[1] Moos WH, Maneta E, Pinkert CA, et al. Epigenetic treatment of neuropsychiatric disorders: autism and schizophrenia[J]. Drug Dev Res, 2016, 77(2): 53–72. doi:  10.1002/ddr.21295
[2] Džoljić E, Grbatinić I, Kostić V. Why is nitric oxide important for our brain?[J]. Funct Neurol, 2015, 30(3): 159–163. doi:  10.11138/fneur/2015.30.3.159
[3] Zhou L, Zhu DY. Neuronal nitric oxide synthase: structure, subcellular localization, regulation, and clinical implications[J]. Nitric Oxide, 2009, 20(4): 223–230. doi:  10.1016/j.niox.2009.03.001
[4] Bredt DS. Endogenous nitric oxide synthesis: biological functions and pathophysiology[J]. Free Radic Res, 1999, 31(6): 577–596. doi:  10.1080/10715769900301161
[5] Luo CX, Zhu DY. Research progress on neurobiology of neuronal nitric oxide synthase[J]. Neurosci Bull, 2011, 27(1): 23–35. doi:  10.1007/s12264-011-1038-0
[6] Zhou QG, Zhu XH, Nemes AD, et al. Neuronal nitric oxide synthase and affective disorders[J]. IBRO Rep, 2018, 5: 116–132. doi:  10.1016/j.ibror.2018.11.004
[7] Chanrion B, Mannoury la Cour C, Bertaso F, et al. Physical interaction between the serotonin transporter and neuronal nitric oxide synthase underlies reciprocal modulation of their activity[J]. Proc Natl Acad Sci U S A, 2007, 104(19): 8119–8124. doi:  10.1073/pnas.0610964104
[8] Langeberg LK, Scott JD. Signalling scaffolds and local organization of cellular behaviour[J]. Nat Rev Mol Cell Biol, 2015, 16(4): 232–244. doi:  10.1038/nrm3966
[9] Doyle DA, Lee A, Lewis J, et al. Crystal structures of a complexed and peptide-free membrane protein-binding domain: molecular basis of peptide recognition by PDZ[J]. Cell, 1996, 85(7): 1067–1076. doi:  10.1016/S0092-8674(00)81307-0
[10] Feng W, Zhang MJ. Organization and dynamics of PDZ-domain-related supramodules in the postsynaptic density[J]. Nat Rev Neurosci, 2009, 10(2): 87–99. doi:  10.1038/nrn2540
[11] Manjunath GP, Ramanujam PL, Galande S. Structure function relations in PDZ-domain-containing proteins: implications for protein networks in cellular signalling[J]. J Biosci, 2018, 43(1): 155–171. doi:  10.1007/s12038-017-9727-0
[12] Zhu LJ, Li TY, Luo CX, et al. CAPON-nNOS coupling can serve as a target for developing new anxiolytics[J]. Nat Med, 2014, 20(9): 1050–1054. doi:  10.1038/nm.3644
[13] Cui ZM, Lv QS, Yan MJ, et al. Elevated expression of CAPON and neuronal nitric oxide synthase in the sciatic nerve of rats following constriction injury[J]. Vet J, 2011, 187(3): 374–380. doi:  10.1016/j.tvjl.2010.01.014
[14] Stricker NL, Christopherson KS, Yi BA, et al. PDZ domain of neuronal nitric oxide synthase recognizes novel C-terminal peptide sequences[J]. Nat Biotechnol, 1997, 15(4): 336–342. doi:  10.1038/nbt0497-336
[15] Tochio H, Zhang Q, Mandal P, et al. Solution structure of the extended neuronal nitric oxide synthase PDZ domain complexed with an associated peptide[J]. Nat Struct Biol, 1999, 6(5): 417–421. doi:  10.1038/8216
[16] Zhou L, Li F, Xu HB, et al. Treatment of cerebral ischemia by disrupting ischemia-induced interaction of nNOS with PSD-95[J]. Nat Med, 2010, 16(12): 1439–1443. doi:  10.1038/nm.2245
[17] Ran X, Gestwicki JE. Inhibitors of protein-protein interactions (PPIs): an analysis of scaffold choices and buried surface area[J]. Curr Opin Chem Biol, 2018, 44: 75–86. doi:  10.1016/j.cbpa.2018.06.004
[18] Manso H, Krug T, Sobral J, et al. Variants within the nitric oxide synthase 1 gene are associated with stroke susceptibility[J]. Atherosclerosis, 2012, 220(2): 443–448. doi:  10.1016/j.atherosclerosis.2011.11.011
[19] Dai YJ, He ZY, Sui RB, et al. Association of nNOS gene polymorphism with ischemic stroke in Han Chinese of North China[J]. Sci World J, 2013, 2013: 891581. doi:  10.1155/2013/891581
[20] Liu HT, Li J, Zhao FY, et al. Nitric oxide synthase in hypoxic or ischemic brain injury[J]. Rev Neurosci, 2015, 26(1): 105–117. doi:  10.1515/revneuro-2014-0041
[21] Eliasson MJL, Huang ZH, Ferrante RJ, et al. Neuronal nitric oxide synthase activation and peroxynitrite formation in ischemic stroke linked to neural damage[J]. J Neurosci, 1999, 19(14): 5910–5918. doi:  10.1523/JNEUROSCI.19-14-05910.1999
[22] Samdani AF, Dawson TM, Dawson VL. Nitric oxide synthase in models of focal ischemia[J]. Stroke, 1997, 28(6): 1283–1288. doi:  10.1161/01.STR.28.6.1283
[23] Luo CX, Zhu XJ, Zhou QG, et al. Reduced neuronal nitric oxide synthase is involved in ischemia-induced hippocampal neurogenesis by up-regulating inducible nitric oxide synthase expression[J]. J Neurochem, 2007, 103(5): 1872–1882. doi:  10.1111/j.1471-4159.2007.04915.x
[24] Tochio H, Mok YK, Zhang Q, et al. Formation of nNOS/PSD-95 PDZ dimer requires a preformed β-finger structure from the nNOS PDZ domain[J]. J Mol Biol, 2000, 303(3): 359–370. doi:  10.1006/jmbi.2000.4148
[25] Wang ZY, Zhao Y, Jiang Y, et al. Enhanced anti-ischemic stroke of ZL006 by T7-conjugated PEGylated liposomes drug delivery system[J]. Sci Rep, 2015, 5: 12651. doi:  10.1038/srep12651
[26] Chen D, Zhao T, Ni K, et al. Metabolic investigation on ZL006 for the discovery of a potent prodrug for the treatment of cerebral ischemia[J]. Bioorg Med Chem Lett, 2016, 26(9): 2152–2155. doi:  10.1016/j.bmcl.2016.03.074
[27] Zhao Y, Jiang Y, Lv W, et al. Dual targeted nanocarrier for brain ischemic stroke treatment[J]. J Control Release, 2016, 233: 64–71. doi:  10.1016/j.jconrel.2016.04.038
[28] Del Arroyo AG, Hadjihambi A, Sanchez J, et al. NMDA receptor modulation of glutamate release in activated neutrophils[J]. EBioMedicine, 2019, 47: 457–469. doi:  10.1016/j.ebiom.2019.08.004
[29] David J, O'Toole E, O'Reilly K, et al. Inhibitors of the NMDA-nitric oxide signaling pathway protect against neuronal atrophy and synapse loss provoked by l-alpha aminoadipic acid-treated astrocytes[J]. Neuroscience, 2018, 392: 38–56. doi:  10.1016/j.neuroscience.2018.09.023
[30] Luo CX, Lin YH, Qian XD, et al. Interaction of nNOS with PSD-95 negatively controls regenerative repair after stroke[J]. J Neurosci, 2014, 34(40): 13535–13548. doi:  10.1523/JNEUROSCI.1305-14.2014
[31] Wang DL, Qian XD, Lin YH, et al. ZL006 promotes migration and differentiation of transplanted neural stem cells in male rats after stroke[J]. J Neurosci Res, 2017, 95(12): 2409–2419. doi:  10.1002/jnr.24068
[32] Lin YH, Dong J, Tang Y, et al. Opening a new time window for treatment of stroke by targeting HDAC2[J]. J Neurosci, 2017, 37(28): 6712–6728. doi:  10.1523/JNEUROSCI.0341-17.2017
[33] Tang Y, Lin YH, Ni HY, et al. Inhibiting histone deacetylase 2 (HDAC2) promotes functional recovery from stroke[J]. J Am Heart Assoc, 2017, 6(10): e007236. doi:  10.1161/JAHA.117.007236
[34] Lin YH, Yao MC, Wu HY, et al. HDAC2 (Histone deacetylase 2): a critical factor in environmental enrichment-mediated stroke recovery[J]. J Neurochem, 2020. doi:  10.1111/jnc.15043. [Epub ahead of print
[35] Clarkson AN, Huang BS, MacIsaac SE, et al. Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke[J]. Nature, 2010, 468(7321): 305–309. doi:  10.1038/nature09511
[36] Lin YH, Liang HY, Xu K, et al. Dissociation of nNOS from PSD-95 promotes functional recovery after cerebral ischaemia in mice through reducing excessive tonic GABA release from reactive astrocytes[J]. J Pathol, 2018, 244(2): 176–188. doi:  10.1002/path.4999
[37] Qu WR, Liu NK, Wu XB, et al. Disrupting nNOS-PSD95 interaction improves neurological and cognitive recoveries after traumatic brain injury[J]. Cereb Cortex, 2020, 30(7): 3859–3871. doi:  10.1093/cercor/bhaa002
[38] Liu SG, Wang YM, Zhang YJ, et al. ZL006 protects spinal cord neurons against ischemia-induced oxidative stress through AMPK-PGC-1α-Sirt3 pathway[J]. Neurochem Int, 2017, 108: 230–237. doi:  10.1016/j.neuint.2017.04.005
[39] Li LL, Ginet V, Liu XN, et al. The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death[J]. J Neurosci, 2013, 33(19): 8185–8201. doi:  10.1523/JNEUROSCI.4578-12.2013
[40] Jaffrey SR, Snowman AM, Eliasson MJL, et al. CAPON: a protein associated with neuronal nitric oxide synthase that regulates its interactions with PSD95[J]. Neuron, 1998, 20(1): 115–124. doi:  10.1016/S0896-6273(00)80439-0
[41] Jiang J, Yan M, Lv Q, et al. Inhibition of nitric oxide-induced nuclear localization of CAPON by NMDA receptor antagonist in cultured rat primary astrocytes[J]. Neurochem Int, 2010, 56(4): 561–568. doi:  10.1016/j.neuint.2009.12.019
[42] Ni HY, Song YX, Lin YH, et al. Dissociating nNOS (neuronal NO synthase)-CAPON (Carboxy-terminal postsynaptic density-95/discs large/zona occludens-1 ligand of nNOS) interaction promotes functional recovery after stroke via enhanced structural neuroplasticity[J]. Stroke, 2019, 50(3): 728–737. doi:  10.1161/STROKEAHA.118.022647
[43] Holmes D. The pain drain[J]. Nature, 2016, 535(7611): S2–S3. doi:  10.1038/535S2a
[44] South SM, Kohno T, Kaspar BK, et al. A conditional deletion of the NR1 subunit of the NMDA receptor in adult spinal cord dorsal horn reduces NMDA currents and injury-induced pain[J]. J Neurosci, 2003, 23(12): 5031–5040. doi:  10.1523/JNEUROSCI.23-12-05031.2003
[45] Zhou HY, Chen SR, Pan HL. Targeting N-methyl-D-aspartate receptors for treatment of neuropathic pain[J]. Expert Rev Clin Pharmacol, 2011, 4(3): 379–388. doi:  10.1586/ecp.11.17
[46] Pal HR, Berry N, Kumar R, et al. Ketamine dependence[J]. Anaesth Intensive Care, 2002, 30(3): 382–384. doi:  10.1177/0310057X0203000323
[47] Carey LM, Lee WH, Gutierrez T, et al. Small molecule inhibitors of PSD95-nNOS protein-protein interactions suppress formalin-evoked Fos protein expression and nociceptive behavior in rats[J]. Neuroscience, 2017, 349: 303–317. doi:  10.1016/j.neuroscience.2017.02.055
[48] Lee WH, Xu ZL, Ashpole NM, et al. Small molecule inhibitors of PSD95-nNOS protein-protein interactions as novel analgesics[J]. Neuropharmacology, 2015, 97: 464–475. doi:  10.1016/j.neuropharm.2015.05.038
[49] Cai WH, Wu SG, Pan ZQ, et al. Disrupting interaction of PSD-95 with nNOS attenuates hemorrhage-induced thalamic pain[J]. Neuropharmacology, 2018, 141: 238–248. doi:  10.1016/j.neuropharm.2018.09.003
[50] Deyama S, Sugano Y, Mori S, et al. Activation of the NMDA receptor-neuronal nitric oxide synthase pathway within the ventral bed nucleus of the stria terminalis mediates the negative affective component of pain[J]. Neuropharmacology, 2017, 118: 59–68. doi:  10.1016/j.neuropharm.2017.03.008
[51] Lee WH, Li LL, Chawla A, et al. Disruption of nNOS-NOS1AP protein-protein interactions suppresses neuropathic pain in mice[J]. Pain, 2018, 159(5): 849–863. doi:  10.1097/j.pain.0000000000001152
[52] Lee WH, Carey LM, Li LL, et al. ZLc002, a putative small-molecule inhibitor of nNOS interaction with NOS1AP, suppresses inflammatory nociception and chemotherapy-induced neuropathic pain and synergizes with paclitaxel to reduce tumor cell viability[J]. Mol Pain, 2018, 14: 1–17. doi:  10.1177/1744806918801224
[53] Li J, Zhang L, Xu C, et al. Prolonged use of NMDAR antagonist develops analgesic tolerance in neuropathic pain via nitric oxide reduction-induced GABAergic disinhibition[J]. Neurotherapeutics, 2020, 17(3): 1016–1030. doi:  10.1007/s13311-020-00883-w
[54] Atri A. The Alzheimer's Disease clinical spectrum: diagnosis and management[J]. Med Clin North Am, 2019, 103(2): 263–293. doi:  10.1016/j.mcna.2018.10.009
[55] Weller J, Budson A. Current understanding of Alzheimer's disease diagnosis and treatment[J]. F1000Res, 2018, 7: 1161. doi:  10.12688/f1000research.14506.1
[56] Zhang Y, Zhu Z, Liang HY, et al. nNOS-CAPON interaction mediates amyloid-β-induced neurotoxicity, especially in the early stages[J]. Aging Cell, 2018, 17(3): e12754. doi:  10.1111/acel.12754
[57] Hashimoto S, Matsuba Y, Kamano N, et al. Author Correction: tau binding protein CAPON induces tau aggregation and neurodegeneration[J]. Nat Commun, 2019, 10(1): 2964. doi:  10.1038/s41467-019-10990-8
[58] Tao WY, Yu LJ, Jiang S, et al. Neuroprotective effects of ZL006 in Aβ1-42-treated neuronal cells[J]. Neural Regen Res, 2020, 15(12): 2296–2305. doi:  10.4103/1673-5374.285006
[59] Smith AE, Xu ZL, Lai YY, et al. Source memory in rats is impaired by an NMDA receptor antagonist but not by PSD95-nNOS protein-protein interaction inhibitors[J]. Behav Brain Res, 2016, 305: 23–29. doi:  10.1016/j.bbr.2016.02.021
[60] Young J, Mendoza M. Parkinson's disease: a treatment guide[J]. J Fam Pract, 2018, 67(5): 276, 279, 284, 286. https://www.mdedge.com/familymedicine/article/164300/neurology/parkinsons-disease-treatment-guide
[61] Dauer W, Przedborski S. Parkinson's disease: mechanisms and models[J]. Neuron, 2003, 39(6): 889–909. doi:  10.1016/S0896-6273(03)00568-3
[62] Jiang PE, Lang QH, Yu QY, et al. Behavioral assessments of spontaneous locomotion in a murine MPTP-induced Parkinson's disease model[J]. J Vis Exp, 2019, (143): e58653. https://www.jove.com/t/58653/behavioral-assessments-spontaneous-locomotion-murine-mptp-induced
[63] Hu W, Guan LS, Dang XB, et al. Small-molecule inhibitors at the PSD-95/nNOS interface attenuate MPP+-induced neuronal injury through Sirt3 mediated inhibition of mitochondrial dysfunction[J]. Neurochem Int, 2014, 79: 57–64. doi:  10.1016/j.neuint.2014.10.005
[64] Millan MJ. The role of monoamines in the actions of established and "novel" antidepressant agents: a critical review[J]. Eur J Pharmacol, 2004, 500(1–3): 371–384.
[65] Yohn CN, Gergues MM, Samuels BA. The role of 5-HT receptors in depression[J]. Mol Brain, 2017, 10(1): 28. doi:  10.1186/s13041-017-0306-y
[66] Baranyi A, Amouzadeh-Ghadikolai O, Rothenhäusler HB, et al. Nitric oxide-related biological pathways in patients with major depression[J]. PLoS One, 2015, 10(11): e0143397. doi:  10.1371/journal.pone.0143397
[67] Ostadhadi S, Khan MI, Norouzi-Javidan A, et al. Involvement of NMDA receptors and L-arginine/nitric oxide/cyclic guanosine monophosphate pathway in the antidepressant-like effects of topiramate in mice forced swimming test[J]. Brain Res Bull, 2016, 122: 62–70. doi:  10.1016/j.brainresbull.2016.03.004
[68] Zhou QG, Hu Y, Hua Y, et al. Neuronal nitric oxide synthase contributes to chronic stress-induced depression by suppressing hippocampal neurogenesis[J]. J Neurochem, 2007, 103(5): 1843–1854. doi:  10.1111/j.1471-4159.2007.04914.x
[69] Lupien SJ, McEwen BS, Gunnar MR, et al. Effects of stress throughout the lifespan on the brain, behaviour and cognition[J]. Nat Rev Neurosci, 2009, 10(6): 434–445. doi:  10.1038/nrn2639
[70] Joseph DN, Whirledge S. Stress and the HPA axis: balancing homeostasis and fertility[J]. Int J Mol Sci, 2017, 18(10): 2224. doi:  10.3390/ijms18102224
[71] Zhou QG, Zhu LJ, Chen C, et al. Hippocampal neuronal nitric oxide synthase mediates the stress-related depressive behaviors of glucocorticoids by downregulating glucocorticoid receptor[J]. J Neurosci, 2011, 31(21): 7579–7590. doi:  10.1523/JNEUROSCI.0004-11.2011
[72] Zhu LJ, Liu MY, Li H, et al. The different roles of glucocorticoids in the hippocampus and hypothalamus in chronic stress-induced HPA axis hyperactivity[J]. PLoS One, 2014, 9(5): e97689. doi:  10.1371/journal.pone.0097689
[73] Hu Y, Wu DL, Luo CX, et al. Hippocampal nitric oxide contributes to sex difference in affective behaviors[J]. Proc Natl Acad Sci U S A, 2012, 109(35): 14224–14229. doi:  10.1073/pnas.1207461109
[74] Doucet MV, Levine H, Dev KK, et al. Small-molecule inhibitors at the PSD-95/nNOS interface have antidepressant-like properties in mice[J]. Neuropsychopharmacology, 2013, 38(8): 1575–1584. doi:  10.1038/npp.2013.57
[75] Dean E. Anxiety[J]. Nurs Stand, 2016, 30(46): 15. doi:  10.7748/ns.30.46.15.s17
[76] Carlezon WA Jr, Duman RS, Nestler EJ. The many faces of CREB[J]. Trends Neurosci, 2005, 28(8): 436–445. doi:  10.1016/j.tins.2005.06.005
[77] Zhang J, Huang XY, Ye ML, et al. Neuronal nitric oxide synthase alteration accounts for the role of 5-HT1A receptor in modulating anxiety-related behaviors[J]. J Neurosci, 2010, 30(7): 2433–2441. doi:  10.1523/JNEUROSCI.5880-09.2010
[78] Zhang J, Cai CY, Wu HY, et al. Correction: corrigendum: CREB-mediated synaptogenesis and neurogenesis is crucial for the role of 5-HT1a receptors in modulating anxiety behaviors[J]. Sci Rep, 2017, 7: 43405. doi:  10.1038/srep43405
[79] Cai CY, Wu HY, Luo CX, et al. Extracellular regulated protein kinaseis critical for the role of 5-HT1a receptor in modulating nNOS expression and anxiety-related behaviors[J]. Behav Brain Res, 2019, 357–358: 88–97. doi:  10.1016/j.bbr.2017.12.017
[80] Zlatković J, Filipović D. Chronic social isolation induces NF-κB activation and upregulation of iNOS protein expression in rat prefrontal cortex[J]. Neurochem Int, 2013, 63(3): 172–179. doi:  10.1016/j.neuint.2013.06.002
[81] Fan JM, Fan XF, Li Y, et al. Blunted inflammation mediated by NF-κB activation in hippocampus alleviates chronic normobaric hypoxia-induced anxiety-like behavior in rats[J]. Brain Res Bull, 2016, 122: 54–61. doi:  10.1016/j.brainresbull.2016.03.001
[82] Pesarico AP, Sartori G, Brüning CA, et al. A novel isoquinoline compound abolishes chronic unpredictable mild stress-induced depressive-like behavior in mice[J]. Behav Brain Res, 2016, 307: 73–83. doi:  10.1016/j.bbr.2016.03.049
[83] Zhu LJ, Ni HY, Chen R, et al. Hippocampal nuclear factor kappa B accounts for stress-induced anxiety behaviors via enhancing neuronal nitric oxide synthase (nNOS)-carboxy-terminal PDZ ligand of nNOS-Dexras1 coupling[J]. J Neurochem, 2018, 146(5): 598–612. doi:  10.1111/jnc.14478
[84] Zhu LJ, Shi HJ, Chang L, et al. nNOS-CAPON blockers produce anxiolytic effects by promoting synaptogenesis in chronic stress-induced animal models of anxiety[J]. Br J Pharmacol, 2020, 177(16): 3674–3690. doi:  10.1111/bph.15084
[85] Liang HY, Chen ZJ, Xiao H, et al. nNOS-expressing neurons in the vmPFC transform pPVT-derived chronic pain signals into anxiety behaviors[J]. Nat Commun, 2020, 11(1): 2501. doi:  10.1038/s41467-020-16198-5
[86] Sumner JA, Edmondson D. Refining our understanding of PTSD in medical settings[J]. Gen Hosp Psychiatry, 2018, 53: 86–87. doi:  10.1016/j.genhosppsych.2018.05.001
[87] Milad M R, Quirk G J. Fear extinction as a model for translational neuroscience: ten years of progress[J]. Annu Rev Psychol, 2012, 63: 129–151. doi:  10.1146/annurev.psych.121208.131631
[88] Burgos-Robles A, Vidal-Gonzalez I, Santini E, et al. Consolidation of fear extinction requires NMDA receptor-dependent bursting in the ventromedial prefrontal cortex[J]. Neuron, 2007, 53(6): 871–880. doi:  10.1016/j.neuron.2007.02.021
[89] Soliman F, Glatt CE, Bath KG, et al. A genetic variant BDNF polymorphism alters extinction learning in both mouse and human[J]. Science, 2010, 327(5967): 863–866. doi:  10.1126/science.1181886
[90] Ji YY, Pang PT, Feng LY, et al. Cyclic AMP controls BDNF-induced TrkB phosphorylation and dendritic spine formation in mature hippocampal neurons[J]. Nat Neurosci, 2005, 8(2): 164–172. doi:  10.1038/nn1381
[91] Cai CY, Chen C, Zhou Y, et al. PSD-95-nNOS Coupling Regulates Contextual Fear Extinction in the Dorsal CA3[J]. Sci Rep, 2018, 8(1): 12775. doi:  10.1038/s41598-018-30899-4
[92] Li J, Han Z, Cao B, et al. Disrupting nNOS-PSD-95 coupling in the hippocampal dentate gyrus promotes extinction memory retrieval[J]. Biochem Biophys Res Commun, 2017, 493(1): 862–868. doi:  10.1016/j.bbrc.2017.09.003
[93] Kostek JA, Beck KD, Gilbertson MW, et al. Acquired equivalence in U.S. veterans with symptoms of posttraumatic stress: reexperiencing symptoms are associated with greater generalization[J]. J Trauma Stress, 2014, 27(6): 717–720. doi:  10.1002/jts.21974
[94] Bian XL, Qin C, Cai CY, et al. Anterior cingulate cortex to ventral hippocampus circuit mediates contextual fear generalization[J]. J Neurosci, 2019, 39(29): 5728–5739. doi:  10.1523/JNEUROSCI.2739-18.2019
[95] Qin C, Bian XL, Cai CY, et al. Uncoupling nNOS-PSD-95 in the ACC can inhibit contextual fear generalization[J]. Biochem Biophys Res Commun, 2019, 513(1): 248–254. doi:  10.1016/j.bbrc.2019.03.184
[96] Li LP, Dustrude ET, Haulcomb MM, et al. PSD95 and nNOS interaction as a novel molecular target to modulate conditioned fear: relevance to PTSD[J]. Transl Psychiatry, 2018, 8(1): 155. doi:  10.1038/s41398-018-0208-5
[97] Song S, Lee J, Park S, et al. Fear renewal requires nitric oxide signaling in the lateral amygdala[J]. Biochem Biophys Res Commun, 2020, 523(1): 86–90. doi:  10.1016/j.bbrc.2019.12.038
[98] Zou ZL, Wang HJ, d'Oleire Uquillas F, et al. Definition of substance and non-substance addiction[J]. Adv Exp Med Biol, 2017, 1010: 21–41. doi:  10.1007/978-981-10-5562-1_2
[99] Liu JF, Li JX. Drug addiction: a curable mental disorder?[J]. Acta Pharmacol Sin, 2018, 39(12): 1823–1829. doi:  10.1038/s41401-018-0180-x
[100] Leri F, Zhou Y, Goddard B, et al. Effects of high-dose methadone maintenance on cocaine place conditioning, cocaine self-administration, and mu-opioid receptor mRNA expression in the rat brain[J]. Neuropsychopharmacology, 2006, 31(7): 1462–1474. doi:  10.1038/sj.npp.1300927
[101] Schroeder JA, Niculescu M, Unterwald EM. Cocaine alters mu but not delta or kappa opioid receptor-stimulated in situ [35S]GTPγS binding in rat brain[J]. Synapse, 2003, 47(1): 26–32. doi:  10.1002/syn.10148
[102] Thériault RK, Leri F, Kalisch B. The role of neuronal nitric oxide synthase in cocaine place preference and mu opioid receptor expression in the nucleus accumbens[J]. Psychopharmacology (Berl), 2018, 235(9): 2675–2685. doi:  10.1007/s00213-018-4961-1
[103] Itzhak Y, Anderson KL, Ali SF. Differential response of nNOS knockout mice to MDMA ("ecstasy")- and methamphetamine-induced psychomotor sensitization and neurotoxicity[J]. Ann N Y Acad Sci, 2004, 1025(1): 119–128. doi:  10.1196/annals.1316.015
[104] Balda MA, Anderson KL, Itzhak Y. Adolescent and adult responsiveness to the incentive value of cocaine reward in mice: role of neuronal nitric oxide synthase (nNOS) gene[J]. Neuropharmacology, 2006, 51(2): 341–349. doi:  10.1016/j.neuropharm.2006.03.026
[105] Koob GF, Volkow ND. Neurocircuitry of addiction[J]. Neuropsychopharmacology, 2010, 35(1): 217–238. doi:  10.1038/npp.2009.110
[106] Smith ACW, Scofield MD, Heinsbroek JA, et al. Accumbens nNOS interneurons regulate cocaine relapse[J]. J Neurosci, 2017, 37(4): 742–756. doi:  10.1523/JNEUROSCI.2673-16.2016
[107] Zou SL, Kumar U. Colocalization of cannabinoid receptor 1 with somatostatin and neuronal nitric oxide synthase in rat brain hippocampus[J]. Brain Res, 2015, 1622: 114–126. doi:  10.1016/j.brainres.2015.06.021
[108] Ribeiro EA, Salery M, Scarpa JR, et al. Transcriptional and physiological adaptations in nucleus accumbens somatostatin interneurons that regulate behavioral responses to cocaine[J]. Nat Commun, 2018, 9(1): 3149. doi:  10.1038/s41467-018-05657-9
[109] Kou XL, Tao Y, Xian JY, et al. Uncoupling nNOS-PSD-95 in mPFC inhibits morphine priming-induced reinstatement after extinction training[J]. Biochem Biophys Res Commun, 2020, 525(2): 520–527. doi:  10.1016/j.bbrc.2020.02.112