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CNS & Neurological Disorders - Drug Targets

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ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

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Review Article

ATP-sensitive Potassium Channel Subunits in Neuroinflammation: Novel Drug Targets in Neurodegenerative Disorders

Author(s): Fatima Maqoud*, Rosa Scala, Malvina Hoxha, Bruno Zappacosta and Domenico Tricarico

Volume 21, Issue 2, 2022

Published on: 24 November, 2021

Page: [130 - 149] Pages: 20

DOI: 10.2174/1871527320666210119095626

Price: $65

Abstract

Arachidonic acids and its metabolites modulate plenty of ligand-gated, voltage-dependent ion channels, and metabolically regulated potassium channels including ATP-sensitive potassium channels (KATP). KATP channels are hetero-multimeric complexes of sulfonylureas receptors (SUR1, SUR2A or SUR2B) and the pore-forming subunits (Kir6.1 and Kir6.2) likewise expressed in the pre-post synapsis of neurons and inflammatory cells, thereby affecting their proliferation and activity. KATP channels are involved in amyloid-β (Aβ)-induced pathology, therefore emerging as therapeutic targets against Alzheimer’s and related diseases. The modulation of these channels can represent an innovative strategy for the treatment of neurodegenerative disorders; nevertheless, the currently available drugs are not selective for brain KATP channels and show contrasting effects. This phenomenon can be a consequence of the multiple physiological roles of the different varieties of KATP channels. Openings of cardiac and muscular KATP channel subunits, are protective against caspase-dependent atrophy in these tissues and some neurodegenerative disorders, whereas in some neuroinflammatory diseases, benefits can be obtained through the inhibition of neuronal KATP channel subunits. For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-α or SUR1-Trpm4/ Nos2/ROS signaling. Despite this strategy being promising, glibenclamide may have limited clinical efficacy due to its unselective blocking action of SUR2A/B subunits also expressed in cardiovascular apparatus with pro-arrhythmic effects and SUR1 expressed in pancreatic beta cells with hypoglycemic risk. Alternatively, neuronal selective dual modulators showing agonist/antagonist actions on KATP channels can be an option.

Keywords: Inflammation, arachidonic acids, ion channel, neurodegeneration, KATP channel, pharmacology

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[1]
Lu Q, Peevey J, Jow F, et al. Disruption of Kv1.1 N-type inactivation by novel small molecule inhibitors (disinactivators). Bioorg Med Chem 2008; 16(6): 3067-75.
[http://dx.doi.org/10.1016/j.bmc.2007.12.031] [PMID: 18226531]
[2]
Illingworth MA, Hanrahan D, Anderson CE, et al. Elevated VGKC-complex antibodies in a boy with fever-induced refractory epileptic encephalopathy in school-age children (FIRES). Dev Med Child Neurol 2011; 53(11): 1053-7.
[http://dx.doi.org/10.1111/j.1469-8749.2011.04008.x] [PMID: 21592118]
[3]
Somers KJ, Lennon VA, Rundell JR, et al. Psychiatric manifestations of voltage-gated potassium-channel complex autoimmunity. J Neuropsychiatry Clin Neurosci 2011; 23(4): 425-33.
[http://dx.doi.org/10.1176/jnp.23.4.jnp425] [PMID: 22231314]
[4]
Imbrici P, D’Adamo MC, Kullmann DM, Pessia M. Episodic ataxia type 1 mutations in the KCNA1 gene impair the fast inactivation properties of the human potassium channels Kv1.4-1.1/Kvbeta1.1 and Kv1.4-1.1/Kvbeta1.2. Eur J Neurosci 2006; 24(11): 3073-83.
[http://dx.doi.org/10.1111/j.1460-9568.2006.05186.x] [PMID: 17156368]
[5]
Brew HM, Hallows JL, Tempel BL. Hyperexcitability and reduced low threshold potassium currents in auditory neurons of mice lacking the channel subunit Kv1.1. J Physiol 2003; 548(Pt 1): 1-20.
[http://dx.doi.org/10.1113/jphysiol.2002.035568] [PMID: 12611922]
[6]
Dodson PD, Billups B, Rusznák Z, Szûcs G, Barker MC, Forsythe ID. Presynaptic rat Kv1.2 channels suppress synaptic terminal hyperexcitability following action potential invasion. J Physiol 2003; 550(Pt 1): 27-33.
[http://dx.doi.org/10.1113/jphysiol.2003.046250] [PMID: 12777451]
[7]
Shah NH, Aizenman E. Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration. Transl Stroke Res 2014; 5(1): 38-58.
[http://dx.doi.org/10.1007/s12975-013-0297-7] [PMID: 24323720]
[8]
Otto JF, Singh NA, Dahle EJ, et al. Electroconvulsive seizure thresholds and kindling acquisition rates are altered in mouse models of human KCNQ2 and KCNQ3 mutations for benign familial neonatal convulsions. Epilepsia 2009; 50(7): 1752-9.
[http://dx.doi.org/10.1111/j.1528-1167.2009.02100.x] [PMID: 19453707]
[9]
McLaughlin B, Hartnett KA, Erhardt JA, et al. Caspase 3 activation is essential for neuroprotection in preconditioning. Proc Natl Acad Sci USA 2003; 100(2): 715-20.
[http://dx.doi.org/10.1073/pnas.0232966100] [PMID: 12522260]
[10]
Redman PT, Jefferson BS, Ziegler CB, et al. A vital role for voltage-dependent potassium channels in dopamine transporter-mediated 6-hydroxydopamine neurotoxicity. Neuroscience 2006; 143(1): 1-6.
[http://dx.doi.org/10.1016/j.neuroscience.2006.08.039] [PMID: 17027171]
[11]
Redman PT, He K, Hartnett KA, et al. Apoptotic surge of potassium currents is mediated by p38 phosphorylation of Kv2.1. Proc Natl Acad Sci USA 2007; 104(9): 3568-73.
[http://dx.doi.org/10.1073/pnas.0610159104] [PMID: 17360683]
[12]
Aras MA, Aizenman E. Obligatory role of ASK1 in the apoptotic surge of K+ currents. Neurosci Lett 2005; 387(3): 136-40.
[http://dx.doi.org/10.1016/j.neulet.2005.06.024] [PMID: 16006035]
[13]
Castel H, Vaudry D, Mei YA, et al. The delayed rectifier channel current IK plays a key role in the control of programmed cell death by PACAP and ethanol in cerebellar granule neurons. Ann N Y Acad Sci 2006; 1070: 173-9.
[http://dx.doi.org/10.1196/annals.1317.008] [PMID: 16888161]
[14]
Monaghan MM, Menegola M, Vacher H, Rhodes KJ, Trimmer JS. Altered expression and localization of hippocampal A-type potassium channel subunits in the pilocarpine-induced model of temporal lobe epilepsy. Neuroscience 2008; 156(3): 550-62.
[http://dx.doi.org/10.1016/j.neuroscience.2008.07.057] [PMID: 18727953]
[15]
Bernard C, Anderson A, Becker A, Poolos NP, Beck H, Johnston D. Acquired dendritic channelopathy in temporal lobe epilepsy. Science 2004; 305(5683): 532-5.
[http://dx.doi.org/10.1126/science.1097065] [PMID: 15273397]
[16]
Lau D, Vega-Saenz de Miera EC, Contreras D, et al. Impaired fast-spiking, suppressed cortical inhibition, and increased susceptibility to seizures in mice lacking Kv3.2 K+ channel proteins. J Neurosci 2000; 20(24): 9071-85.
[http://dx.doi.org/10.1523/JNEUROSCI.20-24-09071.2000] [PMID: 11124984]
[17]
Barnwell LFS, Lugo JN, Lee WL, et al. Kv4.2 knockout mice demonstrate increased susceptibility to convulsant stimulation. Epilepsia 2009; 50(7): 1741-51.
[http://dx.doi.org/10.1111/j.1528-1167.2009.02086.x] [PMID: 19453702]
[18]
Zhang P, Xiang N, Chen Y, et al. Family-based association analysis to finemap bipolar linkage peak on chromosome 8q24 using 2,500 genotyped SNPs and 15,000 imputed SNPs. Bipolar Disord 2010; 12(8): 786-92.
[http://dx.doi.org/10.1111/j.1399-5618.2010.00883.x] [PMID: 21176025]
[19]
Psychiatric GWAS Consortium Bipolar Disorder Working Group. Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4. Nat Genet 2011; 43(10): 977-83.
[http://dx.doi.org/10.1038/ng.943] [PMID: 21926972]
[20]
Kristensen LV, Sandager-Nielsen K, Hansen HH. K(v) 7 (KCNQ) channel openers normalize central 2-deoxyglucose uptake in a mouse model of mania and increase prefrontal cortical and hippocampal serine-9 phosphorylation levels of GSK3β. J Neurochem 2012; 121(3): 373-82.
[http://dx.doi.org/10.1111/j.1471-4159.2012.07704.x] [PMID: 22356228]
[21]
Biervert C, Schroeder BC, Kubisch C, et al. A potassium channel mutation in neonatal human epilepsy. Science 1998; 279(5349): 403-6.
[http://dx.doi.org/10.1126/science.279.5349.403] [PMID: 9430594]
[22]
Ishii A, Fukuma G, Uehara A, et al. A de novo KCNQ2 mutation detected in non-familial benign neonatal convulsions. Brain Dev 2009; 31(1): 27-33.
[http://dx.doi.org/10.1016/j.braindev.2008.05.010] [PMID: 18640800]
[23]
Miranda P, Cadaveira-Mosquera A, González-Montelongo R, et al. The neuronal serum- and glucocorticoid-regulated kinase 1.1 reduces neuronal excitability and protects against seizures through upregulation of the M-current. J Neurosci 2013; 33(6): 2684-96.
[http://dx.doi.org/10.1523/JNEUROSCI.3442-12.2013] [PMID: 23392695]
[24]
Peters HC, Hu H, Pongs O, Storm JF, Isbrandt D. Conditional transgenic suppression of M channels in mouse brain reveals functions in neuronal excitability, resonance and behavior. Nat Neurosci 2005; 8(1): 51-60.
[http://dx.doi.org/10.1038/nn1375] [PMID: 15608631]
[25]
Yamada K, Iwayama Y, Toyota T, et al. Association study of the KCNJ3 gene as a susceptibility candidate for schizophrenia in the Chinese population. Hum Genet 2012; 131(3): 443-51.
[http://dx.doi.org/10.1007/s00439-011-1089-3] [PMID: 21927946]
[26]
Ohno Y, Hibino H, Lossin C, Inanobe A, Kurachi Y. Inhibition of astroglial Kir4.1 channels by selective serotonin reuptake inhibitors. Brain Res 2007; 1178: 44-51.
[http://dx.doi.org/10.1016/j.brainres.2007.08.018] [PMID: 17920044]
[27]
Sicca F, Imbrici P, D’Adamo MC, et al. Autism with seizures and intellectual disability: possible causative role of gain-of-function of the inwardly-rectifying K+ channel Kir4.1. Neurobiol Dis 2011; 43(1): 239-47.
[http://dx.doi.org/10.1016/j.nbd.2011.03.016] [PMID: 21458570]
[28]
Williams DM, Lopes CMB, Rosenhouse-Dantsker A, Connelly HL, Matavel A. Molecular Basis of Decreased Kir4.1 Function in SeSAME/EAST Syndrome. J Am Soc Nephrol 2010; 12
[29]
Sala-Rabanal M, Kucheryavykh LY, Skatchkov SN, Eaton MJ, Nichols CG. Molecular mechanisms of EAST/SeSAME syndrome mutations in Kir4.1 (KCNJ10). J Biol Chem 2010; 285(46): 36040-8.
[http://dx.doi.org/10.1074/jbc.M110.163170] [PMID: 20807765]
[30]
Sun T, Zhao C, Hu G, Li M. Iptakalim: a potential antipsychotic drug with novel mechanisms? Eur J Pharmacol 2010; 634(1-3): 68-76.
[http://dx.doi.org/10.1016/j.ejphar.2010.02.024] [PMID: 20184878]
[31]
Mele A, Mantuano P, De Bellis M, et al. A long-term treatment with taurine prevents cardiac dysfunction in mdx mice. Transl Res 2019; 204: 82-99.
[http://dx.doi.org/10.1016/j.trsl.2018.09.004] [PMID: 30347179]
[32]
Gargus JJ. Ion channel functional candidate genes in multigenic neuropsychiatric disease. Biol Psychiatry 2006; 60(2): 177-85.
[http://dx.doi.org/10.1016/j.biopsych.2005.12.008] [PMID: 16497276]
[33]
Grube S, Gerchen MF, Adamcio B, et al. A CAG repeat polymorphism of KCNN3 predicts SK3 channel function and cognitive performance in schizophrenia. EMBO Mol Med 2011; 3(6): 309-19.
[http://dx.doi.org/10.1002/emmm.201100135] [PMID: 21433290]
[34]
Laumonnier F, Roger S, Guérin P, et al. Association of a functional deficit of the BK Ca Channel, a synaptic regulator of neuronal excitability, with autism and mental retardation. Am J Psychiatry 2006; 163(9): 1622-9.
[http://dx.doi.org/10.1176/ajp.2006.163.9.1622] [PMID: 16946189]
[35]
Behrens R, Nolting A, Reimann F, Schwarz M, Waldschütz R, Pongs O. hKCNMB3 and hKCNMB4, cloning and characterization of two members of the large-conductance calcium-activated potassium channel beta subunit family. FEBS Lett 2000; 474(1): 99-106.
[http://dx.doi.org/10.1016/S0014-5793(00)01584-2] [PMID: 10828459]
[36]
Riazi MA, Brinkman-Mills P, Johnson A, et al. Identification of a putative regulatory subunit of a calcium-activated potassium channel in the dup(3q) syndrome region and a related sequence on 22q11.2. Genomics 1999; 62(1): 90-4.
[http://dx.doi.org/10.1006/geno.1999.5975] [PMID: 10585773]
[37]
Sánchez-Rodríguez I, Gruart A, Delgado-García JM, Jiménez-Díaz L, Navarro-López JD. Role of girk channels in long-term potentiation of synaptic inhibition in an in vivo mouse model of early amyloid- β pathology. Int J Mol Sci 2019; 5: 1168.
[38]
Scala R, Maqoud F, Angelelli M, et al. Zoledronic acid modulation of TRPV1 Channel currents in osteoblast cell line and native rat and mouse bone marrow-derived osteoblasts: cell proliferation and mineralization effect. Cancers (Basel) 2019; 2: E206.
[39]
Maljevic S, Lerche H. Potassium channels: a review of broadening therapeutic possibilities for neurological diseases. J Neurol 2013; 260(9): 2201-11.
[http://dx.doi.org/10.1007/s00415-012-6727-8] [PMID: 23142946]
[40]
Ion Channels. British Journal of Pharmacology 2011; 164(Suppl 1): S137-74.
[41]
Hibino H, Inanobe A, Furutani K, Murakami S, Findlay I, Kurachi Y. Inwardly rectifying potassium channels: their structure, function, and physiological roles. Physiol Rev 2010; 90(1): 291-366.
[http://dx.doi.org/10.1152/physrev.00021.2009] [PMID: 20086079]
[42]
Jan LY, Jan YN. Voltage-gated potassium channels and the diversity of electrical signalling. J Physiol 2012; 590(11): 2591-9.
[http://dx.doi.org/10.1113/jphysiol.2011.224212] [PMID: 22431339]
[43]
Lawson K, McKay NG. Modulation of potassium channels as a therapeutic approach. Curr Pharm Des 2006; 12(4): 459-70.
[http://dx.doi.org/10.2174/138161206775474477] [PMID: 16472139]
[44]
Gutman GA, Chandy KG, Grissmer S, et al. International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels. Pharmacol Rev 2005; 57(4): 473-508.
[http://dx.doi.org/10.1124/pr.57.4.10] [PMID: 16382104]
[45]
Goldstein SAN, Bayliss DA, Kim D, Lesage F, Plant LD, Rajan S. International Union of Pharmacology. LV. Nomenclature and molecular relationships of two-P potassium channels. Pharmacol Rev 2005; 57(4): 527-40.
[http://dx.doi.org/10.1124/pr.57.4.12] [PMID: 16382106]
[46]
Maqoud F, Curci A, Scala R, et al. Cell Cycle Regulation by Ca(2+)-Activated K(+) (BK) channels modulators in SH-SY5Y Neuroblastoma Cells. Int J Mol Sci 2018; 8: 2442.
[47]
Curci A, Mele A, Camerino GM, Dinardo MM, Tricarico D. The large conductance Ca(2+) -activated K(+) (BKCa) channel regulates cell proliferation in SH-SY5Y neuroblastoma cells by activating the staurosporine-sensitive protein kinases. Front Physiol 2014; 5: 476.
[http://dx.doi.org/10.3389/fphys.2014.00476] [PMID: 25538629]
[48]
Tricarico D, Mele A, Calzolaro S, et al. Emerging role of calcium-activated potassium channel in the regulation of cell viability following potassium ions challenge in HEK293 cells and pharmacological modulation. PLoS One 2013; 7: e69551.
[49]
Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet 2013; 4: 76.
[http://dx.doi.org/10.3389/fgene.2013.00076] [PMID: 23675382]
[50]
Imbrici P, D’Adamo MC, Cusimano A, Pessia M. Episodic ataxia type 1 mutation F184C alters Zn2+-induced modulation of the human K+ channel Kv1.4-Kv1.1/Kvbeta1.1. Am J Physiol Cell Physiol 2007; 292(2): C778-87.
[http://dx.doi.org/10.1152/ajpcell.00259.2006] [PMID: 16956965]
[51]
Imbrici P, Liantonio A, Camerino GM, et al. Therapeutic approaches to genetic ion channelopathies and perspectives in drug discovery. Front Pharmacol 2016; 7: 121.
[http://dx.doi.org/10.3389/fphar.2016.00121]
[52]
Ashcroft FM, Harrison DE, Ashcroft SJ. Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells. Nature 1984; 312(5993): 446-8.
[http://dx.doi.org/10.1038/312446a0] [PMID: 6095103]
[53]
Nichols CG. KATP channels as molecular sensors of cellular metabolism. Nature 2006; 440(7083): 470-6.
[http://dx.doi.org/10.1038/nature04711] [PMID: 16554807]
[54]
Ashcroft FM, Gribble FM. ATP-sensitive K+ channels and insulin secretion: their role in health and disease. Diabetologia 1999; 42(8): 903-19.
[http://dx.doi.org/10.1007/s001250051247] [PMID: 10491749]
[55]
Ashcroft FM. ATP-sensitive K+ channels and disease: from molecule to malady. Am J Physiol Endocrinol Metab 2007; 293(4): E880-9.
[http://dx.doi.org/10.1152/ajpendo.00348.2007] [PMID: 17652156]
[56]
Liss B, Haeckel O, Wildmann J, Miki T, Seino S, Roeper J. K-ATP channels promote the differential degeneration of dopaminergic midbrain neurons. Nat Neurosci 2005; 8(12): 1742-51.
[http://dx.doi.org/10.1038/nn1570] [PMID: 16299504]
[57]
Kanno T, Rorsman P, Göpel SO. Glucose-dependent regulation of rhythmic action potential firing in pancreatic β-cells by K(ATP)-channel modulation. J Physiol 2002; 545(2): 501-7.
[http://dx.doi.org/10.1113/jphysiol.2002.031344] [PMID: 12456829]
[58]
Hillmann K, Garcia Bartels N, Kottner J, Stroux A, Canfield D, Blume-Peytavi U. A Single-centre, randomized, double-blind, placebo-controlled clinical trial to investigate the efficacy and safety of minoxidil topical foam in frontotemporal and vertex androgenetic alopecia in men. Skin Pharmacol Physiol 2015; 28(5): 236-44.
[http://dx.doi.org/10.1159/000375320] [PMID: 25765348]
[59]
Dragicevic E, Schiemann J, Liss B. Dopamine midbrain neurons in health and Parkinson’s disease: emerging roles of voltage-gated calcium channels and ATP-sensitive potassium channels. Neuroscience 2015; 284: 798-814.
[http://dx.doi.org/10.1016/j.neuroscience.2014.10.037] [PMID: 25450964]
[60]
Yamada K, Inagaki N. Neuroprotection by KATP channels. J Mol Cell Cardiol 2005; 38(6): 945-9.
[http://dx.doi.org/10.1016/j.yjmcc.2004.11.020] [PMID: 15910879]
[61]
Soundarapandian MM, Zhong X, Peng L, Wu D, Lu Y. Role of K(ATP) channels in protection against neuronal excitatory insults. J Neurochem 2007; 103(5): 1721-9.
[http://dx.doi.org/10.1111/j.1471-4159.2007.04963.x] [PMID: 17944875]
[62]
Huang Y, McClenaghan C, Harter TM, et al. Cardiovascular consequences of KATP overactivity in Cantu syndrome. JCI insight 2018; 15: e121153.
[http://dx.doi.org/10.1172/jci.insight.121153]
[63]
Smeland MF, McClenaghan C, Roessler HI, et al. ABCC9-related Intellectual disability Myopathy Syndrome is a K(ATP) channelopathy with loss-of-function mutations in ABCC9. Nat Commun 2019; 1: 4457.
[64]
Shimomura K, Flanagan SE, Zadek B, et al. Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinism. EMBO Mol Med 2009; 1(3): 166-77.
[http://dx.doi.org/10.1002/emmm.200900018] [PMID: 20049716]
[65]
Grange DK, Nichols CG, Singh GK. Cantu syndrome and related disorders. GeneReviews® 2014; 1993-2020.
[66]
Nguyen HM, Grössinger EM, Horiuchi M, et al. Differential Kv1.3, KCa3.1, and Kir2.1 expression in “classically” and “alternatively” activated microglia. Glia 2017; 65(1): 106-21.
[http://dx.doi.org/10.1002/glia.23078] [PMID: 27696527]
[67]
Blomster LV, Strøbaek D, Hougaard C, et al. Quantification of the functional expression of the Ca2+ -activated K+ channel KCa 3.1 on microglia from adult human neocortical tissue. Glia 2016; 64(12): 2065-78.
[http://dx.doi.org/10.1002/glia.23040] [PMID: 27470924]
[68]
Wulff H, Miller MJ, Hänsel W, Grissmer S, Cahalan MD, Chandy KG. Design of a Potent and Selective Inhibitor of the Intermediate-Conductance Ca2+ -activated K+ Channel, IKCa1: A Potential Immunosuppressant. Proc Natl Acad Sci 2000; 97(14): 8151.
[69]
Kettenmann H, Hanisch UK, Noda M, Verkhratsky A. Physiology of microglia. Physiol Rev 2011; 91(2): 461-553.
[http://dx.doi.org/10.1152/physrev.00011.2010] [PMID: 21527731]
[70]
Du RH, Sun HB, Hu ZL, Lu M, Ding JH, Hu G. Kir6.1/K-ATP channel modulates microglia phenotypes: implication in Parkinson’s disease. Cell Death Dis 2018; 9(3): 404.
[71]
Zhou Y, Lu M, Du RH, et al. MicroRNA-7 targets Nod-like receptor protein 3 inflammasome to modulate neuroinflammation in the pathogenesis of Parkinson’s disease. Mol Neurodegener 2016; 11: 28.
[http://dx.doi.org/10.1186/s13024-016-0094-3] [PMID: 27084336]
[72]
Colton CA. Heterogeneity of microglial activation in the innate immune response in the brain. J neuroimmune Pharmacol 2009; 4(4): 399-418.
[73]
Block ML, Zecca L, Hong JS. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nat Rev Neurosci 2007; 8(1): 57-69.
[http://dx.doi.org/10.1038/nrn2038] [PMID: 17180163]
[74]
Li R, Huang YG, Fang D, Le WD. (-)-Epigallocatechin gallate inhibits lipopolysaccharide-induced microglial activation and protects against inflammation-mediated dopaminergic neuronal injury. J Neurosci Res 2004; 78(5): 723-31.
[http://dx.doi.org/10.1002/jnr.20315] [PMID: 15478178]
[75]
Colton C, Wilcock DM. Assessing activation states in microglia. CNS Neurol Disord Drug Targets 2010; 9(2): 174-91.
[http://dx.doi.org/10.2174/187152710791012053] [PMID: 20205642]
[76]
Ponomarev ED, Maresz K, Tan Y, Dittel BN. CNS-derived interleukin-4 is essential for the regulation of autoimmune inflammation and induces a state of alternative activation in microglial cells. J Neurosci 2007; 27(40): 10714-21.
[http://dx.doi.org/10.1523/JNEUROSCI.1922-07.2007] [PMID: 17913905]
[77]
Colton CA, Mott RT, Sharpe H, Xu Q, Van Nostrand WE, Vitek MP. Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD. J Neuroinflammation 2006; 3(1): 27.
[78]
Sawada M, Suzumura A, Hosoya H, Marunouchi T, Nagatsu T. Interleukin-10 inhibits both production of cytokines and expression of cytokine receptors in microglia. J Neurochem 1999; 72(4): 1466-71.
[http://dx.doi.org/10.1046/j.1471-4159.1999.721466.x] [PMID: 10098850]
[79]
Orihuela R, McPherson CA, Harry GJ. Microglial M1/M2 polarization and metabolic states. Br J Pharmacol 2016; 173(4): 649-65.
[http://dx.doi.org/10.1111/bph.13139] [PMID: 25800044]
[80]
Butovsky O, Jedrychowski MP, Moore CS, et al. Identification of a unique TGF-β-dependent molecular and functional signature in microglia. Nat Neurosci 2014; 17(1): 131-43.
[http://dx.doi.org/10.1038/nn.3599] [PMID: 24316888]
[81]
Nguyen HM, Blomster LV, Christophersen P, Wulff H. Potassium channel expression and function in microglia: Plasticity and possible species variations. Channels (Austin) 2017; 11(4): 305-15.
[http://dx.doi.org/10.1080/19336950.2017.1300738] [PMID: 28277939]
[82]
Rangaraju S, Gearing M, Jin LW, Levey A. Potassium channel Kv1.3 is highly expressed by microglia in human Alzheimer’s disease. J Alzheimers Dis 2015; 44(3): 797-808.
[http://dx.doi.org/10.3233/JAD-141704] [PMID: 25362031]
[83]
Rus H, Pardo CA, Hu L, et al. The voltage-gated potassium channel Kv1.3 is highly expressed on inflammatory infiltrates in multiple sclerosis brain.sss Proc Natl Acad Sci 2005; 102(31): 11094-9.
[84]
Rassendren F, Audinat E. Purinergic signaling in epilepsy. J Neurosci Res 2016; 94(9): 781-93.
[http://dx.doi.org/10.1002/jnr.23770] [PMID: 27302739]
[85]
Ferreira R, Lively S, Schlichter LC. IL-4 type 1 receptor signaling up-regulates KCNN4 expression, and increases the KCa3.1 current and its contribution to migration of alternative-activated microglia. Front Cell Neurosci 2014; 8: 183.
[http://dx.doi.org/10.3389/fncel.2014.00183] [PMID: 25071444]
[86]
Schlichter LC, Kaushal V, Moxon-Emre I, Sivagnanam V, Vincent C. The Ca2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro. J Neuroinflammation 2010; 7: 1-4.
[87]
Yang JZ, Huang X, Zhao FF, Xu Q, Hu G. Iptakalim enhances adult mouse hippocampal neurogenesis via opening Kir6.1-composed K-ATP channels expressed in neural stem cells. CNS Neurosci Ther 2012; 18(9): 737-44.
[http://dx.doi.org/10.1111/j.1755-5949.2012.00359.x] [PMID: 22742873]
[88]
Crous-Bou M, Minguillón C, Gramunt N, Molinuevo JL. Alzheimer’s disease prevention: from risk factors to early intervention. Alzheimers Res Ther 2017; 9(1): 71.
[http://dx.doi.org/10.1186/s13195-017-0297-z]
[89]
Mangialasche F, Solomon A, Winblad B, Mecocci P, Kivipelto M. Alzheimer’s disease: clinical trials and drug development. Lancet Neurol 2010; 9(7): 702-16.
[http://dx.doi.org/10.1016/S1474-4422(10)70119-8] [PMID: 20610346]
[90]
Mecocci P, Baroni M, Senin U, Boccardi V. Brain aging and late-onset alzheimer’s disease: a matter of increased amyloid or reduced energy? J Alzheimers Dis 2018; 64(s1): S397-404.
[http://dx.doi.org/10.3233/JAD-179903] [PMID: 29562513]
[91]
Huang Y, Mucke L. Alzheimer mechanisms and therapeutic strategies. Cell 2012; 148(6): 1204-22.
[http://dx.doi.org/10.1016/j.cell.2012.02.040] [PMID: 22424230]
[92]
Tönnies E, Trushina E. Oxidative stress, synaptic dysfunction, and Alzheimer’s Disease. J Alzheimers Dis 2017; 57(4): 1105-21.
[http://dx.doi.org/10.3233/JAD-161088] [PMID: 28059794]
[93]
Reddy PH, Tripathi R, Troung Q, et al. Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer’s disease: implications to mitochondria-targeted antioxidant therapeutics. Biochim Biophys Acta 2012; 1822(5): 639-49.
[http://dx.doi.org/10.1016/j.bbadis.2011.10.011] [PMID: 22037588]
[94]
Reddy PH. A Critical assessment of research on neurotransmitters in Alzheimer’s Disease. J Alzheimers Dis 2017; 57(4): 969-74.
[http://dx.doi.org/10.3233/JAD-170256] [PMID: 28409748]
[95]
Frazzini V, Guarnieri S, Bomba M, et al. Altered Kv2.1 functioning promotes increased excitability in hippocampal neurons of an Alzheimer’s disease mouse model. Cell Death Dis 2016; 7(2): e2100.
[http://dx.doi.org/10.1038/cddis.2016.18] [PMID: 26890139]
[96]
Palop JJ, Chin J, Roberson ED, et al. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer’s disease. Neuron 2007; 55(5): 697-711.
[http://dx.doi.org/10.1016/j.neuron.2007.07.025] [PMID: 17785178]
[97]
Charolidi N, Schilling T, Eder C. Microglial Kv1.3 Channels and P2Y12 receptors differentially regulate cytokine and chemokine release from brain slices of young Adult and aged mice. PLoS One 2015; 10(5): e01287463.
[98]
Bruunsgaard H, Pedersen M, Pedersen BK. Aging and proinflammatory cytokines. Curr Opin Hematol 2001; 8(3): 131-6.
[http://dx.doi.org/10.1097/00062752-200105000-00001] [PMID: 11303144]
[99]
Sesti F. Oxidation of K(+) Channels in Aging and Neurodegeneration. Aging Dis 2016; 7(2): 130-5.
[http://dx.doi.org/10.14336/AD.2015.0901] [PMID: 27114846]
[100]
Hornberger M, Wong S, Tan R, et al. In vivo and post-mortem memory circuit integrity in frontotemporal dementia and Alzheimer’s disease. Brain 2012; 135(Pt 10): 3015-25.
[http://dx.doi.org/10.1093/brain/aws239] [PMID: 23012333]
[101]
Ikeda M, Dewar D, McCulloch J. Selective reduction of [125I]apamin binding sites in Alzheimer hippocampus: a quantitative autoradiographic study. Brain Res 1991; 567(1): 51-6.
[http://dx.doi.org/10.1016/0006-8993(91)91434-3] [PMID: 1667746]
[102]
Plant LD, Webster NJ, Boyle JP, et al. Amyloid β peptide as a physiological modulator of neuronal ‘A’-type K+ current. Neurobiol Aging 2006; 27(11): 1673-83.
[http://dx.doi.org/10.1016/j.neurobiolaging.2005.09.038] [PMID: 16271805]
[103]
Ramsden M, Henderson Z, Pearson HA. Modulation of Ca2+ channel currents in primary cultures of rat cortical neurones by amyloid β protein (1-40) is dependent on solubility status. Brain Res 2002; 956(2): 254-61.
[http://dx.doi.org/10.1016/S0006-8993(02)03547-3] [PMID: 12445693]
[104]
Chung S, Lee J, Joe EH, Uhm DY. β-amyloid peptide induces the expression of voltage dependent outward rectifying K+ channels in rat microglia. Neurosci Lett 2001; 300(2): 67-70.
[http://dx.doi.org/10.1016/S0304-3940(01)01516-6] [PMID: 11207376]
[105]
Schilling T, Eder C. Amyloid-β-induced reactive oxygen species production and priming are differentially regulated by ion channels in microglia. J Cell Physiol 2011; 226(12): 3295-302.
[http://dx.doi.org/10.1002/jcp.22675] [PMID: 21321937]
[106]
Franciosi S, Ryu JK, Choi HB, Radov L, Kim SU, McLarnon JG. Broad-spectrum Effects of 4-aminopyridine to Modulate Amyloid beta1-42-induced Cell Signaling and Functional Responses in Human Microglia. J Neurosci 2006; 45: 11652-64.
[107]
Maezawa I, Jenkins DP, Jin BE, Wulff H. Microglial KCa3.1 Channels as a potential therapeutic target for Alzheimer’s Disease. Int J Alzheimers Dis 2012; 2012
[http://dx.doi.org/10.1155/2012/868972] [PMID: 22675649]
[108]
Frautschy SA, Yang F, Irrizarry M, et al. Microglial response to amyloid plaques in APPsw transgenic mice. Am J Pathol 1998; 152(1): 307-17.
[PMID: 9422548]
[109]
Lucin KM, Wyss-Coray T. Immune activation in brain aging and neurodegeneration: too much or too little? Neuron 2009; 64(1): 110-22.
[http://dx.doi.org/10.1016/j.neuron.2009.08.039] [PMID: 19840553]
[110]
Cameron B, Landreth GE. Inflammation, microglia, and Alzheimer’s disease. Neurobiol Dis 2010; 37(3): 503-9.
[http://dx.doi.org/10.1016/j.nbd.2009.10.006] [PMID: 19833208]
[111]
Okello A, Edison P, Archer HA, et al. Microglial activation and amyloid deposition in mild cognitive impairment. Neurology 2009; 72(1): 56-62.
[http://dx.doi.org/10.1212/01.wnl.0000338622.27876.0d]
[112]
Rogers J. The inflammatory response in Alzheimer’s disease. J Periodontol 2008; 79(8)(Suppl.): 1535-43.
[http://dx.doi.org/10.1902/jop.2008.080171] [PMID: 18673008]
[113]
Jimenez S, Baglietto-Vargas D, Caballero C, et al. Inflammatory Response in the Hippocampus of PS1M146L/APP751SL Mouse Model of Alzheimer's Disease: Age-dependent switch in the microglial phenotype from alternative to classic. J Neurosci 2008; 45: 11650-61.
[114]
McGeer EG, McGeer PL. Neuroinflammation in Alzheimer’s disease and mild cognitive impairment: a field in its infancy. J Alzheimers Dis 2010; 19(1): 355-61.
[http://dx.doi.org/10.3233/JAD-2010-1219] [PMID: 20061650]
[115]
Martin BK, Szekely C, Brandt J, et al. ADAPT Research Group. Cognitive function over time in the Alzheimer’s Disease Anti-inflammatory Prevention Trial (ADAPT): results of a randomized, controlled trial of naproxen and celecoxib. Arch Neurol 2008; 65(7): 896-905.
[http://dx.doi.org/10.1001/archneur.2008.65.7.nct70006] [PMID: 18474729]
[116]
Lyketsos CG, Breitner J C S, Green R C, et al. ADAPT Research Group. Naproxen and celecoxib do not prevent AD in early results from a randomized controlled trial. Neurology 2007; 68(21): 1800-8.
[117]
Nörenberg W, Gebicke-Haerter PJ, Illes P. Voltage-dependent potassium channels in activated rat microglia. J Physiol 1994; 475(1): 15-32.
[http://dx.doi.org/10.1113/jphysiol.1994.sp020046] [PMID: 7514664]
[118]
Mayordomo-Cava J, Yajeya J, Navarro-López JD, Jiménez-Díaz L. Amyloid-β(25-35) Modulates the Expression of GirK and KCNQ channel genes in the hippocampus. PLoS One 2015; 10(7): e0134385.
[119]
May LM, Anggono V, Gooch HM, et al. G-Protein-coupled inwardly rectifying Potassium (GIRK) channel activation by the p75 neurotrophin receptor is required for Amyloid β Toxicity. Front Neurosci 2017; 11: 455.
[http://dx.doi.org/10.3389/fnins.2017.00455] [PMID: 28848381]
[120]
Wilcock DM, Vitek MP, Colton CA. Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer’s disease. Neuroscience 2009; 159(3): 1055-69.
[http://dx.doi.org/10.1016/j.neuroscience.2009.01.023] [PMID: 19356689]
[121]
Ma G, Gao J, Fu Q, et al. Diazoxide reverses the enhanced expression of KATP subunits in cholinergic neurons caused by exposure to Aβ1-42. Neurochem Res 2009; 34(12): 2133.
[http://dx.doi.org/10.1007/s11064-009-0007-8]
[122]
Liu D, Pitta M, Lee JH, et al. The KATP channel activator diazoxide ameliorates amyloid-β and tau pathologies and improves memory in the 3xTgAD mouse model of Alzheimer’s disease. J Alzheimers Dis 2010; 22(2): 443-57.
[http://dx.doi.org/10.3233/JAD-2010-101017] [PMID: 20847430]
[123]
Griffith CM, Xie MX, Qiu WY, et al. Aberrant expression of the pore-forming KATP channel subunit Kir6.2 in hippocampal reactive astrocytes in the 3xTg-AD mouse model and human Alzheimer’s disease. Neuroscience 2016; 336: 81-101.
[http://dx.doi.org/10.1016/j.neuroscience.2016.08.034] [PMID: 27586053]
[124]
Moriguchi S, Ishizuka T, Yabuki Y, et al. Blockade of the KATP channel Kir6.2 by memantine represents a novel mechanism relevant to Alzheimer’s disease therapy. Mol Psychiatry 2018; 23(2): 211-21.
[http://dx.doi.org/10.1038/mp.2016.187] [PMID: 27777420]
[125]
Esmaeili MH, Bahari B, Salari AA. ATP-sensitive potassium-channel inhibitor glibenclamide attenuates HPA axis hyperactivity, depression- and anxiety-related symptoms in a rat model of Alzheimer’s disease. Brain Res Bull 2018; 137: 265-76.
[http://dx.doi.org/10.1016/j.brainresbull.2018.01.001] [PMID: 29307659]
[126]
Li Y, Ba M, Du Y, et al. Aβ1-42 increases the expression of neural KATP subunits Kir6.2/SUR1 via the NF-κB, p38 MAPK and PKC signal pathways in rat primary cholinergic neurons. Hum Exp Toxicol 2019; 38(6): 665-74.
[http://dx.doi.org/10.1177/0960327119833742] [PMID: 30868916]
[127]
Thei L, Imm J, Kaisis E, Dallas ML, Kerrigan TL. Microglia in Alzheimer’s Disease: A Role for Ion Channels. Front Neurosci 2018; 12: 676.
[http://dx.doi.org/10.3389/fnins.2018.00676] [PMID: 30323735]
[128]
Rangaraju S, Dammer EB, Raza SA, et al. Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer’s disease. Mol Neurodegener 2018; 13(1): 24.
[http://dx.doi.org/10.1186/s13024-018-0254-8]
[129]
Pannasch U, Färber K, Nolte C, et al. The potassium channels Kv1.5 and Kv1.3 modulate distinct functions of microglia. Mol Cell Neurosci 2006; 33(4): 401-11.
[http://dx.doi.org/10.1016/j.mcn.2006.08.009] [PMID: 17055293]
[130]
Lowinus T, Bose T, Busse S, et al. Immunomodulation by memantine in therapy of Alzheimer’s disease is mediated through inhibition of Kv1.3 channels and T cell responsiveness. Oncotarget 2016; 7(33): 53797-807.
[http://dx.doi.org/10.18632/oncotarget.10777] [PMID: 27462773]
[131]
Poulopoulou C, Markakis I, Davaki P, et al. Aberrant modulation of a delayed rectifier potassium channel by glutamate in Alzheimer’s disease. Neurobiol Dis 2010; 37(2): 339-48.
[http://dx.doi.org/10.1016/j.nbd.2009.10.012] [PMID: 19850126]
[132]
Pan Y, Xu X, Tong X, Wang X. Messenger RNA and protein expression analysis of voltage-gated potassium channels in the brain of Abeta(25-35)-treated rats. J Neurosci Res 2004; 77(1): 94-9.
[http://dx.doi.org/10.1002/jnr.20134] [PMID: 15197742]
[133]
Campolongo P, Ratano P, Ciotti MT, et al. Systemic administration of substance P recovers beta amyloid-induced cognitive deficits in rat: involvement of Kv potassium channels. PLoS One 2013; 8(11): e78036s.
[134]
de Silva HA, Aronson JK, Grahame-Smith DG, Jobst KA, Smith AD. Abnormal function of potassium channels in platelets of patients with Alzheimer’s disease. Lancet 1998; 352(9140): 1590-3.
[http://dx.doi.org/10.1016/S0140-6736(98)03200-0] [PMID: 9843105]
[135]
Etcheberrigaray R, Ito E, Oka K, Tofel-Grehl B, Gibson GE, Alkon DL. Potassium channel dysfunction in fibroblasts identifies patients with Alzheimer disease. Proc Natl Acad Sci 1993; 90(17): 8209-13.
[http://dx.doi.org/10.1073/pnas.90.17.8209]
[136]
Wei Y, Shin MR, Sesti F. Oxidation of KCNB1 channels in the human brain and in mouse model of Alzheimer’s disease. Cell Death Dis 2018; 9(8): 820.
[http://dx.doi.org/10.1038/s41419-018-0886-1]
[137]
Yang CT, Lu GL, Hsu SF, et al. Paeonol promotes hippocampal synaptic transmission: The role of the Kv2.1 potassium channel. Eur J Pharmacol 2018; 827: 227-37.
[http://dx.doi.org/10.1016/j.ejphar.2018.03.020] [PMID: 29550337]
[138]
Boscia F, Pannaccione A, Ciccone R, et al. The expression and activity of KV3.4 channel subunits are precociously upregulated in astrocytes exposed to Aβ oligomers and in astrocytes of Alzheimer’s disease Tg2576 mice. Neurobiol Aging 2017; 54: 187-98.
[http://dx.doi.org/10.1016/j.neurobiolaging.2017.03.008] [PMID: 28390823]
[139]
Boda E, Hoxha E, Pini A, Montarolo F, Tempia F. Brain expression of Kv3 subunits during development, adulthood and aging and in a murine model of Alzheimer’s disease. J Mol Neurosci 2012; 46(3): 606-15.
[http://dx.doi.org/10.1007/s12031-011-9648-6] [PMID: 21912965]
[140]
Pannaccione A, Boscia F, Scorziello A, et al. Up-regulation and Increased Activity of KV3.4 Channels and Their Accessory Subunit MinK-related peptide 2 induced by amyloid peptide are involved in apoptotic neuronal death. Mol Pharmacol 2007; 72(3): 665-73.
[141]
Hall AM, Throesch BT, Buckingham SC, et al. Tau-dependent Kv4.2 Depletion and dendritic hyperexcitability in a mouse model of Alzheimer's Disease. J Neurosci 2015; 35(15): 6221-30.
[142]
Chen T, Gai WP, Abbott CA. Dipeptidyl peptidase 10 (DPP10(789)): a voltage gated potassium channel associated protein is abnormally expressed in Alzheimer’s and other neurodegenerative diseases. BioMed Res Int 2014; 2014: 209398.
[PMID: 25025038]
[143]
Durán-González J, Michi ED, Elorza B, et al. Amyloid β peptides modify the expression of antioxidant repair enzymes and a potassium channel in the septohippocampal system. Neurobiol Aging 2013; 34(8): 2071-6.
[http://dx.doi.org/10.1016/j.neurobiolaging.2013.02.005] [PMID: 23473707]
[144]
Proulx É, Fraser P, McLaurin J, Lambe EK. Impaired cholinergic excitation of prefrontal attention circuitry in the TgCRND8 Model of Alzheimer's Disease. J Neurosci 2015; 35(37): 12779-23791.
[145]
Chakroborty S, Kim J, Schneider C, Jacobson C, Molgó J, Stutzmann GE. Early presynaptic and postsynaptic calcium signaling abnormalities mask underlying synaptic depression in presymptomatic Alzheimer's Disease Mice. J Neurosci 2012; 32(24): 8341-53.
[146]
Kaushal V, Koeberle PD, Wang Y, Schlichter LC. The Ca2+-activated K+ Channel KCNN4/KCa3.1 contributes to microglia activation and nitric oxide-dependent neurodegeneration. J Neurosci 2007; 27(1): 234-44.
[147]
Yu Z, Dou F, Wang Y, Hou L, Chen H. Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling. J Neuroinflammation 2018; 15(1): 316.
[148]
Jin LW, Lucente JD, Nguyen HM, et al. Repurposing the KCa3.1 inhibitor senicapoc for Alzheimer’s disease. Ann Clin Transl Neurol 2019; 6(4): 723-38.
[http://dx.doi.org/10.1002/acn3.754] [PMID: 31019997]
[149]
Reich EP, Cui L, Yang L, et al. Blocking ion channel KCNN4 alleviates the symptoms of experimental autoimmune encephalomyelitis in mice. Eur J Immunol 2005; 35(4): 1027-36.
[http://dx.doi.org/10.1002/eji.200425954] [PMID: 15770697]
[150]
Ye H, Jalini S, Mylvaganam S, Carlen P. Activation of large-conductance Ca(2+)-activated K(+) channels depresses basal synaptic transmission in the hippocampal CA1 area in APP (swe/ind) TgCRND8 mice. Neurobiol Aging 2010; 31(4): 591-604.
[http://dx.doi.org/10.1016/j.neurobiolaging.2008.05.012] [PMID: 18547679]
[151]
Yamamoto K, Ueta Y, Wang L, et al. Suppression of a neocortical potassium channel activity by intracellular amyloid-β and its rescue with homer1a. J Neurosci 2011; 31(31): 11100-9.
[152]
Yu Y, Maureira C, Liu X, McCormick D. P/Q and N channels control baseline and spike-triggered calcium levels in neocortical axons and synaptic Boutons. J Neurosci 2010; 30(35): 11858-69.
[153]
Honrath B, Matschke L, Meyer T, et al. SK2 channels regulate mitochondrial respiration and mitochondrial Ca2+ uptake. Cell Death Differ 2017; 24(5): 761-73.
[http://dx.doi.org/10.1038/cdd.2017.2] [PMID: 28282037]
[154]
Dolga AM, Netter MF, Perocchi F, et al. Mitochondrial small conductance SK2 channels prevent glutamate-induced oxytosis and mitochondrial dysfunction. J Biol Chem 2013; 288(15): 10792-804.
[http://dx.doi.org/10.1074/jbc.M113.453522] [PMID: 23430260]
[155]
Przedborski S. The two-century journey of Parkinson disease research. Nat Rev Neurosci 2017; 18(4): 251-9.
[http://dx.doi.org/10.1038/nrn.2017.25] [PMID: 28303016]
[156]
Pires AO, Teixeira FG, Mendes-Pinheiro B, Serra SC, Sousa N, Salgado AJ. Old and new challenges in Parkinson’s disease therapeutics. Prog Neurobiol 2017; 156: 69-89.
[http://dx.doi.org/10.1016/j.pneurobio.2017.04.006] [PMID: 28457671]
[157]
Kieburtz K, Wunderle KB. Parkinson’s disease: evidence for environmental risk factors. Mov Disord 2013; 28(1): 8-13.
[http://dx.doi.org/10.1002/mds.25150] [PMID: 23097348]
[158]
Deleidi M, Gasser T. The role of inflammation in sporadic and familial Parkinson’s disease. Cell Mol Life Sci 2013; 70(22): 4259-73.
[http://dx.doi.org/10.1007/s00018-013-1352-y] [PMID: 23665870]
[159]
Gasser T, Hardy J, Mizuno Y. Milestones in PD genetics. Mov Disord 2011; 26(6): 1042-8.
[http://dx.doi.org/10.1002/mds.23637] [PMID: 21626549]
[160]
Winklhofer KF, Haass C. Mitochondrial dysfunction in Parkinson’s disease. Biochim Biophys Acta 2010; 1802(1): 29-44.
[http://dx.doi.org/10.1016/j.bbadis.2009.08.013] [PMID: 19733240]
[161]
Hardy J. Genetic analysis of pathways to Parkinson disease. Neuron 2010; 68(2): 201-6.
[http://dx.doi.org/10.1016/j.neuron.2010.10.014] [PMID: 20955928]
[162]
Hirsch EC, Hunot S. Neuroinflammation in Parkinson’s disease: a target for neuroprotection? Lancet Neurol 2009; 8(4): 382-97.
[http://dx.doi.org/10.1016/S1474-4422(09)70062-6] [PMID: 19296921]
[163]
Gan-Or Z, Dion PA, Rouleau GA. Genetic perspective on the role of the autophagy-lysosome pathway in Parkinson disease. Autophagy 2015; 11(9): 1443-57.
[http://dx.doi.org/10.1080/15548627.2015.1067364] [PMID: 26207393]
[164]
Sulzer D. Multiple hit hypotheses for dopamine neuron loss in Parkinson’s disease. Trends Neurosci 2007; 30(5): 244-50.
[http://dx.doi.org/10.1016/j.tins.2007.03.009] [PMID: 17418429]
[165]
Roselli F, Caroni P. From intrinsic firing properties to selective neuronal vulnerability in neurodegenerative diseases. Neuron 2015; 85(5): 901-10.
[http://dx.doi.org/10.1016/j.neuron.2014.12.063] [PMID: 25741719]
[166]
Pacelli C, Giguère N, Bourque MJ, Lévesque M, Slack RS, Trudeau LE. Elevated mitochondrial bioenergetics and axonal arborization size are key contributors to the vulnerability of dopamine neurons. Curr Biol 2015; 25(18): 2349-60.
[http://dx.doi.org/10.1016/j.cub.2015.07.050] [PMID: 26320949]
[167]
Chen X, Xue B, Wang J, Liu H, Shi L, Xie J. Potassium channels: a potential therapeutic target for Parkinson’s Disease. Neurosci Bull 2018; 34(2): 341-8.
[http://dx.doi.org/10.1007/s12264-017-0177-3] [PMID: 28884460]
[168]
Bajgar R, Seetharaman S, Kowaltowski AJ, Garlid KD, Paucek P. Identification and properties of a novel intracellular (mitochondrial) ATP-sensitive potassium channel in brain. J Biol Chem 2001; 276(36): 33369-74.
[http://dx.doi.org/10.1074/jbc.M103320200] [PMID: 11441006]
[169]
Bednarczyk P. Potassium channels in brain mitochondria. Acta Biochim Pol 2009; 56(3): 385-92.
[http://dx.doi.org/10.18388/abp.2009_2471] [PMID: 19759922]
[170]
Rodriguez-Pallares J, Parga JA, Joglar B, Guerra MJ, Labandeira-Garcia JL. Mitochondrial ATP-sensitive potassium channels enhance angiotensin-induced oxidative damage and dopaminergic neuron degeneration. Relevance for aging-associated susceptibility to Parkinson’s disease. Age (Dordr) 2012; 34(4): 863-80.
[http://dx.doi.org/10.1007/s11357-011-9284-7] [PMID: 21713375]
[171]
Qin L, Liu Y, Wang T, et al. NADPH oxidase mediates lipopolysaccharide-induced neurotoxicity and proinflammatory gene expression in activated microglia. J Biol Chem 2004; 279(2): 1415-21.
[http://dx.doi.org/10.1074/jbc.M307657200] [PMID: 14578353]
[172]
de Cavanagh EMV, Inserra F, Ferder M, Ferder L. From mitochondria to disease: role of the renin-angiotensin system. Am J Nephrol 2007; 27(6): 545-53.
[http://dx.doi.org/10.1159/000107757] [PMID: 17785964]
[173]
Daiber A. Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species. Biochim Biophys Acta 1797; 1797: 897-906.
[174]
Collier TJ, Kanaan NM, Kordower JH. Ageing as a primary risk factor for Parkinson’s disease: evidence from studies of non-human primates. Nat Rev Neurosci 2011; 12(6): 359-66.
[http://dx.doi.org/10.1038/nrn3039] [PMID: 21587290]
[175]
Shulman JM, De Jager PL, Feany MB. Parkinson’s disease: genetics and pathogenesis. Annu Rev Pathol 2011; 6(1): 193-222.
[http://dx.doi.org/10.1146/annurev-pathol-011110-130242] [PMID: 21034221]
[176]
Burke RE, O’Malley K. Axon degeneration in Parkinson’s disease. Exp Neurol 2013; 246: 72-83.
[http://dx.doi.org/10.1016/j.expneurol.2012.01.011] [PMID: 22285449]
[177]
Liss B, Roeper J. Molecular physiology of neuronal K-ATP channels (review). Mol Membr Biol 2001; 18(2): 117-27.
[http://dx.doi.org/10.1080/09687680110047373] [PMID: 11463204]
[178]
Sharma N, Crane A, Clement JP IV, et al. The C terminus of SUR1 is required for trafficking of KATP channels. J Biol Chem 1999; 274(29): 20628-32.
[http://dx.doi.org/10.1074/jbc.274.29.20628] [PMID: 10400694]
[179]
Schiemann J, Schlaudraff F, Klose V, et al. K-ATP channels in dopamine substantia nigra neurons control bursting and novelty-induced exploration. Nat Neurosci 2012; 15(9): 1272-80.
[http://dx.doi.org/10.1038/nn.3185] [PMID: 22902720]
[180]
Peng K, Hu J, Xiao J, et al. Mitochondrial ATP-sensitive potassium channel regulates mitochondrial dynamics to participate in neurodegeneration of Parkinson’s disease. Biochim Biophys Acta Mol Basis Dis 2018; 1864(4 Pt A): 1086-103.
[http://dx.doi.org/10.1016/j.bbadis.2018.01.013] [PMID: 29353068]
[181]
Dragicevic E, Poetschke C, Duda J, et al. Cav1.3 channels control D2-autoreceptor responses via NCS-1 in substantia nigra dopamine neurons. Brain 2014; 137(Pt 8): 2287-302.
[http://dx.doi.org/10.1093/brain/awu131] [PMID: 24934288]
[182]
de Candia M, Zaetta G, Denora N, et al. New azepino[4,3-b]indole derivatives as nanomolar selective inhibitors of human butyrylcholinesterase showing protective effects against NMDA-induced neurotoxicity. Eur J Med Chem 2017; 125: 288-98.
[http://dx.doi.org/10.1016/j.ejmech.2016.09.037] [PMID: 27688184]
[183]
Zhou F, Yao HH, Wu JY, Ding JH, Sun T, Hu G. Opening of microglial K(ATP) channels inhibits rotenone-induced neuroinflammation. J Cell Mol Med 2008; 12(5A): 1559-70.
[http://dx.doi.org/10.1111/j.1582-4934.2007.00144.x] [PMID: 19012619]
[184]
Maurice N, Deltheil T, Melon C, et al. Bee venom alleviates motor deficits and modulates the transfer of cortical information through the basal ganglia in rat models of Parkinson’s Disease. PLoS One 2015; 10(11): e0142838.
[185]
Sarpal D, Koenig JI, Adelman JP, Brady D, Prendeville LC, Shepard PD. Regional distribution of SK3 mRNA-containing neurons in the adult and adolescent rat ventral midbrain and their relationship to dopamine-containing cells. Synapse 2004; 53(2): 104-13.
[http://dx.doi.org/10.1002/syn.20042] [PMID: 15170822]
[186]
Mourre C, Manrique C, Camon J, et al. Changes in SK channel expression in the basal ganglia after partial nigrostriatal dopamine lesions in rats: Functional consequences. Neuropharmacology 2017; 113(Pt A): 519-32.
[http://dx.doi.org/10.1016/j.neuropharm.2016.11.003] [PMID: 27825825]
[187]
Doo AR, Kim ST, Kim SN, et al. Neuroprotective effects of bee venom pharmaceutical acupuncture in acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson’s disease. Neurol Res 2010; 32: 88-91.
[188]
Serôdio P, Rudy B. Differential expression of Kv4 K+ channel subunits mediating subthreshold transient K+ (A-type) currents in rat brain. J Neurophysiol 1998; 79(2): 1081-91.
[http://dx.doi.org/10.1152/jn.1998.79.2.1081] [PMID: 9463463]
[189]
Subramaniam M, Althof D, Gispert S, et al. Mutant α-synuclein enhances firing frequencies in dopamine substantia nigra neurons by oxidative impairment of a-type potassium channels. J Neurosci 2014; 34(41): 13586-99.
[190]
Tkatch T, Baranauskas G, Surmeier DJ. Kv4.2 mRNA abundance and A-type K(+) current amplitude are linearly related in basal ganglia and basal forebrain neurons. J Neurosci 2000; 20(2): 579-88.
[http://dx.doi.org/10.1523/JNEUROSCI.20-02-00579.2000] [PMID: 10632587]
[191]
Maffie JK, Dvoretskova E, Bougis PE, Martin-Eauclaire MF, Rudy B. Dipeptidyl-peptidase-like-proteins confer high sensitivity to the scorpion toxin AmmTX3 to Kv4-mediated A-type K+ channels. J Physiol 2013; 591(10): 2419-27.
[http://dx.doi.org/10.1113/jphysiol.2012.248831] [PMID: 23440961]
[192]
Hansen HH, Weikop P, Mikkelsen MD, Rode F, Mikkelsen JD. The pan-Kv7 (KCNQ) channel opener retigabine inhibits striatal excitability by direct action on striatal neurons in vivo. Basic Clin Pharmacol Toxicol 2017; 120(1): 46-51.
[http://dx.doi.org/10.1111/bcpt.12636] [PMID: 27377794]
[193]
Shen W, Hamilton SE, Nathanson NM, Surmeier DJ. Cholinergic Suppression of KCNQ Channel Currents Enhances Excitability of Striatal Medium Spiny Neurons. J Neurosci 2005; 25(32): 7449-58.
[194]
Saganich MJ, Machado E, Rudy B. Differential expression of genes encoding subthreshold-operating voltage-gated K+ channels in brain. J Neurosci 2001; 21(13): 4609-24.
[http://dx.doi.org/10.1523/JNEUROSCI.21-13-04609.2001] [PMID: 11425889]
[195]
Martire M, D’Amico M, Panza E, et al. Involvement of KCNQ2 subunits in [3H]dopamine release triggered by depolarization and pre-synaptic muscarinic receptor activation from rat striatal synaptosomes. J Neurochem 2007; 102(1): 179-93.
[http://dx.doi.org/10.1111/j.1471-4159.2007.04562.x] [PMID: 17437547]
[196]
Weber YG, Geiger J, Kämpchen K, Landwehrmeyer B, Sommer C, Lerche H. Immunohistochemical analysis of KCNQ2 potassium channels in adult and developing mouse brain. Brain Res 2006; 1077(1): 1-6.
[http://dx.doi.org/10.1016/j.brainres.2006.01.023] [PMID: 16500630]
[197]
Cooper EC, Harrington E, Jan YN, Jan LY. M channel KCNQ2 subunits are localized to key sites for control of neuronal network oscillations and synchronization in mouse brain. J Neurosci 2001; 21(24): 9529-40.
[http://dx.doi.org/10.1523/JNEUROSCI.21-24-09529.2001] [PMID: 11739564]
[198]
Hansen HH, Ebbesen C, Mathiesen C, et al. The KCNQ channel opener retigabine inhibits the activity of mesencephalic dopaminergic systems of the rat. J Pharmacol Exp Ther 2006; 318(3): 1006-19.
[199]
Wong M, Martin LJ. Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice. Hum Mol Genet 2010; 19(11): 2284-302.
[http://dx.doi.org/10.1093/hmg/ddq106] [PMID: 20223753]
[200]
Musarò A. Understanding ALS: new therapeutic approaches. FEBS J 2013; 280(17): 4315-22.
[http://dx.doi.org/10.1111/febs.12087] [PMID: 23217177]
[201]
Dobrowolny G, Aucello M, Musarò A. Muscle atrophy induced by SOD1G93A expression does not involve the activation of caspase in the absence of denervation. Skelet Muscle 2011; 1(1): 3.
[http://dx.doi.org/10.1186/2044-5040-1-3]
[202]
Kanai K, Kuwabara S, Misawa S, et al. Altered axonal excitability properties in amyotrophic lateral sclerosis: impaired potassium channel function related to disease stage. Brain 2006; 129(Pt 4): 953-62.
[http://dx.doi.org/10.1093/brain/awl024] [PMID: 16467388]
[203]
Jiang K, Yu Z, Shui Q. The pattern of ATP-sensitive K+ channel subunits, Kir6.2 and SUR1 mRNA expressions in DG region is different from those in CA1-3 regions of chronic epilepsy induced by picrotoxin in rats. Neuropathology 2007; 27(6): 531-8.
[http://dx.doi.org/10.1111/j.1440-1789.2007.00823.x] [PMID: 18021373]
[204]
Camerino GM, Fonzino A, Conte E, et al. Elucidating the Contribution of skeletal muscle ion channels to amyotrophic lateral sclerosis in search of new therapeutic options. Sci Rep 2019; 9(1): 3185.
[http://dx.doi.org/10.1038/s41598-019-39676-3]
[205]
Mehta RI, Ivanova S, Tosun C, Castellani RJ, Gerzanich V, Simard JM. Sulfonylurea receptor 1 expression in human cerebral infarcts. J Neuropathol Exp Neurol 2013; 72(9): 871-83.
[http://dx.doi.org/10.1097/NEN.0b013e3182a32e40] [PMID: 23965746]
[206]
Simard JM, Castellani RJ, Ivanova S, Koltz MT, Gerzanich V. Sulfonylurea receptor 1 in the germinal matrix of premature infants. Pediatr Res 2008; 64(6): 648-52.
[http://dx.doi.org/10.1203/PDR.0b013e318186e5a9] [PMID: 18679166]
[207]
Simard JM, Woo SK, Bhatta S, Gerzanich V. Drugs acting on SUR1 to treat CNS ischemia and trauma. Curr Opin Pharmacol 2008; 8(1): 42-9.
[http://dx.doi.org/10.1016/j.coph.2007.10.004] [PMID: 18032110]
[208]
Simard JM, Woo SK, Schwartzbauer GT, Gerzanich V. Sulfonylurea receptor 1 in central nervous system injury: a focused review. J Cereb Blood Flow Metab 2012; 32(9): 1699-717.
[http://dx.doi.org/10.1038/jcbfm.2012.91] [PMID: 22714048]
[209]
Tosun C, Kurland DB, Mehta R, et al. Inhibition of the Sur1-Trpm4 channel reduces neuroinflammation and cognitive impairment in subarachnoid hemorrhage. Stroke 2013; 44(12): 3522-8.
[http://dx.doi.org/10.1161/STROKEAHA.113.002904] [PMID: 24114458]
[210]
Bryan J, Muñoz A, Zhang X, et al. ABCC8 and ABCC9: ABC transporters that regulate K+ channels. Pflugers Arch 2007; 453(5): 703-18.
[http://dx.doi.org/10.1007/s00424-006-0116-z] [PMID: 16897043]
[211]
Bonfanti DH, Alcazar LP, Arakaki PA, et al. ATP-dependent potassium channels and type 2 diabetes mellitus. Clin Biochem 2015; 48(7-8): 476-82.
[http://dx.doi.org/10.1016/j.clinbiochem.2014.12.026] [PMID: 25583094]
[212]
Haghvirdizadeh P, Sadat Haerian M, Haghvirdizadeh P, Sadat H B. ABCC8 genetic variants and risk of diabetes mellitus. Gene 2014; 545(2): 198-204.
[http://dx.doi.org/10.1016/j.gene.2014.04.040] [PMID: 24768178]
[213]
Remedi MS, Nichols CG. Hyperinsulinism and diabetes: genetic dissection of β cell metabolism-excitation coupling in mice. Cell Metab 2009; 10(6): 442-53.
[http://dx.doi.org/10.1016/j.cmet.2009.10.011] [PMID: 19945402]
[214]
Schmid D, Svoboda M, Sorgner A, et al. Glibenclamide reduces proinflammatory cytokines in an ex vivo model of human endotoxinaemia under hypoxaemic conditions. Life Sci 2011; 89: 725-34.
[http://dx.doi.org/10.1016/j.lfs.2011.08.017]
[215]
Zhang G, Lin X, Zhang S, Xiu H, Pan C, Cui W. A protective role of glibenclamide in inflammation-associated injury. Mediators Inflamm 2017; 2017
[http://dx.doi.org/10.1155/2017/3578702] [PMID: 28740332]
[216]
Lamas JA, Fernández-Fernández D. Tandem pore TWIK-related potassium channels and neuroprotection. Neural Regen Res 2019; 14(8): 1293-308.
[http://dx.doi.org/10.4103/1673-5374.253506] [PMID: 30964046]
[217]
Mule NK, Orjuela Leon AC, Falck JR, Arand M, Marowsky A. 11,12 -Epoxyeicosatrienoic acid (11,12 EET) reduces excitability and excitatory transmission in the hippocampus. Neuropharmacology 2017; 123: 310-21.
[http://dx.doi.org/10.1016/j.neuropharm.2017.05.013] [PMID: 28526610]
[218]
Gantz SC, Bean BP. Cell-autonomous excitation of midbrain dopamine neurons by endocannabinoid-dependent lipid signaling. Neuron 2017; 93(6): 1375-1387.e2.
[http://dx.doi.org/10.1016/j.neuron.2017.02.025] [PMID: 28262417]
[219]
Bukiya AN, McMillan J, Liu J, Shivakumar B, Parrill AL, Dopico AM. Activation of calcium- and voltage-gated potassium channels of large conductance by leukotriene B4. J Biol Chem 2014; 289(51): 35314-25.
[http://dx.doi.org/10.1074/jbc.M114.577825] [PMID: 25371198]
[220]
Qu YY, Yuan MY, Liu Y, Xiao XJ, Zhu YL. The protective effect of epoxyeicosatrienoic acids on cerebral ischemia/reperfusion injury is associated with PI3K/Akt pathway and ATP-sensitive potassium channels. Neurochem Res 2015; 40(1): 1-14.
[http://dx.doi.org/10.1007/s11064-014-1456-2] [PMID: 25366463]
[221]
Batchu SN, Chaudhary KR, El-Sikhry H, et al. Role of PI3Kα and sarcolemmal ATP-sensitive potassium channels in epoxyeicosatrienoic acid mediated cardioprotection. J Mol Cell Cardiol 2012; 53(1): 43-52.
[http://dx.doi.org/10.1016/j.yjmcc.2012.04.008] [PMID: 22561102]
[222]
Batchu SN, Law E, Brocks DR, Falck JR, Seubert JM. Epoxyeicosatrienoic acid prevents postischemic electrocardiogram abnormalities in an isolated heart model. J Mol Cell Cardiol 2009; 46(1): 67-74.
[http://dx.doi.org/10.1016/j.yjmcc.2008.09.711] [PMID: 18973759]
[223]
Wang XL, Lu T, Cao S, Shah VH, Lee HC. Inhibition of ATP binding to the carboxyl terminus of Kir6.2 by epoxyeicosatrienoic acids. Biochim Biophys Acta 2006; 1761(9): 1041-9.
[http://dx.doi.org/10.1016/j.bbalip.2006.06.005] [PMID: 16904368]
[224]
Centeno JM, Miranda-Gómez L, López-Morales MA, et al. Diabetes modifies the role of prostanoids and potassium channels which regulate the hypereactivity of the rabbit renal artery to BNP. Naunyn Schmiedebergs Arch Pharmacol 2018; 391(5): 501-11.
[http://dx.doi.org/10.1007/s00210-018-1478-4] [PMID: 29464270]
[225]
Liu Y, Zhang J, Yu L, et al. A soluble epoxide hydrolase inhibitor--8-HUDE increases pulmonary vasoconstriction through inhibition of K(ATP) channels. Pulm Pharmacol Ther 2012; 25(1): 69-76.
[http://dx.doi.org/10.1016/j.pupt.2011.11.005] [PMID: 22155000]
[226]
Morin C, Sirois M, Echave V, Rizcallah E, Rousseau E. Relaxing effects of 17(18)-EpETE on arterial and airway smooth muscles in human lung. Am J Physiol Lung Cell Mol Physiol 2009; 296(1): L130-9.
[http://dx.doi.org/10.1152/ajplung.90436.2008] [PMID: 18978038]
[227]
Lu T, Ye D, Wang X, et al. Cardiac and vascular KATP channels in rats are activated by endogenous epoxyeicosatrienoic acids through different mechanisms. J Physiol 2006; 575(Pt 2): 627-44.
[http://dx.doi.org/10.1113/jphysiol.2006.113985] [PMID: 16793897]
[228]
Da Silva-Santos JE, Santos-Silva MC, Cunha FdeQ, Assreuy J. The role of ATP-sensitive potassium channels in neutrophil migration and plasma exudation. J Pharmacol Exp Ther 2002; 300(3): 946-51.
[http://dx.doi.org/10.1124/jpet.300.3.946] [PMID: 11861802]
[229]
Tricarico D, Capriulo R, Camerino DC. Involvement of K(Ca2+) channels in the local abnormalities and hyperkalemia following the ischemia-reperfusion injury of rat skeletal muscle. Neuromuscul Disord 2002; 12(3): 258-65.
[http://dx.doi.org/10.1016/S0960-8966(01)00270-X] [PMID: 11801397]
[230]
Dinardo MM, Camerino GM, Mele A, Latorre R, Conte Camerino D, Tricarico D. Splicing of the rSlo gene affects the molecular composition and drug response of Ca2+-activated K+ channels in skeletal muscle. PLoS One 2012; 7(7): e40235.
[231]
Bondarenko AI, Panasiuk O, Okhai I, Montecucco F, Brandt KJ, Mach F. Direct activation of Ca2+ and voltage-gated potassium channels of large conductance by anandamide in endothelial cells does not support the presence of endothelial atypical cannabinoid receptor. Eur J Pharmacol 2017; 805: 14-24.
[http://dx.doi.org/10.1016/j.ejphar.2017.03.038] [PMID: 28327344]
[232]
Masi A, Narducci R, Mannaioni G. Harnessing ionic mechanisms to achieve disease modification in neurodegenerative disorders. Pharmacol Res 2019; 147: 104343.
[http://dx.doi.org/10.1016/j.phrs.2019.104343] [PMID: 31279830]
[233]
Salgado-Puga K, Rodríguez-Colorado J, Prado-Alcalá RA, Peña-Ortega F. Subclinical doses of ATP-Sensitive potassium channel modulators prevent alterations in memory and synaptic plasticity induced by amyloid-β. J Alzheimers Dis 2017; 57(1): 205-26.
[http://dx.doi.org/10.3233/JAD-160543] [PMID: 28222502]
[234]
Katsumata Y, Nelson PT, Ellingson SR, Fardo DW. Gene-based association study of genes linked to hippocampal sclerosis of aging neuropathology: GRN, TMEM106B, ABCC9, and KCNMB2. Neurobiol Aging 2017; 53: 193.e17-25.
[http://dx.doi.org/10.1016/j.neurobiolaging.2017.01.003] [PMID: 28131462]
[235]
Kong J, Ren G, Jia N, et al. Effects of nicorandil in neuroprotective activation of PI3K/AKT pathways in a cellular model of Alzheimer’s disease. Eur Neurol 2013; 70: 233-41.
[236]
Villoslada P, Rovira A, Montalban X, et al. NeuroAdvan study.. Effects of diazoxide in multiple sclerosis: A randomized, double-blind phase 2 clinical trial. Neurol Neuroimmunol neuroinflammation 2015; 2(5): e147.
[237]
Mele A, Camerino GM, Calzolaro S, Cannone M, Conte D, Tricarico D. Dual response of the KATP channels to staurosporine: a novel role of SUR2B, SUR1 and Kir6.2 subunits in the regulation of the atrophy in different skeletal muscle phenotypes. Biochem Pharmacol 2014; 91(2): 266-75.
[http://dx.doi.org/10.1016/j.bcp.2014.06.023] [PMID: 24998494]
[238]
Cetrone M, Mele A, Tricarico D. Effects of the antidiabetic drugs on the age-related atrophy and sarcopenia associated with diabetes type II. Curr Diabetes Rev 2014; 10(4): 231-7.
[http://dx.doi.org/10.2174/1573399810666140918121022] [PMID: 25245021]
[239]
Tricarico D, Rolland JF, Cannone G, et al. Structural nucleotide analogs are potent activators/inhibitors of pancreatic β cell KATP channels: an emerging mechanism supporting their use as antidiabetic drugs. J Pharmacol Exp Ther 2012; 340(2): 266-76.
[http://dx.doi.org/10.1124/jpet.111.185835] [PMID: 22028392]
[240]
Tricarico D, Mele A, Camerino GM, et al. Molecular determinants for the activating/blocking actions of the 2H-1,4-benzoxazine derivatives, a class of potassium channel modulators targeting the skeletal muscle KATP channels. Mol Pharmacol 2008; 74(1): 50-8.
[http://dx.doi.org/10.1124/mol.108.046615] [PMID: 18403717]

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