[1] C. J. B. daCosta, C. R. Free, J. Corradi, C. Bouzat, és S. M. Sine (2011) „Single-channel and structural foundations of neuronal α7 acetylcholine receptor potentiation”, J. Neurosci., köt. 31, sz.
39, o. 13870–13879.
[2] M. D. Isaacson, N. A. Horenstein, C. Stokes, W. R. Kem, és R. L. Papke (2013) „Point-to-point ligand–receptor interactions across the subunit interface modulate the induction and stabilization of conformational states of alpha7 nAChR by benzylidene anabaseines”, Biochem. Pharmacol., köt. 85, sz. 6, o. 817–828.
[3] J. Wang, R. L. Papke, C. Stokes, és N. A. Horenstein (2012) „Potential state-selective hydrogen bond formation can modulate activation and desensitization of the α7 nicotinic acetylcholine receptor”, J. Biol. Chem., köt. 287, sz. 26, o. 21957–21969.
[4] D. K. Williams, J. Wang, és R. L. Papke (2011) „Investigation of the molecular mechanism of the α7 nicotinic acetylcholine receptor positive allosteric modulator PNU-120596 provides evidence for two distinct desensitized states”, Mol. Pharmacol., köt. 80, sz. 6, o. 1013–1032.
[5] M. Jindrichova, S. J. Lansdell, és N. S. Millar (2012) „Changes in Temperature Have Opposing Effects on Current Amplitude in α7 and α4β2 Nicotinic Acetylcholine Receptors”, PLoS ONE, köt.
7, sz. 2, o. e32073.
[6] F. Sitzia, J. T. Brown, A. D. Randall, és J. Dunlop (2011) „Voltage- and Temperature-Dependent Allosteric Modulation of α7 Nicotinic Receptors by PNU120596”, Front. Pharmacol., 2:81.
[7] D. K. Williams, C. Peng, M. R. Kimbrell, és R. L. Papke (2012) „Intrinsically low open probability of α7 nicotinic acetylcholine receptors can be overcome by positive allosteric modulation and serum factors leading to the generation of excitotoxic currents at physiological temperatures”, Mol.
Pharmacol., köt. 82, sz. 4, o. 746–759.
[8] C. Bouzat, M. Bartos, J. Corradi, és S. M. Sine (2008) „The interface between extracellular and transmembrane domains of homomeric Cys-loop receptors governs open-channel lifetime and rate of desensitization”, J. Neurosci., köt. 28, sz. 31, o. 7808–7819.
[9] R. L. Papke, W. R. Kem, F. Soti, G. Y. López-Hernández, és N. A. Horenstein (2009) „Activation and desensitization of nicotinic alpha7-type acetylcholine receptors by benzylidene anabaseines and nicotine”, J. Pharmacol. Exp. Ther., köt. 329, sz. 2, o. 791–807.
[10] D. K. Williams, J. Wang, és R. L. Papke (2011) „Positive allosteric modulators as an approach to nicotinic acetylcholine receptor-targeted therapeutics: advantages and limitations”, Biochem.
Pharmacol., köt. 82, sz. 8, o. 915–930.
[11] F. Maingret, B. Coste, F. Padilla, N. Clerc, M. Crest, S. M. Korogod, és P. Delmas (2008)
„Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism”, J. Gen. Physiol., köt. 131, sz. 3, o. 211–225.
[12] S. Lolignier, M. Amsalem, F. Maingret, F. Padilla, M. Gabriac, E. Chapuy, A. Eschalier, P. Delmas, és J. Busserolles (2011) „Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation”, PloS One, köt. 6, sz. 8, o. e23083.
150
[13] C. E. Morris, P.-A. Boucher, és B. Joós (2012) „Left-shifted nav channels in injured bilayer: primary targets for neuroprotective nav antagonists?”, Front. Pharmacol., köt. 3, o. 19.
[14] B. T. Priest (2009) „Future potential and status of selective sodium channel blockers for the treatment of pain.”, Curr. Opin. Drug Discov. Devel., köt. 12, sz. 5, o. 682–92.
[15] M. Mantegazza és W. A. Catterall (2010) „Voltage-gated Na+ channels and epilepsy”, Epilepsia, köt. 51, o. 9–9.
[16] J. Lai, F. Porreca, J. C. Hunter, és M. S. Gold (2004) „VOLTAGE-GATED SODIUM CHANNELS AND HYPERALGESIA”, Annu. Rev. Pharmacol. Toxicol., köt. 44, sz. 1, o. 371–397.
[17] G. Cruccu, T. Z. Aziz, L. Garcia-Larrea, P. Hansson, T. S. Jensen, J.-P. Lefaucheur, B. A. Simpson, és R. S. Taylor (2007) „EFNS guidelines on neurostimulation therapy for neuropathic pain”, Eur. J.
Neurol., köt. 14, sz. 9, o. 952–970.
[18] S. England és M. J. de Groot (2009) „Subtype-selective targeting of voltage-gated sodium channels”, Br. J. Pharmacol., köt. 158, sz. 6, o. 1413–1425.
[19] J. A. Kaczmarski és B. Corry (2014) „Investigating the size and dynamics of voltage-gated sodium channel fenestrations”, Channels Austin Tex, köt. 8, sz. 3, o. 264–277.
[20] T. L. Wallace és R. H. P. Porter (2011) „Targeting the nicotinic alpha7 acetylcholine receptor to enhance cognition in disease”, Biochem. Pharmacol., köt. 82, sz. 8, o. 891–903.
[21] N. S. Philip, L. L. Carpenter, A. R. Tyrka, és L. H. Price (2010) „Nicotinic acetylcholine receptors and depression: a review of the preclinical and clinical literature”, Psychopharmacology (Berl.), köt.
212, sz. 1, o. 1–12.
[22] A. Taly, P.-J. Corringer, D. Guedin, P. Lestage, és J.-P. Changeux (2009) „Nicotinic receptors:
allosteric transitions and therapeutic targets in the nervous system”, Nat. Rev. Drug Discov., köt. 8, sz. 9, o. 733–750.
[23] S. Sahdeo, T. Wallace, R. Hirakawa, F. Knoflach, D. Bertrand, H. Maag, D. Misner, G. C.
Tombaugh, L. Santarelli, K. Brameld, M. E. Milla, és D. C. Button (2014) „Characterization of RO5126946, a Novel α7 nicotinic acetylcholine receptor-positive allosteric modulator”, J.
Pharmacol. Exp. Ther., köt. 350, sz. 2, o. 455–468.
[24] H. D. Mansvelder, K. I. van Aerde, J. J. Couey, és A. B. Brussaard (2006) „Nicotinic modulation of neuronal networks: from receptors to cognition”, Psychopharmacology (Berl.), köt. 184, sz. 3–4, o.
292–305.
[25] E. D. del Toro, J. M. Juiz, X. Peng, J. Lindstrom, és M. Criado (1994) „Immunocytochemical localization of the ?7 subunit of the nicotinic acetylcholine receptor in the rat central nervous system”, J. Comp. Neurol., köt. 349, sz. 3, o. 325–342.
[26] R. Fabian-Fine, P. Skehel, M. L. Errington, H. A. Davies, E. Sher, M. G. Stewart, és A. Fine (2001)
„Ultrastructural distribution of the alpha7 nicotinic acetylcholine receptor subunit in rat hippocampus”, J. Neurosci. Off. J. Soc. Neurosci., köt. 21, sz. 20, o. 7993–8003.
[27] D. K. Berg és W. G. Conroy (2002) „Nicotinic alpha 7 receptors: synaptic options and downstream signaling in neurons”, J. Neurobiol., köt. 53, sz. 4, o. 512–523.
151
[28] N. A. Horenstein, R. L. Papke, A. R. Kulkarni, G. U. Chaturbhuj, C. Stokes, K. Manther, és G. A.
Thakur (2016) „Critical Molecular Determinants of α7 Nicotinic Acetylcholine Receptor Allosteric Activation: SEPARATION OF DIRECT ALLOSTERIC ACTIVATION AND POSITIVE ALLOSTERIC MODULATION”, J. Biol. Chem., köt. 291, sz. 10, o. 5049–5067.
[29] J. A. Dickinson, K. E. Hanrott, M. H. S. Mok, J. N. C. Kew, és S. Wonnacott (2007) „Differential coupling of alpha7 and non-alpha7 nicotinic acetylcholine receptors to calcium-induced calcium release and voltage-operated calcium channels in PC12 cells”, J. Neurochem., köt. 100, sz. 4, o.
1089–1096.
[30] E. X. Albuquerque, E. F. R. Pereira, M. Alkondon, és S. W. Rogers (2009) „Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function”, Physiol. Rev., köt. 89, sz. 1, o. 73–120.
[31] G. D. Cymes és C. Grosman (2012) „The unanticipated complexity of the selectivity-filter glutamates of nicotinic receptors”, Nat. Chem. Biol., köt. 8, sz. 12, o. 975–981.
[32] M. Paolini, M. De Biasi, és J. A. Dani „Nicotinic Acetylcholine Receptors and the Roles of the Alpha7 Subunit”. In R. A. J. Lester (Szerk.). Nicotinic Receptors, Springer New York, New York, 2014: 255–277.
[33] G. T. Young, R. Zwart, A. S. Walker, E. Sher, és N. S. Millar (2008) „Potentiation of alpha7 nicotinic acetylcholine receptors via an allosteric transmembrane site”, Proc. Natl. Acad. Sci. U. S.
A., köt. 105, sz. 38, o. 14686–14691.
[34] D. Bertrand, S. Bertrand, S. Cassar, E. Gubbins, J. Li, és M. Gopalakrishnan (2008) „Positive allosteric modulation of the alpha7 nicotinic acetylcholine receptor: ligand interactions with distinct binding sites and evidence for a prominent role of the M2-M3 segment”, Mol. Pharmacol., köt. 74, sz. 5, o. 1407–1416.
[35] N. Andersen, J. Corradi, S. M. Sine, és C. Bouzat (2013) „Stoichiometry for activation of neuronal α7 nicotinic receptors”, Proc. Natl. Acad. Sci. U. S. A., köt. 110, sz. 51, o. 20819–20824.
[36] A. Mike, N. G. Castro, és E. X. Albuquerque (2000) „Choline and acetylcholine have similar kinetic properties of activation and desensitization on the alpha7 nicotinic receptors in rat hippocampal neurons”, Brain Res., köt. 882, sz. 1–2, o. 155–168.
[37] R. Giniatullin, A. Nistri, és J. L. Yakel (2005) „Desensitization of nicotinic ACh receptors: shaping cholinergic signaling”, Trends Neurosci., köt. 28, sz. 7, o. 371–378.
[38] V. V. Uteshev, E. M. Meyer, és R. L. Papke (2002) „Activation and inhibition of native neuronal alpha-bungarotoxin-sensitive nicotinic ACh receptors”, Brain Res., köt. 948, sz. 1–2, o. 33–46.
[39] A. A. Mazurov, J. D. Speake, és D. Yohannes (2011) „Discovery and Development of α7 Nicotinic Acetylcholine Receptor Modulators”, J. Med. Chem., köt. 54, sz. 23, o. 7943–7961.
[40] A. S. Vallés, M. V. Borroni, és F. J. Barrantes (2014) „Targeting brain α7 nicotinic acetylcholine receptors in Alzheimer’s disease: rationale and current status”, CNS Drugs, köt. 28, sz. 11, o. 975–
987.
[41] A. Auerbach (2015) „Agonist activation of a nicotinic acetylcholine receptor”, Neuropharmacology, köt. 96, o. 150–156.
152
[42] A. Auerbach (2013) „The energy and work of a ligand-gated ion channel”, J. Mol. Biol., köt. 425, sz.
9, o. 1461–1475.
[43] C. B. Marotta, H. A. Lester, és D. A. Dougherty (2015) „An Unaltered Orthosteric Site and a Network of Long-Range Allosteric Interactions for PNU-120596 in α7 Nicotinic Acetylcholine Receptors”, Chem. Biol., köt. 22, sz. 8, o. 1063–1073.
[44] T. Dinklo, H. Shaban, J. W. Thuring, H. Lavreysen, K. E. Stevens, L. Zheng, C. Mackie, C.
Grantham, I. Vandenberk, G. Meulders, L. Peeters, H. Verachtert, E. De Prins, és A. S. J. Lesage (2011) „Characterization of 2-[[4-fluoro-3-(trifluoromethyl)phenyl]amino]-4-(4-pyridinyl)-5-thiazolemethanol (JNJ-1930942), a novel positive allosteric modulator of the alpha7 nicotinic acetylcholine receptor”, J. Pharmacol. Exp. Ther., köt. 336, sz. 2, o. 560–574.
[45] A. Chatzidaki és N. S. Millar (2015) „Allosteric modulation of nicotinic acetylcholine receptors”, Biochem. Pharmacol., köt. 97, sz. 4, o. 408–417.
[46] J. Dunlop, T. Lock, B. Jow, F. Sitzia, S. Grauer, F. Jow, A. Kramer, M. R. Bowlby, A. Randall, D.
Kowal, A. Gilbert, T. A. Comery, J. Larocque, V. Soloveva, J. Brown, és R. Roncarati (2009) „Old and new pharmacology: positive allosteric modulation of the alpha7 nicotinic acetylcholine receptor by the 5-hydroxytryptamine(2B/C) receptor antagonist SB-206553 (3,5-dihydro-5-methyl-N-3-pyridinylbenzo[1,2-b:4,5-b’]di pyrrole-1(2H)-carboxamide)”, J. Pharmacol. Exp. Ther., köt. 328, sz.
3, o. 766–776.
[47] J. K. Gill-Thind, P. Dhankher, J. M. D’Oyley, T. D. Sheppard, és N. S. Millar (2015) „Structurally Similar Allosteric Modulators of α7 Nicotinic Acetylcholine Receptors Exhibit Five Distinct Pharmacological Effects”, J. Biol. Chem., köt. 290, sz. 6, o. 3552–3562.
[48] R. S. Hurst, M. Hajós, M. Raggenbass, T. M. Wall, N. R. Higdon, J. A. Lawson, K. L. Rutherford-Root, M. B. Berkenpas, W. E. Hoffmann, D. W. Piotrowski, V. E. Groppi, G. Allaman, R. Ogier, S.
Bertrand, D. Bertrand, és S. P. Arneric (2005) „A novel positive allosteric modulator of the alpha7 neuronal nicotinic acetylcholine receptor: in vitro and in vivo characterization”, J. Neurosci. Off. J.
Soc. Neurosci., köt. 25, sz. 17, o. 4396–4405.
[49] V. Echeverria, A. Yarkov, és G. Aliev (2016) „Positive modulators of the α7 nicotinic receptor against neuroinflammation and cognitive impairment in Alzheimer’s disease”, Prog. Neurobiol.
(nyomtatás alatt)
[50] F. H. Yu és W. A. Catterall (2004) „The VGL-chanome: a protein superfamily specialized for electrical signaling and ionic homeostasis”, Sci. STKE Signal Transduct. Knowl. Environ., köt. 2004, sz. 253, o. re15.
[51] M. H. Meisler és J. A. Kearney (2005) „Sodium channel mutations in epilepsy and other neurological disorders”, J. Clin. Invest., köt. 115, sz. 8, o. 2010–2017.
[52] D. A. Beneski és W. A. Catterall (1980) „Covalent labeling of protein components of the sodium channel with a photoactivable derivative of scorpion toxin”, Proc. Natl. Acad. Sci. U. S. A., köt. 77, sz. 1, o. 639–643.
[53] H. A. Fozzard, M. F. Sheets, és D. A. Hanck (2011) „The sodium channel as a target for local anesthetic drugs”, Front. Pharmacol., köt. 2, o. 68.
153
[54] D. A. Doyle, J. Morais Cabral, R. A. Pfuetzner, A. Kuo, J. M. Gulbis, S. L. Cohen, B. T. Chait, és R.
MacKinnon (1998) „The structure of the potassium channel: molecular basis of K+ conduction and selectivity”, Science, köt. 280, sz. 5360, o. 69–77.
[55] Y. Jiang, A. Lee, J. Chen, M. Cadene, B. T. Chait, és R. MacKinnon (2002) „The open pore conformation of potassium channels”, Nature, köt. 417, sz. 6888, o. 523–526.
[56] W. Ulbricht (2005) „Sodium channel inactivation: molecular determinants and modulation”, Physiol.
Rev., köt. 85, sz. 4, o. 1271–1301.
[57] K. McCormack, S. Santos, M. L. Chapman, D. S. Krafte, B. E. Marron, C. W. West, M. J. Krambis, B. M. Antonio, S. G. Zellmer, D. Printzenhoff, K. M. Padilla, Z. Lin, P. K. Wagoner, N. A. Swain, P. A. Stupple, M. de Groot, R. P. Butt, és N. A. Castle (2013) „Voltage sensor interaction site for selective small molecule inhibitors of voltage-gated sodium channels”, Proc. Natl. Acad. Sci. U. S.
A., köt. 110, sz. 29, o. E2724-2732.
[58] G. A. Patino és L. L. Isom (2010) „Electrophysiology and beyond: multiple roles of Na+ channel β subunits in development and disease”, Neurosci. Lett., köt. 486, sz. 2, o. 53–59.
[59] A. L. Hodgkin és A. F. Huxley (1952) „A quantitative description of membrane current and its application to conduction and excitation in nerve”, J. Physiol., köt. 117, sz. 4, o. 500–544.
[60] J. Payandeh, T. Scheuer, N. Zheng, és W. A. Catterall (2011) „The crystal structure of a voltage-gated sodium channel”, Nature, köt. 475, sz. 7356, o. 353–358.
[61] C. A. Ahern, J. Payandeh, F. Bosmans, és B. Chanda (2016) „The hitchhiker’s guide to the voltage-gated sodium channel galaxy”, J. Gen. Physiol., köt. 147, sz. 1, o. 1–24.
[62] E. C. McCusker, C. Bagnéris, C. E. Naylor, A. R. Cole, N. D’Avanzo, C. G. Nichols, és B. A.
Wallace (2012) „Structure of a bacterial voltage-gated sodium channel pore reveals mechanisms of opening and closing”, Nat. Commun., köt. 3, o. 1102.
[63] J. Payandeh, T. M. Gamal El-Din, T. Scheuer, N. Zheng, és W. A. Catterall (2012) „Crystal structure of a voltage-gated sodium channel in two potentially inactivated states”, Nature., 486(7401):135-9 [64] X. Zhang, W. Ren, P. DeCaen, C. Yan, X. Tao, L. Tang, J. Wang, K. Hasegawa, T. Kumasaka, J.
He, J. Wang, D. E. Clapham, és N. Yan (2012) „Crystal structure of an orthologue of the NaChBac voltage-gated sodium channel”, Nature, köt. 486, sz. 7401, o. 130–134.
[65] C.-J. Tsai, K. Tani, K. Irie, Y. Hiroaki, T. Shimomura, D. G. McMillan, G. M. Cook, G. F. X.
Schertler, Y. Fujiyoshi, és X.-D. Li (2013) „Two Alternative Conformations of a Voltage-Gated Sodium Channel”, J. Mol. Biol., köt. 425, sz. 22, o. 4074–4088.
[66] A. O. O’Reilly, E. Eberhardt, C. Weidner, C. Alzheimer, B. A. Wallace, és A. Lampert (2012)
„Bisphenol A Binds to the Local Anesthetic Receptor Site to Block the Human Cardiac Sodium Channel”, PLoS ONE, köt. 7, sz. 7, o. e41667.
[67] J. Payandeh és D. L. Minor (2015) „Bacterial Voltage-Gated Sodium Channels (BacNaVs) from the Soil, Sea, and Salt Lakes Enlighten Molecular Mechanisms of Electrical Signaling and Pharmacology in the Brain and Heart”, J. Mol. Biol., köt. 427, sz. 1, o. 3–30.
[68] P. C. Ruben. Voltage Gated Sodium Channels. Springer Berlin. Heidelberg, 2014: 400-406.
154
[69] S. Ahuja, S. Mukund, L. Deng, K. Khakh, E. Chang, H. Ho, S. Shriver, C. Young, S. Lin, J. P.
Johnson, P. Wu, J. Li, M. Coons, C. Tam, B. Brillantes, H. Sampang, K. Mortara, K. K. Bowman, K.
R. Clark, A. Estevez, Z. Xie, H. Verschoof, M. Grimwood, C. Dehnhardt, J.-C. Andrez, T. Focken, D. P. Sutherlin, B. S. Safina, M. A. Starovasnik, D. F. Ortwine, Y. Franke, C. J. Cohen, D. H.
Hackos, C. M. Koth, és J. Payandeh (2015) „Structural basis of Nav1.7 inhibition by an isoform-selective small-molecule antagonist”, Science, köt. 350, sz. 6267, o. aac5464.
[70] M. Arcisio-Miranda, Y. Muroi, S. Chowdhury, és B. Chanda (2010) „Molecular mechanism of allosteric modification of voltage-dependent sodium channels by local anesthetics”, J. Gen. Physiol., köt. 136, sz. 5, o. 541–554.
[71] C. Boiteux, I. Vorobyov, és T. W. Allen (2014) „Ion conduction and conformational flexibility of a bacterial voltage-gated sodium channel”, Proc. Natl. Acad. Sci. U. S. A., köt. 111, sz. 9, o. 3454–
3459.
[72] M. F. Sheets, H. A. Fozzard, G. M. Lipkind, és D. A. Hanck (2010) „Sodium channel molecular conformations and antiarrhythmic drug affinity”, Trends Cardiovasc. Med., köt. 20, sz. 1, o. 16–21.
[73] D. S. Ragsdale, J. C. McPhee, T. Scheuer, és W. A. Catterall (1994) „Molecular determinants of state-dependent block of Na+ channels by local anesthetics”, Science, köt. 265, sz. 5179, o. 1724–
1728.
[74] A. Mike és P. Lukacs (2010) „The enigmatic drug binding site for sodium channel inhibitors”, Curr.
Mol. Pharmacol., köt. 3, sz. 3, o. 129–144.
[75] S. B. Long, E. B. Campbell, és R. Mackinnon (2005) „Crystal structure of a mammalian voltage-dependent Shaker family K+ channel”, Science, köt. 309, sz. 5736, o. 897–903.
[76] R. W. Aldrich, D. P. Corey, és C. F. Stevens (1983) „A reinterpretation of mammalian sodium channel gating based on single channel recording”, Nature, köt. 306, sz. 5942, o. 436–441.
[77] M. Zhou, J. H. Morais-Cabral, S. Mann, és R. MacKinnon (2001) „Potassium channel receptor site for the inactivation gate and quaternary amine inhibitors”, Nature, köt. 411, sz. 6838, o. 657–661.
[78] Y. Zhou és R. MacKinnon (2003) „The occupancy of ions in the K+ selectivity filter: charge balance and coupling of ion binding to a protein conformational change underlie high conduction rates”, J.
Mol. Biol., köt. 333, sz. 5, o. 965–975.
[79] Z.-Y. Ye, K.-Q. Zhou, T.-L. Xu, és J.-N. Zhou (2008) „Fluoxetine potentiates GABAergic IPSCs in rat hippocampal neurons”, Neurosci. Lett., köt. 442, sz. 1, o. 24–29.
[80] A. Toib, V. Lyakhov, és S. Marom (1998) „Interaction between duration of activity and time course of recovery from slow inactivation in mammalian brain Na+ channels”, J. Neurosci. Off. J. Soc.
Neurosci., köt. 18, sz. 5, o. 1893–1903.
[81] W. Xiong, Y. Z. Farukhi, Y. Tian, D. Disilvestre, R. A. Li, és G. F. Tomaselli (2006) „A conserved ring of charge in mammalian Na+ channels: a molecular regulator of the outer pore conformation during slow inactivation”, J. Physiol., köt. 576, sz. Pt 3, o. 739–754.
[82] S. A. Pless, J. D. Galpin, A. Frankel, és C. A. Ahern (2011) „Molecular basis for class Ib anti-arrhythmic inhibition of cardiac sodium channels”, Nat. Commun., köt. 2, o. 351.
155
[83] K. Gyires, Z. Fürst, és G. Pethő, Szerk., „A farmakológia alapjai”. Medicina Könyvkiadó Zrt., Budapest, 2011: 202-204.
[84] L. S. Milescu, G. Akk, és F. Sachs (2005) „Maximum likelihood estimation of ion channel kinetics from macroscopic currents”, Biophys. J., köt. 88, sz. 4, o. 2494–2515.
[85] A. Destexhe, Z. F. Mainen, és T. J. Sejnowski (1994) „Synthesis of models for excitable membranes, synaptic transmission and neuromodulation using a common kinetic formalism”, J. Comput.
Neurosci., köt. 1, sz. 3, o. 195–230.
[86] D. Colquhoun és A. G. Hawkes (1977) „Relaxation and fluctuations of membrane currents that flow through drug-operated channels”, Proc. R. Soc. Lond. B Biol. Sci., köt. 199, sz. 1135, o. 231–262.
[87] Z. Benyó. "Kompartment modellek adaptív szabályozások". Budapesti Műszaki Egyetem, Budapest, 1990. (oktatási anyag)
[88] N. Mukhtasimova, C. Free, és S. M. Sine (2005) „Initial coupling of binding to gating mediated by conserved residues in the muscle nicotinic receptor”, J. Gen. Physiol., köt. 126, sz. 1, o. 23–39.
[89] D. Colquhoun és A. Hawkes. „A Q-Matrix Cookbook”. In B. Sakmann, E. Neher (szerk.), Single-Channel Recording. Plenum Press, New York, 1995: 589-633.
[90] K. Arning, „Mathematical Modelling and Simulation of Ion Channels.”, Linz, 2009. (PhD disszertáció)
[91] L. Goldman (2006) „Quantitative analysis of a fully generalized four-state kinetic scheme”, Biophys.
J., köt. 91, sz. 1, o. 173–178.
[92] G. Póta. „Modern fizikai kémia". Debreceni Egyetem, Debrecen, 2013.
[93] Turányi Tamás. "Reakciómechanizmusok vizsgálata [reakciókinetika - bizonytalanságanalízis - mechnaizmusredukció". Akadémiai Kiadó, Budapest, 2010: 52-57.
[94] M. Fink és D. Noble (2009) „Markov models for ion channels: versatility versus identifiability and speed”, Philos. Transact. A Math. Phys. Eng. Sci., köt. 367, sz. 1896, o. 2161–2179.
[95] K. J. Gingrich és L. E. Wagner (2016) „Fast-onset lidocaine block of rat NaV1.4 channels suggests involvement of a second high-affinity open state”, Biochim. Biophys. Acta, köt. 1858, sz. 6, o. 1175–
1188.
[96] J. J. Celentano és A. G. Hawkes (2004) „Use of the covariance matrix in directly fitting kinetic parameters: application to GABAA receptors”, Biophys. J., köt. 87, sz. 1, o. 276–294.
[97] P. d’Alcantara, L. M. Cardenas, S. Swillens, és R. S. Scroggs (2002) „Reduced transition between open and inactivated channel states underlies 5HT increased I(Na+) in rat nociceptors”, Biophys. J., köt. 83, sz. 1, o. 5–21.
[98] J. D. Moreno, T. J. Lewis, és C. E. Clancy (2016) „Parameterization for In-Silico Modeling of Ion Channel Interactions with Drugs”, PloS One, köt. 11, sz. 3, o. e0150761.
[99] C. Erdősné Sélley, G. Gyurecz, J. Janik, és G. Körtélyesi," Mérnöki optimalizáció”. Typotex, Budapest, 2012: 64-69.
[100] V. Menon, N. Spruston, és W. L. Kath (2009) „A state-mutating genetic algorithm to design ion-channel models”, Proc. Natl. Acad. Sci. U. S. A., köt. 106, sz. 39, o. 16829–16834.
156
[101] M. Gurkiewicz és A. Korngreen (2007) „A Numerical Approach to Ion Channel Modelling Using Whole-Cell Voltage-Clamp Recordings and a Genetic Algorithm”, PLoS Comput. Biol., köt. 3, sz. 8, o. e169.
[102] R. A. Alberty (2004) „Principle of Detailed Balance in Kinetics”, J. Chem. Educ., köt. 81, sz. 8, o.
1206.
[103] F. P. Kelly. Reversibility and stochastic networks. Rev. ed. Cambridge University Press, New York, 2011:77-79.
[104] Tóth János és Simon L. Péter. Differenciálegyenletek: bevezetés az elméletbe és az alkalmazásokba.
Typotex, Budapest, 2009: 101-102.
[105] M. Feinberg (1989) „Necessary and sufficient conditions for detailed balancing in mass action systems of arbitrary complexity”, Chem. Eng. Sci., köt. 44, sz. 9, o. 1819–1827.
[106] D. Colquhoun, K. A. Dowsland, M. Beato, és A. J. R. Plested (2004) „How to impose microscopic reversibility in complex reaction mechanisms”, Biophys. J., köt. 86, sz. 6, o. 3510–3518.
[107] E. A. Richard és C. Miller (1990) „Steady-state coupling of ion-channel conformations to a transmembrane ion gradient”, Science, köt. 247, sz. 4947, o. 1208–1210.
[108] D. J. Wyllie, P. Béhé, M. Nassar, R. Schoepfer, és D. Colquhoun (1996) „Single-channel currents from recombinant NMDA NR1a/NR2D receptors expressed in Xenopus oocytes”, Proc. Biol. Sci., köt. 263, sz. 1373, o. 1079–1086.
[109] P. Kienker (1989) „Equivalence of aggregated Markov models of ion-channel gating”, Proc. R. Soc.
Lond. B Biol. Sci., köt. 236, sz. 1284, o. 269–309.
[110] M. P. Saccomani, S. Audoly, G. Bellu, és L. D’Angiò (2010) „Examples of testing global identifiability of biological and biomedical models with the DAISY software”, Comput. Biol. Med., köt. 40, sz. 4, o. 402–407.
[111] M. Fink, J. J. Batzel, és H. Tran (2008) „A respiratory system model: parameter estimation and sensitivity analysis”, Cardiovasc. Eng. Dordr. Neth., köt. 8, sz. 2, o. 120–134.
[112] C. Cobelli és J. J. DiStefano (1980) „Parameter and structural identifiability concepts and ambiguities: a critical review and analysis”, Am. J. Physiol., köt. 239, sz. 1, o. R7-24.
[113] J. Reid (1977) „Structural identifiability in linear time-invariant systems”, IEEE Trans. Autom.
Control, köt. 22, sz. 2, o. 242–246.
[114] J. Monod és F. Jacob (1961) „Teleonomic mechanisms in cellular metabolism, growth, and differentiation”, Cold Spring Harb. Symp. Quant. Biol., köt. 26, o. 389–401.
[115] D. Colquhoun és R. Lape (2012) „Allosteric coupling in ligand-gated ion channels”, J. Gen.
[118] F. Bezanilla (1985) „Gating of sodium and potassium channels”, J. Membr. Biol., köt. 88, sz. 2, o.
97–111.
157
[119] B. Hille (1977) „Local anesthetics: hydrophilic and hydrophobic pathways for the drug-receptor reaction”, J. Gen. Physiol., köt. 69, sz. 4, o. 497–515.
[120] L. M. Hondeghem és B. G. Katzung (1977) „Time- and voltage-dependent interactions of antiarrhythmic drugs with cardiac sodium channels”, Biochim. Biophys. Acta, köt. 472, sz. 3–4, o.
373–398.
[121] C. F. Starmer, A. O. Grant, és H. C. Strauss (1984) „Mechanisms of use-dependent block of sodium channels in excitable membranes by local anesthetics”, Biophys. J., köt. 46, sz. 1, o. 15–27.
[122] J. R. Balser, H. B. Nuss, D. W. Orias, D. C. Johns, E. Marban, G. F. Tomaselli, és J. H. Lawrence (1996) „Local anesthetics as effectors of allosteric gating. Lidocaine effects on inactivation-deficient rat skeletal muscle Na channels”, J. Clin. Invest., köt. 98, sz. 12, o. 2874–2886.
[123] K. J. Gingrich, D. Beardsley, és D. T. Yue (1993) „Ultra-deep blockade of Na+ channels by a
„Coupling between fast and slow inactivation revealed by analysis of a point mutation (F1304Q) in mu 1 rat skeletal muscle sodium channels”, J. Physiol., köt. 494 ( Pt 2), o. 411–429.
[126] C. F. Starmer (1987) „Theoretical characterization of ion channel blockade. Competitive binding to periodically accessible receptors”, Biophys. J., köt. 52, sz. 3, o. 405–412.
[127] C. F. Starmer, D. L. Packer, és A. O. Grant (1987) „Ligand binding to transiently accessible sites:
mechanisms for varying apparent binding rates”, J. Theor. Biol., köt. 124, sz. 3, o. 335–341.
[128] C. F. Starmer és K. R. Courtney (1986) „Modeling ion channel blockade at guarded binding sites:
application to tertiary drugs”, Am. J. Physiol., köt. 251, sz. 4 Pt 2, o. H848-856.
[129] C. F. Starmer és A. O. Grant (1985) „Phasic ion channel blockade. A kinetic model and parameter estimation procedure”, Mol. Pharmacol., köt. 28, sz. 4, o. 348–356.
[130] J. H. Grønlien, M. Håkerud, H. Ween, K. Thorin-Hagene, C. A. Briggs, M. Gopalakrishnan, és J.
Malysz (2007) „Distinct profiles of alpha7 nAChR positive allosteric modulation revealed by structurally diverse chemotypes”, Mol. Pharmacol., köt. 72, sz. 3, o. 715–724.
[131] J. Malysz, J. H. Grønlien, D. B. Timmermann, M. Håkerud, K. Thorin-Hagene, H. Ween, J. D.
Trumbull, Y. Xiong, C. A. Briggs, P. K. Ahring, T. Dyhring, és M. Gopalakrishnan (2009)
„Evaluation of alpha7 nicotinic acetylcholine receptor agonists and positive allosteric modulators using the parallel oocyte electrophysiology test station”, Assay Drug Dev. Technol., köt. 7, sz. 4, o.
374–390.
[132] R. L. Papke, E. Meyer, T. Nutter, és V. V. Uteshev (2000) „α7 Receptor-selective agonists and modes of α7 receptor activation”, Eur. J. Pharmacol., köt. 393, sz. 1–3, o. 179–195.
[133] R. L. Papke és J. S. Thinschmidt (1998) „The correction of alpha7 nicotinic acetylcholine receptor concentration-response relationships in Xenopus oocytes”, Neurosci. Lett., köt. 256, sz. 3, o. 163–
166.
158
[134] L. D. Islas és W. N. Zagotta (2006) „Short-range molecular rearrangements in ion channels detected by tryptophan quenching of bimane fluorescence”, J. Gen. Physiol., köt. 128, sz. 3, o. 337–346.
[135] J. Mészáros. „Numerikus módszerek”. Miskolci Egyetem Földtudományi Kar. Magyarország, 2011.
[136] G. Geda, „Modellezés és szimuláció az oktatásban”. Educatio Kht., Budapest, 2011: 28.
[137] B. Paláncz. „Közönséges differenciálegyenletek”. In Numerikus módszerek, 2011. (online jegyzet) [138] W. H. Press. Numerical recipes in C++: the art of scientific computing, 2nd ed. Cambridge
University Press, Cambridge, 2002: 70-72.
[139] A. K. Szabo, K. Pesti, A. Mike, és E. S. Vizi (2014) „Mode of action of the positive modulator PNU-120596 on α7 nicotinic acetylcholine receptors”, Neuropharmacology, köt. 81, o. 42–54.
[140] K. Pesti, A. K. Szabo, A. Mike, és E. S. Vizi (2014) „Kinetic properties and open probability of α7 nicotinic acetylcholine receptors”, Neuropharmacology, köt. 81, o. 101–115.
[141] C. J. B. daCosta és S. M. Sine (2013) „Stoichiometry for drug potentiation of a pentameric ion channel”, Proc. Natl. Acad. Sci. U. S. A., köt. 110, sz. 16, o. 6595–6600.
[142] R. Karoly, N. Lenkey, A. O. Juhasz, E. S. Vizi, és A. Mike (2010) „Fast- or Slow-inactivated State Preference of Na+ Channel Inhibitors: A Simulation and Experimental Study”, PLoS Comput. Biol., köt. 6, sz. 6, o. e1000818.
[143] N. Lenkey, R. Karoly, P. Lukacs, E. S. Vizi, M. Sunesen, L. Fodor, és A. Mike (2010)
„Classification of Drugs Based on Properties of Sodium Channel Inhibition: A Comparative Automated Patch-Clamp Study”, PLoS ONE, köt. 5, sz. 12, o. e15568.
[144] T. Anno és L. M. Hondeghem (1990) „Interactions of flecainide with guinea pig cardiac sodium channels. Importance of activation unblocking to the voltage dependence of recovery”, Circ. Res., köt. 66, sz. 3, o. 789–803.
[145] H. Liu, J. Atkins, és R. S. Kass (2003) „Common Molecular Determinants of Flecainide and Lidocaine Block of Heart Na + Channels: Evidence from Experiments with Neutral and Quaternary Flecainide Analogues”, J. Gen. Physiol., köt. 121, sz. 3, o. 199–214.
[146] H. Liu, M. Tateyama, C. E. Clancy, H. Abriel, és R. S. Kass (2002) „Channel Openings Are Necessary but not Sufficient for Use-dependent Block of Cardiac Na + Channels by Flecainide:
Evidence from the Analysis of Disease-linked Mutations”, J. Gen. Physiol., köt. 120, sz. 1, o. 39–51.
[147] D. S. Ragsdale, J. C. McPhee, T. Scheuer, és W. A. Catterall (1996) „Common molecular determinants of local anesthetic, antiarrhythmic, and anticonvulsant block of voltage-gated Na+
channels”, Proc. Natl. Acad. Sci. U. S. A., köt. 93, sz. 17, o. 9270–9275.
[148] D. A. Hanck, E. Nikitina, M. M. McNulty, H. A. Fozzard, G. M. Lipkind, és M. F. Sheets (2009)
„Using lidocaine and benzocaine to link sodium channel molecular conformations to state-dependent antiarrhythmic drug affinity”, Circ. Res., köt. 105, sz. 5, o. 492–499.
[149] M. G. Mujtaba, S.-Y. Wang, és G. K. Wang (2002) „Prenylamine block of Nav1.5 channel is mediated via a receptor distinct from that of local anesthetics”, Mol. Pharmacol., köt. 62, sz. 2, o.
415–422.
[150] S. N. Wright (2001) „Irreversible block of human heart (hH1) sodium channels by the plant alkaloid lappaconitine”, Mol. Pharmacol., köt. 59, sz. 2, o. 183–192.
159
[151] M. F. Sheets és D. A. Hanck (2007) „Outward stabilization of the S4 segments in domains III and IV enhances lidocaine block of sodium channels”, J. Physiol., köt. 582, sz. Pt 1, o. 317–334.
[152] T. Mickus, H. y Jung, és N. Spruston (1999) „Properties of slow, cumulative sodium channel inactivation in rat hippocampal CA1 pyramidal neurons”, Biophys. J., köt. 76, sz. 2, o. 846–860.
[153] P. W. Lenkowski, T. W. Batts, M. D. Smith, S.-H. Ko, P. J. Jones, C. H. Taylor, A. K. McCusker, G.
C. Davis, H. A. Hartmann, H. S. White, M. L. Brown, és M. K. Patel (2007) „A pharmacophore derived phenytoin analogue with increased affinity for slow inactivated sodium channels exhibits a desired anticonvulsant profile”, Neuropharmacology, köt. 52, sz. 3, o. 1044–1054.
[154] C. C. Kuo és B. P. Bean (1994) „Na+ channels must deactivate to recover from inactivation”, Neuron, köt. 12, sz. 4, o. 819–829.
[155] T. A. Ban (2006) „The role of serendipity in drug discovery”, Dialogues Clin. Neurosci., köt. 8, sz.
3, o. 335–344.
[156] E. Hargrave-Thomas, B. Yu, és J. Reynisson (2012) „The Effect of Serendipity in Drug Discovery and Development”.
[157] M. Gurkiewicz, A. Korngreen, S. G. Waxman, és A. Lampert (2011) „Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation”, J. Neurophysiol., köt. 105, sz. 4, o. 1546–1557.
[158] A. Taddese és B. P. Bean (2002) „Subthreshold sodium current from rapidly inactivating sodium channels drives spontaneous firing of tuberomammillary neurons”, Neuron, köt. 33, sz. 4, o. 587–
600.
[159] C. A. Vandenberg és F. Bezanilla (1991) „A sodium channel gating model based on single channel, macroscopic ionic, and gating currents in the squid giant axon”, Biophys. J., köt. 60, sz. 6, o. 1511–
1533.
[160] C. M. Armstrong (2006) „Na channel inactivation from open and closed states”, Proc. Natl. Acad.
Sci. U. S. A., köt. 103, sz. 47, o. 17991–17996.
160