Y Acad Sci, 2013, 1279(1): 90-96.
22 WangL, LiS, LiuY, et al. Motor neuron degeneration following glycine-mediated excitotoxicity induces spastic paralysis after spinal cord ischemia/reperfusion injury in rabbit [J]. Am J Transl Res, 2017, 9(7): 3411-3421.
23 GackièreF, VinayL. Contribution of the potassium-chloride cotransporter KCC2 to the strength of inhibition in the neonatal rodent spinal cord in vitro [J]. J Neurosci, 2015, 35(13): 5307-5316.
24 KiehnO. Decoding the organization of spinal circuits that control locomotion [J]. Nat Rev Neurosci, 2016, 17(4): 224-238.
25 TashiroS, ShinozakiM, MukainoM, et al. BDNF induced by treadmill training contributes to the suppression of spasticity and allodynia after spinal cord injury via upregulation of KCC2 [J]. Neurorehabil Neural Repair, 2015, 29(7): 677-689.
26 MendeM, FletcherE V, BelluardoJ L, et al. Sensory-derived glutamate regulates presynaptic inhibitory terminals in mouse spinal cord [J]. Neuron, 2016, 90(6): 1189-1202.
27 KakinohanaO, HefferanM P, MiyanoharaA, et al. Combinational spinal GAD65 gene delivery and systemic GABA-mimetic treatment for modulation of spasticity [J]. PLoS One, 2012, 7(1): e30561.
28 KopachO, MedvedievV, KrotovV, et al. Opposite, bidirectional shifts in excitation and inhibition in specific types of dorsal horn interneurons are associated with spasticity and pain post-SCI [J]. Sci Rep, 2017, 7(1): 5884.
29 BellarditaC, CaggianoV, LeirasR, et al. Spatiotemporal correlation of spinal network dynamics underlying spasms in chronic spinalized mice [J]. eLife, 2017, 6: e23011
30 TakeokaA, VollenweiderI, CourtineG, et al. Muscle spindle feedback directs locomotor recovery and circuit reorganization after spinal cord injury [J]. Cell, 2014, 159(7): 1626-1639.
31 RossignolS, FrigonA. Recovery of locomotion after spinal cord injury: some facts and mechanisms [J]. Annu Rev Neurosci, 2011, 34(1): 413-440.
32 KatheC, HutsonT H, McmahonS B, et al. Intramuscular neurotrophin-3 normalizes low threshold spinal reflexes, reduces spasms and improves mobility after bilateral corticospinal tract injury in rats [J]. eLife, 2016, 5: e18146.
33 NielsenJ B, CroneC, HultbornH. The spinal pathophysiology of spasticity: from a basic science point of view [J]. Acta Physiol (Oxf), 2007, 189: 171-180.
34 TodaT, IshidaK, KiyamaH, et al. Down-regulation of KCC2 expression and phosphorylation in motoneurons, and increases the number of in primary afferent projections to motoneurons in mice with post-stroke spasticity [J]. PLoS One, 2014, 9(12): e114328.
35 JiangY Q, ZaaimiB, MartinJ H. Competition with primary sensory afferents drives remodeling of corticospinal axons in mature spinal motor circuits [J]. J Neurosci, 2016, 36(1): 193-203.
36 BrownstoneR M, BuiT V . Spinal interneurons providing input to the final common path during locomotion [J]. Prog Brain Res, 2010, 187: 81-95.
37 BandaruS P, LiuS, WaxmanS G, et al. Dendritic spine dysgenesis contributes to hyperrefiexia after spinal cord injury [J]. J Neurophysiol, 2015, 113: 1598-1615.
38 PetruskaJ C, KitayB, BoyceV S, et al. Intramuscular AAV delivery of NT-3 alters synaptic transmission to motoneurons in adult rats [J]. Eur J Neurosci, 2010, 32(6): 997-1005.
39 BoyceV S, MendellL M. Neurotrophins and spinal circuit function [J]. Front Neural Circuits, 2014, 8: 59.
40 DurickiD A, HutsonT H, KatheC, et al. Delayed intramuscular human neurotrophin-3 improves recovery in adult and elderly rats after stroke [J]. Brain, 2016, 139(1): 259-275.
41 JanineB, RubiaV D B, QuentinB, et al. Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury [J]. Brain, 2013, 136(11): 3347-3361.
42 MedinaI, FriedelP, RiveraC, et al. Current view on the functional regulation of the neuronal K+-Cl- cotransporter KCC2 [J]. Front Cell Neurosci, 2014, 8: 27.
