［1］Yang Y, Wang H, Hu J, et al. Lateral habenula in the pathophysiology of depression［J］. Curr Opin Neurobiol, 2017, 48: 90-96.
［2］Smith K. Mental health: a world of depression［J］. Nature, 2014, 515(7526): 181.
［3］Jetté N, Amoozegar F, Patten SB. Depression in epilepsy, migraine, and multiple sclerosis: Epidemiology and how to screen for it［J］. Neurol Clin Pract, 2017, 7(2): 118-127.
［4］Dhir A. Investigational drugs for treating major depressive disorder［J］. Expert Opin Investig Drugs, 2017, 26(1): 9-24.
［5］Owens MJ. Selectivity of antidepressants: from the monoamine hypothesis of depression to the SSRI revolution and beyond［J］. J Clin Psychiatry, 2004, 65 Suppl 4: 5-10.
［6］Lin FB, Hou DR, Tang QP. Research progress of depression and the application of esketamine［J］. Nan Fang Yi Ke Da Xue Xue Bao, 2016, 37(4): 567-inside back cover.
［7］Lieve KV,Wilde AA.Inherited ion channel diseases: a brief review［J］.Europace,2015,17 Suppl 2:ii1-6.
［8］Neverisky DL, Abbott GW. Ion channel-transporter interactions［J］. Crit Rev Biochem Mol Biol, 2015, 51(4): 257-267.
［9］Hull JM, Isom LL. Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease［J］. Neuropharmacology. 2018, 132:43-57.
［10］Prica C, Hascoet M, Bourin M. Antidepressant-like effect of lamotrigine is reversed by veratrine: a possible role of sodium channels in bipolar depression［J］. Behav Brain Res, 2008, 191(1): 49-54.
［11］Ji X, Saha S, Gao G, et al. The sodium channel β4 auxiliary sucbunit selectively controls long-term depression in core nucleus accumbens medium spiny neurons［J］. Front Cell Neurosci, 2017, 11:17.
［12］Wu A, Fujikawa DG. Effects of AMPA-receptor and voltage-sensitive sodium channel blockade on high potassium-induced glutamate release and neuronal death in vivo［J］. Brain Res, 2002, 946(1): 119-129.
［13］Prakriya M, Mennerick S. Selective depression of low-release probability excitatory synapses by sodium channel blockers［J］. Neuron, 2000,26(3):671-682.
［14］Chen X, Xue B, Wang J, et al. Potassium channels: a potential therapeutic target for parkinson's disease［J］. Neurosci Bull, 2018, 34(2):341-348.
［15］Bortolatto CF, Jesse CR, Wilhelm EA, et al. Involvement of potassium channels in the antidepressant-like effect of venlafaxine in mice［J］. Life Sci, 2010, 86(9/10): 372-376.
［16］Donato F, Borges FC, Giacomeli R, et al. Evidence for the involvement of potassium channel inhibition in the antidepressant-like effects of hesperidin in the tail suspension test in mice［J］. J Med Food, 2015, 18(7): 818-823.
［17］Nikoui V, Ostadhadi S, Azhand P, et al. The effect of nitrazepam on depression and curiosity in behavioral tests in mice: The role of potassium channels［J］. Eur J Pharmacol, 2016, 791: 369-376.
［18］Borsotto M,Veyssiere J,Moha OMH,et al.Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression:a new therapeutic concept［J］.Br J Pharmacol,2015,172(3):771-784.
［19］Tsai SJ. Sipatrigine could have therapeutic potential for major depression and bipolar depression through antagonism of the two-pore-domain K+ channel TREK-1［J］. Med Hypotheses，2008，70(3): 548-550.
［20］Lin DH, Zhang XR, Ye DQ, et al. The role of the two-pore domain potassium channel TREK-1 in the therapeutic effects of escitalopram in a rat model of poststroke depression［J］. CNS Neurosci Ther, 2015, 21(6): 504-512.
［21］Vallée N, Lambrechts K, De Maistre S, et al. Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the "spadin" antidepressant［J］. Front Physiol, 2016,7: 42.
［22］Kabir ZD, Martínez-Rivera A, Rajadhyaksha AM. From gene to behavior: L-type calcium channel mechanisms underlying neuropsychiatric symptoms［J］. Neurotherapeutics, 2017, 14(3): 588-613.
［23］Mizerna OP, Fedulova SA, Veselovs'kyi MS. Nonuniform distribution and contribution of the P- and P/Q-type calcium channels to short-term inhibitory synaptic transmission in cultured hippocampal neurons［J］. Fiziol Zh, 2010, 56(6): 3-11.
［24］Normann C, Peckys D, Schulze CH, et al. Associative long-term depression in the hippocampus is dependent on postsynaptic N-type Ca2+ channels［J］. J Neurosci, 2000, 20(22): 8290-8297.
［25］Jaso BA, Niciu MJ, Iadarola ND, et al. Therapeutic modulation of glutamate receptors in major depressive disorder［J］. Curr Neuropharmacol, 2017, 15(1): 57-70.
［26］Deutschenbaur L,Beck J,Kiyhankhadiv A,et al.Role of calcium,glutamate and NMDA in major depression and therapeutic application［J］.Prog Neuropsychopharmacol Biol Psychiatry,2016,64:325-333.
［27］Pochwat B, Szewczyk B, Sowa-Kucma M, et al. Antidepressant-like activity of magnesium in the chronic mild stress model in rats: alterations in the NMDA receptor subunits［J］. Int J Neuropsychopharmacol, 2014, 17(3): 393-405.
［28］Weiland NG, Orchinik M, Tanapat P. Chronic corticosterone treatment induces parallel changes in N-methyl-D-aspartate receptor subunit messenger RNA levels and antagonist binding sites in the hippocampus［J］. Neuroscience, 1997, 78(3):653-662.
［29］Jalini S, Ye H, Tonkikh AA, et al. Raised intracellular calcium contributes to ischemia-induced depression of evoked synaptic transmission［J］. PLoS One, 2016, 11(3):e0148110.
［30］Lisman J, Raghavachari S. Biochemical principles underlying the stable maintenance of LTP by the CaMKII/NMDAR complex［J］. Brain Res, 2015, 1621:51-61.
［31］Vasilescu AN, Schweinfurth N, Borgwardt S, et al. Modulation of the activity of N-methyl-d-aspartate receptors as a novel treatment option for depression: current clinical evidence and therapeutic potential of rapastinel (GLYX-13)［J］. Neuropsychiatr Dis Treat, 2017, 13: 973-980.
［32］Pochwat B, Paucha-Poniewiera A, Szewczyk B, et al. NMDA antagonists under investigation for the treatment of major depressive disorder［J］. Expert Opin Investig Drugs,  2014, 23(9): 1181-1192.
［33］Moskal JR, Burch R, Burgdorf JS, et al. GLYX-13, an NMDA receptor glycine site functional partial agonist enhances cognition and produces antidepressant effects without the psychotomimetic side effects of NMDA receptor antagonists［J］. Expert Opin Investig Drugs, 2014, 23(2):243-254.
［34］Chan SY,Matthews E,Burnet PW.ON or OFF?:Modulating the N-methyl-D-aspartate receptor in major depression［J］.Front Mol Neurosci,2016,9:169.
［35］Freudenberg F, Celikel T, Reif A. The role of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in depression: central mediators of pathophysiology and antidepressant activity［J］. Neurosci Biobehav Rev, 2015, 52: 193-206.
［36］Treccani G, Gaarn dJK, Wegener G, et al. Differential expression of postsynaptic NMDA and AMPA receptor subunits in the hippocampus and prefrontal cortex of the flinders sensitive line rat model of depression［J］. Synapse, 2016, 70(11): 471-474.
［37］Yi ES,Oh S,Lee JK,Leem YH.Chronic stress-induced dendritic reorganization and abundance of synaptosomal PKA-dependent CP-AMPA receptor in the basolateral amygdala in a mouse model of depression［J］.Biochem Biophys Res Commun,2017,486(3):671-678.
［38］Salari AA,Bakhtiari A,Homberg JR.Activation of GABA-A receptors during postnatal brain development increases anxiety- and depression-related behaviors in a time- and dose-dependent manner in adult mice［J］.Eur Neuropsychopharmacol,2015,25(8):1260-1274.
［39］Brymer KJ, Fenton EY, Kalynchuk LE, et al. Peripheral etanercept administration normalizes behavior, hippocampal neurogenesis, and hippocampal reelin and GABAA receptor expression in a preclinical model of depression［J］. Front Pharmacol, 2018, 9:121.
［40］Stratton MS, Staros M, Budefeld T, et al. Embryonic GABA(B) receptor blockade alters cell migration, adult hypothalamic structure, and anxiety- and depression-like behaviors sex specifically in mice［J］. PLoS One, 2014, 9(8): e106015.
［41］Sun H, Lu L, Zuo Y, et al. Kainate receptor activation induces glycine receptor endocytosis through PKC deSUMOylation［J］. Nat Commun, 2014, 5: 4980.
［42］Du J, Lü W, Wu S, et al. Glycine receptor mechanism elucidated by electron cryo-microscopy［J］. Nature. 2015, 526(7572): 224-229.
［43］Chang HK, Kim KH, Kang KW, et al. Antidepressants modulate glycine action in rat hippocampus［J］. J Exerc Rehabil, 2015, 11(6): 311-319.
［44］Sluyter R. The P2X7 Receptor［J］. Adv Exp Med Biol, 2017, 1051:17-53.
［45］Burnstock G. P2X ion channel receptors and inflammation［J］. Purinergic Signal, 2016, 12(1): 59-67.
［46］Wang W, Xiang ZH, Jiang CL, et al. Effects of antidepressants on P2X7 receptors［J］. Psychiatry Res, 2016, 242: 281-287.
［47］Otrokocsi L, Kittel , Sperlágh B. P2X7 Receptors Drive Spine Synapse Plasticity in the Learned Helplessness Model of Depression［J］. Int J Neuropsychopharmacol, 2017, 20(10): 813-822.
［48］Zhang K,Liu J,You X,et al.P2X7 as a new target for chrysophanol to treat lipopolysaccharide-induced depression in mice［J］. Neurosci Lett, 2016, 613: 60-65.
［49］Yue N, Huang H, Zhu X, et al. Activation of P2X7 receptor and NLRP3 inflammasome assembly in hippocampal glial cells mediates chronic stress-induced depressive-like behaviors［J］. J Neuroinflammation, 2017, 14(1): 102.
［50］Yohn CN,Gergues MM,Samuels BA.The role of 5-HT receptors in depression［J］.Mol Brain,2017,10(1): 28.
［51］Pytka K, Gluch-Lutwin M, Kotańska M, et al. Single administration of HBK-15-a triple 5-HT1A, 5-HT7, and 5-HT3 receptor antagonist-reverses depressive-like behaviors in mouse model of depression induced by corticosterone［J］. Mol Neurobiol, 2018, 55(5):3931-3945.
［52］Radu BM, Banciu A, Banciu DD, et al. Acid-sensing ion channels as potential pharmacological targets in peripheral and central nervous system diseases［J］. Adv Protein Chem Struct Biol, 2016, 103: 137-167.
［53］Mango D, Braksator E, Battaglia G, et al. Acid-sensing ion channel 1a is required for mGlu receptor dependent long-term depression in the hippocampus［J］. Pharmacol Res, 2017, 119: 12-19.
［54］Li WG, Xu TL. Acid-sensing ion channels: a novel therapeutic target for pain and anxiety［J］. Curr Pharm Des, 2015, 21(7): 885-894.
［55］Urbano FJ, Lino NG, González-Inchauspe CM, et al. Acid-sensing ion channels 1a (ASIC1a) inhibit neuromuscular transmission in female mice［J］. Am J Physiol Cell Physiol, 2014, 306(4):C396-406.