Voltage-gated Na⁺ channels in neuropathic pain

Bibliography

• STUCKY CL, GOLD MS, ZHANG X: Mechanisms of pain. Proc. Natl. Acad. Sci. USA (2001) 98:11845-11846.
   PubMed Web of Science ®Google Scholar
• WOOLF CJ, MANNION RJ: Neuropathic pain: aetiology, symptoms, mechanisms, and management. Lancet (1999) 353:1959-1964.
   PubMed Web of Science ®Google Scholar
• LAI J, PORRECA F, HUNTER JC, GOLD MS: Voltage-gated sodium channels and hyperalgesia. Ann. Rev. Pharmacol. Toxicol. (2004) 44:371-397.
   PubMed Web of Science ®Google Scholar
• BENNETT GJ: Can we distinguish between inflammatory and neuropathic pain? Pain Res. Manag. (2006) 11(Suppl. A):11A-15A.
   PubMedGoogle Scholar
• LAWSON SN: Phenotype and function of somatic primary afferent nociceptive neurones with C-, αδ- or α/β-fibres. Exp. Physiol. (2002) 87:239-244.
   PubMed Web of Science ®Google Scholar
• DOMBOURIAN MG, TURNER NA, GEROVAC TA et al.: B1 and TRPV-1 receptor genes and their relationship to hyperalgesia following spinal cord injury. Spine (2006) 31:2778-2782.
   PubMed Web of Science ®Google Scholar
• KAGE K, NIFORATOS W, ZHU CZ, LYNCH KJ, HONORE P, JARVIS MF: Alteration of dorsal root ganglion P2X3 receptor expression and function following spinal nerve ligation in the rat. Exp. Brain Res. (2002) 147:511-519.
   PubMed Web of Science ®Google Scholar
• OLSON TH, RIEDL MS, VULCHANOVA L, ORTIZ-GONZALEZ XR, ELDE R: An acid sensing ion channel (ASIC) localizes to small primary afferent neurons in rats. Neuroreport (1998) 9:1109-1113.
   PubMed Web of Science ®Google Scholar
• NESS TJ: Pharmacology of peripheral analgesia. Pain Pract. (2001) 1:243-254.
   PubMedGoogle Scholar
• JI RR, KOHNO T, MOORE KA, WOOLF CJ: Central sensitization and LTP: do pain and memory share similar mechanisms? Trends Neurosci. (2003) 26:696-705.
   PubMed Web of Science ®Google Scholar
• AMIR R, ARGOFF CE, BENNETT GJ et al.: The role of sodium channels in chronic inflammatory and neuropathic pain. J. Pain (2006) 7:S1-S29.
   PubMed Web of Science ®Google Scholar
• CATTERALL WA: From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron (2000) 26:13-25.
   PubMed Web of Science ®Google Scholar
• KO SH, LENKOWSKI PW, LEE HC, MOUNSEY JP, PATEL MK: Modulation of Nav1.5 by β1- and β3-subunit co-expression in mammalian cells. Pflugers Arch. (2005) 449:403-412.
   PubMed Web of Science ®Google Scholar
• QU Y, ROGERS JC, CHEN SF, MCCORMICK KA, SCHEUER T, CATTERALL WA: Functional roles of the extracellular segments of the sodium channel α subunit in voltage-dependent gating and modulation by β1 subunits. J. Biol. Chem. (1999) 274:32647-32654.
   PubMed Web of Science ®Google Scholar
• GOLDIN AL, BARCHI RL, CALDWELL JH et al.: Nomenclature of voltage-gated sodium channels. Neuron (2000) 28:365-368.
   PubMed Web of Science ®Google Scholar
• ISOM LL, DE JONGH KS, PATTON DE et al.: Primary structure and functional expression of the β 1 subunit of the rat brain sodium channel. Science (1992) 256:839-842.
   PubMed Web of Science ®Google Scholar
• ISOM LL, RAGSDALE DS, DE JONGH KS et al.: Structure and function of the β 2 subunit of brain sodium channels, a transmembrane glycoprotein with a CAM motif. Cell (1995) 83:433-442.
   PubMed Web of Science ®Google Scholar
• MORGAN K, STEVENS EB, SHAH B et al.: β3: an additional auxiliary subunit of the voltage-sensitive sodium channel that modulates channel gating with distinct kinetics. Proc. Natl. Acad. Sci. USA (2000) 97:2308-2313.
   PubMed Web of Science ®Google Scholar
• YU FH, WESTENBROEK RE, SILOS-SANTIAGO I et al.: Sodium channel β4, a new disulfide-linked auxiliary subunit with similarity to β2. J. Neurosci. (2003) 23:7577-7585.
   PubMed Web of Science ®Google Scholar
• STÜHMER W, CONTI F, SUZUKI H et al.: Structural parts involved in activation and inactivation of the sodium channel. Nature (1989) 339:597-603.
   PubMed Web of Science ®Google Scholar
• YANG N, GEORGE ALJ, HORN R: Molecular basis of charge movement in voltage-gated sodium channels. Neuron (1996) 16:113-122.
   PubMed Web of Science ®Google Scholar
• HEINEMANN SH, TERLAU H, STUHMER W, IMOTO K, NUMA S: Calcium channel characteristics conferred on the sodium channel by single mutations. Nature (1992) 356:441-443.
   PubMed Web of Science ®Google Scholar
• WEST JW, PATTON DE, SCHEUER T, WANG Y, GOLDIN AL, CATTERALL WA: A cluster of hydrophobic amino acid residues required for fast Na+-channel inactivation. Proc. Natl. Acad. Sci. USA (1992) 89:10910-10914.
   PubMed Web of Science ®Google Scholar
• WEST JW, NUMANN R, MURPHY BJ, SCHEUER T, CATTERALL WA: A phosphorylation site in the Na+ channel required for modulation by protein kinase C. Science (1991) 254:866-868.
   PubMed Web of Science ®Google Scholar
• MURPHY BJ, ROSSIE S, DE JONGH KS, CATTERALL WA: Identification of the sites of selective phosphorylation and dephosphorylation of the rat brain Na+ channel α subunit by cAMP-dependent protein kinase and phosphoprotein phosphatases. J. Biol. Chem. (1993) 268:27355-27362.
   PubMed Web of Science ®Google Scholar
• YAJIMA Y, NARITA M, SHIMAMURA M, NARITA M, KUBOTA C, SUZUKI T: Differential involvement of spinal protein kinase C and protein kinase A in neuropathic and inflammatory pain in mice. Brain Res. (2003) 992:288-293.
   PubMed Web of Science ®Google Scholar
• GOLDIN AL: Resurgence of sodium channel research. Ann. Rev. Physiol. (2001) 63:871-894.
   PubMed Web of Science ®Google Scholar
• MILLER JR, PATEL MK, JOHN JE, MOUNSEY JP, MOORMAN JR: Contributions of charged residues in a cytoplasmic linking region to Na channel gating. Biochim. Biophys. Acta (2000) 1509:275-291.
   PubMed Web of Science ®Google Scholar
• MCPHEE JC, RAGSDALE DS, SCHEUER T, CATTERALL WA: A mutation in segment IVS6 disrupts fast inactivation of sodium channels. Proc. Natl. Acad. Sci. USA (1994) 91:12346-12350.
   PubMed Web of Science ®Google Scholar
• MCPHEE JC, RAGSDALE DS, SCHEUER T, CATTERALL WA: A critical role for transmembrane segment IVS6 of the sodium channel α subunit in fast inactivation. J. Biol. Chem. (1995) 270:12025-12034.
   PubMed Web of Science ®Google Scholar
• MCPHEE JC, RAGSDALE DS, SCHEUER T, CATTERALL WA: A critical role for the S4-S5 intracellular loop in domain IV of the sodium channel α-subunit in fast inactivation. J. Biol. Chem. (1998) 273:1121-1129.
   PubMed Web of Science ®Google Scholar
• MCCOLLUM IJ, VILIN YY, SPACKMAN E, FUJIMOTO E, RUBEN PC: Negatively charged residues adjacent to IFM motif in the DIII-DIV linker of hNaV1.4 differentially affect slow inactivation. FEBS Lett. (2003) 552:163-169.
   PubMed Web of Science ®Google Scholar
• ULBRICHT W: Sodium channel inactivation: molecular determinants and modulation. Physiol. Rev. (2005) 85:1271-1301.
   PubMed Web of Science ®Google Scholar
• O’REILLY JP, WANG SY, WANG GK: Residue-specific effects on slow inactivation at V787 in D2-S6 of Nav1.4 sodium channels. Biophys. J. (2001) 81:2100-2111.
   PubMed Web of Science ®Google Scholar
• CHEN Y, YU FH, SURMEIER DJ, SCHEUER T, CATTERALL WA: Neuromodulation of Na+ channel slow inactivation via cAMP-dependent protein kinase and protein kinase C. Neuron (2006) 49:409-420.
   PubMed Web of Science ®Google Scholar
• ROGAWSKI MA, LOSCHER W: The neurobiology of antiepileptic drugs. Nat. Rev. Neurosci. (2004) 5:553-564.
   PubMed Web of Science ®Google Scholar
• NAU C, WANG GK: Interactions of local anesthetics with voltage-gated Na+ channels. J. Membr. Biol. (2004) 201:1-8.
   PubMed Web of Science ®Google Scholar
• BLACK JA, DIB-HAJJ S, MCNABOLA K et al.: Spinal sensory neurons express multiple sodium channel α-subunit mRNAs. Brain Res. Mol. Brain Res. (1996) 43:117-131.
   PubMedGoogle Scholar
• DICKENSON AH, MATTHEWS EA, SUZUKI R: Neurobiology of neuropathic pain: mode of action of anticonvulsants. Eur. J. Pain (2002) 6(Suppl. A):51-60.
   PubMed Web of Science ®Google Scholar
• MATZNER O, DEVOR M: Hyperexcitability at sites of nerve injury depends on voltage-sensitive Na+ channels. J. Neurophysiol. (1994) 72:349-359.
   PubMed Web of Science ®Google Scholar
• LIU CN, WALL PD, BEN DOR E, MICHAELIS M, AMIR R, DEVOR M: Tactile allodynia in the absence of C-fiber activation: altered firing properties of DRG neurons following spinal nerve injury. Pain (2000) 85:503-521.
   PubMed Web of Science ®Google Scholar
• WAXMAN SG, DIB-HAJJ S, CUMMINS TR, BLACK JA: Sodium channels and pain. Proc. Natl. Acad. Sci. USA (1999) 96:7635-7639.
   PubMed Web of Science ®Google Scholar
• CUMMINS TR, WAXMAN SG: Downregulation of tetrodotoxin-resistant sodium currents and upregulation of a rapidly repriming tetrodotoxin-sensitive sodium current in small spinal sensory neurons after nerve injury. J. Neurosci. (1997) 17:3503-3514.
   PubMed Web of Science ®Google Scholar
• DIB-HAJJ SD, FJELL J, CUMMINS TR et al.: Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain. Pain (1999) 83:591-600.
   PubMed Web of Science ®Google Scholar
• WAXMAN SG, CUMMINS TR, DIB-HAJJ S, FJELL J, BLACK JA: Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain. Muscle Nerve (1999) 22:1177-1187.
   PubMed Web of Science ®Google Scholar
• BLACK JA, CUMMINS TR, PLUMPTON C et al.: Upregulation of a silent sodium channel after peripheral, but not central, nerve injury in DRG neurons. J. Neurophysiol. (1999) 82:2776-2785.
   PubMed Web of Science ®Google Scholar
• SLEEPER AA, CUMMINS TR, DIB-HAJJ SD et al.: Changes in expression of two tetrodotoxin-resistant sodium channels and their currents in dorsal root ganglion neurons after sciatic nerve injury but not rhizotomy. J. Neurosci. (2000) 20:7279-7289.
   PubMed Web of Science ®Google Scholar
• BLACK JA, LIU S, TANAKA M, CUMMINS TR, WAXMAN SG: Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain. Pain (2004) 108:237-247.
   PubMed Web of Science ®Google Scholar
• WAXMAN SG, KOCSIS JD, BLACK JA: Type III sodium channel mRNA is expressed in embryonic but not adult spinal sensory neurons, and is reexpressed following axotomy. J. Neurophysiol. (1994) 72:466-470.
   PubMed Web of Science ®Google Scholar
• DIB-HAJJ S, BLACK JA, FELTS P, WAXMAN SG: Down-regulation of transcripts for Na channel α-SNS in spinal sensory neurons following axotomy. Proc. Natl. Acad. Sci. USA (1996) 93:14950-14954.
   PubMed Web of Science ®Google Scholar
• DIB-HAJJ SD, TYRRELL L, BLACK JA, WAXMAN SG: NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy. Proc. Natl. Acad. Sci. USA (1998) 95:8963-8968.
   PubMed Web of Science ®Google Scholar
• KIM CH, OH Y, CHUNG JM, CHUNG K: The changes in expression of three subtypes of TTX sensitive sodium channels in sensory neurons after spinal nerve ligation. Brain Res. Mol. Brain Res. (2001) 95:153-161.
   PubMedGoogle Scholar
• HAINS BC, KLEIN JP, SAAB CY, CRANER MJ, BLACK JA, WAXMAN SG: Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury. J. Neurosci. (2003) 23:8881-8892.
   PubMed Web of Science ®Google Scholar
• HAINS BC, SAAB CY, KLEIN JP, CRANER MJ, WAXMAN SG: Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury. J. Neurosci. (2004) 24:4832-4839.
   PubMed Web of Science ®Google Scholar
• LINDIA JA, KOHLER MG, MARTIN WJ, ABBADIE C: Relationship between sodium channel NaV1.3 expression and neuropathic pain behavior in rats. Pain (2005) 117:145-153.
   PubMed Web of Science ®Google Scholar
• NASSAR MA, BAKER MD, LEVATO A et al.: Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice. Mol. Pain (2006) 2:33.
   PubMed Web of Science ®Google Scholar
• TOLEDO-ARAL JJ, MOSS BL, HE ZJ et al.: Identification of PN1, a predominant voltage-dependent sodium channel expressed principally in peripheral neurons. Proc. Natl. Acad. Sci. USA (1997) 94:1527-1532.
   PubMed Web of Science ®Google Scholar
• SANGAMESWARAN L, FISH LM, KOCH BD et al.: A novel tetrodotoxin-sensitive, voltage-gated sodium channel expressed in rat and human dorsal root ganglia. J. Biol. Chem. (1997) 272:14805-14809.
   PubMed Web of Science ®Google Scholar
• NASSAR MA, STIRLING LC, FORLANI G et al.: Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proc. Natl. Acad. Sci. USA (2004) 101:12706-12711.
   PubMed Web of Science ®Google Scholar
• NASSAR MA, LEVATO A, STIRLING LC, WOOD JN: Neuropathic pain develops normally in mice lacking both Nav1.7 and Nav1.8. Mol. Pain (2005) 1:24.
   PubMed Web of Science ®Google Scholar
• YANG Y, WANG Y, LI S et al.: Mutations in SCN9A, encoding a Na channel α subunit, in patients with primary erythermalgia. J. Med. Genet. (2004) 41:171-174.
   PubMed Web of Science ®Google Scholar
• CUMMINS TR, DIB-HAJJ SD, WAXMAN SG: Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. J. Neurosci. (2004) 24:8232-8236.
   PubMed Web of Science ®Google Scholar
• FERTLEMAN CR, BAKER MD, PARKER KA et al.: SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron (2006) 52:767-774.
   PubMed Web of Science ®Google Scholar
• COX JJ, REIMANN F, NICHOLAS AK et al.: An SCN9A channelopathy causes congenital inability to experience pain. Nature (2006) 444:894-898.
   PubMed Web of Science ®Google Scholar
• AKOPIAN AN, SIVILOTTI L, WOOD JN: A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons. Nature (1996) 379:257-262.
   PubMed Web of Science ®Google Scholar
• GOLD MS, WEINREICH D, KIM CS et al.: Redistribution of NaV1.8 in uninjured axons enables neuropathic pain. J. Neurosci. (2003) 23:158-166.
   PubMed Web of Science ®Google Scholar
• LAI J, GOLD MS, KIM CS et al.: Inhibition of neuropathic pain by decreased expression of the tetrodotoxin-resistant sodium channel, NaV1.8. Pain (2002) 95:143-152.
   PubMed Web of Science ®Google Scholar
• ABDULLA FA, SMITH PA: Changes in Na+ channel currents of rat dorsal root ganglion neurons following axotomy and axotomy-induced autotomy. J. Neurophysiol. (2002) 88:2518-2529.
   PubMed Web of Science ®Google Scholar
• DECOSTERD I, JI RR, ABDI S, TATE S, WOOLF CJ: The pattern of expression of the voltage-gated sodium channels Nav1.8 and Nav1.9 does not change in uninjured primary sensory neurons in experimental neuropathic pain models. Pain (2002) 96:269-277.
   PubMed Web of Science ®Google Scholar
• NOVAKOVIC SD, TZOUMAKA E, MCGIVERN JG et al.: Distribution of the tetrodotoxin-resistant sodium channel PN3 in rat sensory neurons in normal and neuropathic conditions. J. Neurosci. (1998) 18:2174-2187.
   PubMed Web of Science ®Google Scholar
• PORRECA F, LAI J, BIAN D et al.: A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of chronic pain. Proc. Natl. Acad. Sci. USA (1999) 96:7640-7644.
   PubMed Web of Science ®Google Scholar
• PRIEST BT, MURPHY BA, LINDIA JA et al.: Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior. Proc. Natl. Acad. Sci. USA (2005) 102:9382-9387.
   PubMed Web of Science ®Google Scholar
• HILLE B: Local anesthetics: hydrophilic and hydrophobic pathways for the drug-receptor reaction. J. Gen. Physiol. (1977) 69:497-515.
   PubMed Web of Science ®Google Scholar
• HONDEGHEM LM, KATZUNG BG: Time-and voltage-dependent interactions of antiarrhythmic drugs with cardiac sodium channels. Biochim. Biophys. Acta (1977) 472:373-398.
   PubMed Web of Science ®Google Scholar
• KO SH, JOCHNOWITZ N, LENKOWSKI PW et al.: Reversal of neuropathic pain by α-hydroxyphenylamide: a novel sodium channel antagonist. Neuropharmacology (2006) 50:865-873.
   PubMed Web of Science ®Google Scholar
• ILYIN VI, POMONIS JD, WHITESIDE GT et al.: Pharmacology of 2-[4-(4-chloro-2-fluorophenoxy)phenyl]- pyrimidine-4-carboxamide: a potent, broad-spectrum state-dependent sodium channel blocker for treating pain states. J. Pharmacol. Exp. Ther. (2006) 318:1083-1093.
   PubMed Web of Science ®Google Scholar
• LENKOWSKI PW, BATTS TW, SMITH MD et al.: A pharmacophore derived phenytoin analogue with increased affinity for slow inactivated sodium channels exhibits a desired anticonvulsant profile. Neuropharmacology (2007) 52:1044-1054.
   PubMed Web of Science ®Google Scholar
• BACKONJA MM: Anticonvulsants (antineuropathics) for neuropathic pain syndromes. Clin. J. Pain (2000) 16:S67-S72.
   PubMedGoogle Scholar
• BACKONJA MM: Use of anticonvulsants for treatment of neuropathic pain. Neurology (2002) 59:S14-S17.
   PubMed Web of Science ®Google Scholar
• TREMONT-LUKATS IW, MEGEFF C, BACKONJA MM: Anticonvulsants for neuropathic pain syndromes: mechanisms of action and place in therapy. Drugs (2000) 60:1029-1052.
   PubMed Web of Science ®Google Scholar
• HARATI Y, GOOCH C, SWENSON M et al.: Double-blind randomized trial of tramadol for the treatment of the pain of diabetic neuropathy. Neurology (1998) 50:1842-1846.
   PubMed Web of Science ®Google Scholar
• SIMPSON DM, OLNEY R, MCARTHUR JC, KHAN A, GODBOLD J, EBEL-FROMMER K: A placebo-controlled trial of lamotrigine for painful HIV-associated neuropathy. Neurology (2000) 54:2115-2119.
   PubMed Web of Science ®Google Scholar
• VESTERGAARD K, ANDERSEN G, GOTTRUP H, KRISTENSEN BT, JENSEN TS: Lamotrigine for central poststroke pain: a randomized controlled trial. Neurology (2001) 56:184-190.
   PubMed Web of Science ®Google Scholar
• RASKIN P, DONOFRIO PD, ROSENTHAl NR et al.: Topiramate versus placebo in painful diabetic neuropathy: analgesic and metabolic effects. Neurology (2004) 63:865-873.
   PubMed Web of Science ®Google Scholar
• KHOROMI S, PATSALIDES A, PARADA S, SALEHI V, MEEGAN JM, MAX MB: Topiramate in chronic lumbar radicular pain. J. Pain (2005) 6:829-836.
   PubMed Web of Science ®Google Scholar
• GILRON I, BOOHER SL, ROWAN JS, MAX MB: Topiramate in trigeminal neuralgia: a randomized, placebo-controlled multiple crossover pilot study. Clin. Neuropharmacol. (2001) 24:109-112.
   PubMed Web of Science ®Google Scholar
• VENERONI O, MAJ R, CALABRESI M, FARAVELLI L, FARIELLO RG, SALVATI P: Anti-allodynic effect of NW-1029, a novel Na+ channel blocker, in experimental animal models of inflammatory and neuropathic pain. Pain (2003) 102:17-25.
   PubMed Web of Science ®Google Scholar
• SABIDO-DAVID C, FARAVELLI L, SALVATI P: The therapeutic potential of Na+ and Ca2+ channel blockers in pain management. Expert Opin. Investig. Drugs (2004) 13(10):1249-1261.
   PubMed Web of Science ®Google Scholar
• KOHANE DS, SMITH SE, LOUIS DN et al.: Prolonged duration local anesthesia from tetrodotoxin-enhanced local anesthetic microspheres. Pain (2003) 104:415-421.
   PubMed Web of Science ®Google Scholar
• FERRANTE FM, PAGGIOLI J, CHERUKURI S, ARTHUR GR: The analgesic response to intravenous lidocaine in the treatment of neuropathic pain. Anesth. Analg. (1996) 82:91-97.
   PubMed Web of Science ®Google Scholar
• BACH FW, JENSEN TS, KASTRUP J, STIGSBY B, DEJGARD A: The effect of intravenous lidocaine on nociceptive processing in diabetic neuropathy. Pain (1990) 40:29-34.
   PubMed Web of Science ®Google Scholar
• DEVULDER JE, GHYS L, DHONDT W, ROLLY G: Neuropathic pain in a cancer patient responding to subcutaneously administered lignocaine. Clin. J. Pain (1993) 9:220-223.
   PubMed Web of Science ®Google Scholar
• SHORVON S: Oxcarbazepine: a review. Seizure (2000) 9:75-79.
   PubMed Web of Science ®Google Scholar
• AMBROSIO AF, SOARES-DA-SILVA P, CARVALHO CM, CARVALHO AP: Mechanisms of action of carbamazepine and its derivatives, oxcarbazepine, BIA 2-093, and BIA 2-024. Neurochem. Res. (2002) 27:121-130.
   PubMed Web of Science ®Google Scholar
• BEYDOUN A, KOBETZ SA, CARRAZANA EJ: Efficacy of oxcarbazepine in the treatment of painful diabetic neuropathy. Clin. J. Pain (2004) 20:174-178.
   PubMed Web of Science ®Google Scholar
• SUDOH Y, CAHOON EE, GERNER P, WANG GK: Tricyclic antidepressants as long-acting local anesthetics. Pain (2003) 103:49-55.
   PubMed Web of Science ®Google Scholar
• MAX MB, LYNCH SA, MUIR J, SHOAF SE, SMOLLER B, DUBNER R: Effects of desipramine, amitriptyline, and fluoxetine on pain in diabetic neuropathy. N. Engl. J. Med. (1992) 326:1250-1256.
   PubMed Web of Science ®Google Scholar
• TURKINGTON RW: Depression masquerading as diabetic neuropathy. JAMA (1980) 243:1147-1150.
   PubMed Web of Science ®Google Scholar
• MAX MB, SCHAFER SC, CULNANE M, SMOLLER B, DUBNER R, GRACELY RH: Amitriptyline, but not lorazepam, relieves postherpetic neuralgia. Neurology (1988) 38:1427-1432.
   PubMed Web of Science ®Google Scholar
• WATSON CP, EVANS RJ, REED K, MERSKEY H, GOLDSMITH L, WARSH J: Amitriptyline versus placebo in postherpetic neuralgia. Neurology (1982) 32:671-673.
   PubMed Web of Science ®Google Scholar
• LEIJON G, BOIVIE J: Central post-stroke pain – a controlled trial of amitriptyline and carbamazepine. Pain (1989) 36:27-36.
   PubMed Web of Science ®Google Scholar
• KALSO E, TASMUTH T, NEUVONEN PJ: Amitriptyline effectively relieves neuropathic pain following treatment of breast cancer. Pain (1996) 64:293-302.
   PubMed Web of Science ®Google Scholar
• SINDRUP SH, JENSEN TS: Efficacy of pharmacological treatments of neuropathic pain: an update and effect related to mechanism of drug action. Pain (1999) 83:389-400.
   PubMed Web of Science ®Google Scholar