A novel mechanism of inhibition of high-voltage activated calcium channels by α-conotoxins contributes to relief of nerve injury-induced neuropathic pain

[1]  C. Goodchild,et al.  CNSB004 (Leconotide) causes antihyperalgesia without side effects when given intravenously: a comparison with ziconotide in a rat model of diabetic neuropathic pain. , 2010, Pain medicine.

[2]  David John Adams,et al.  Analgesic α-conotoxins Vc1.1 and Rg1A inhibit N-type calcium channels in sensory neurons of α9 nicotinic receptor knockout mice , 2010, Channels.

[3]  A. Braun.  Coordinate regulation of stretch-activated channels and myogenic tone by polycystins 1 and 2 , 2010, Channels.

[4]  N. Absalom,et al.  Alpha9 nicotinic acetylcholine receptors and the treatment of pain. , 2009, Biochemical pharmacology.

[5]  Stephen B. H. Kent,et al.  In situ neutralization in Boc-chemistry solid phase peptide synthesis. Rapid, high yield assembly of difficult sequences. , 2009 .

[6]  Alison Haythornthwaite,et al.  Analgesic α-Conotoxins Vc1.1 and Rg1A Inhibit N-Type Calcium Channels in Rat Sensory Neurons via GABAB Receptor Activation , 2008, The Journal of Neuroscience.

[7]  J. McIntosh,et al.  Spinal α3β2* nicotinic acetylcholine receptors tonically inhibit the transmission of nociceptive mechanical stimuli , 2008, Brain Research.

[8]  D. Craik,et al.  Are α9α10 Nicotinic Acetylcholine Receptors a Pain Target for α-Conotoxins? , 2007, Molecular Pharmacology.

[9]  J. Dunlop,et al.  Targeting the cholinergic system as a therapeutic strategy for the treatment of pain , 2007, Neuropharmacology.

[10]  J. McIntosh,et al.  Targeting the α9α10 nicotinic acetylcholine receptor to treat severe pain , 2007 .

[11]  J. McIntosh,et al.  Molecular mechanism for analgesia involving specific antagonism of α9α10 nicotinic acetylcholine receptors , 2006, Proceedings of the National Academy of Sciences.

[12]  D. Craik,et al.  The Synthesis, Structural Characterization, and Receptor Specificity of the α-Conotoxin Vc1.1* , 2006, Journal of Biological Chemistry.

[13]  J. McGivern.  Targeting N-type and T-type calcium channels for the treatment of pain. , 2006, Drug discovery today.

[14]  K. Gayler,et al.  Alpha-conotoxin Vc1.1 alleviates neuropathic pain and accelerates functional recovery of injured neurones , 2005, Brain Research.

[15]  E. Eisenberg,et al.  Efficacy and safety of opioid agonists in the treatment of neuropathic pain of nonmalignant origin: systematic review and meta-analysis of randomized controlled trials. , 2005, JAMA.

[16]  P. M. Lang,et al.  A conus peptide blocks nicotinic receptors of unmyelinated axons in human nerves , 2005, NeuroReport.

[17]  D. Keays,et al.  Molecular prospecting for drugs from the sea , 2005, IEEE Engineering in Medicine and Biology Magazine.

[18]  K. K. Rau,et al.  Nicotinic AChR in subclassified capsaicin-sensitive and -insensitive nociceptors of the rat DRG. , 2005, Journal of neurophysiology.

[19]  D. Carr,et al.  Pain relief: a universal human right , 2004, Pain.

[20]  C. Altier,et al.  Targeting Ca2+ channels to treat pain: T-type versus N-type. , 2004, Trends in pharmacological sciences.

[21]  M. Gassmann,et al.  Molecular Structure and Physiological Functions of GABAB Receptors , 2004 .

[22]  K. Gayler,et al.  Drugs from the sea: conopeptides as potential therapeutics. , 2004, Current medicinal chemistry.

[23]  A. Gomes,et al.  Determinants of Potency on α-Conotoxin MII, a Peptide Antagonist of Neuronal Nicotinic Receptors , 2004 .

[24]  T. Tanabe,et al.  Plastic Change of N-type Ca Channel Expression after Preconditioning Is Responsible for Prostaglandin E2-induced Long-lasting Allodynia , 2003, Anesthesiology.

[25]  P. M. Lang,et al.  Characterization of neuronal nicotinic acetylcholine receptors in the membrane of unmyelinated human C-fiber axons by in vitro studies. , 2003, Journal of neurophysiology.

[26]  Z. Khalil,et al.  Drugs from the sea: conotoxins as drug leads for neuropathic pain and other neurological conditions. , 2003, Mini reviews in medicinal chemistry.

[27]  D. Keays,et al.  A novel alpha-conotoxin identified by gene sequencing is active in suppressing the vascular response to selective stimulation of sensory nerves in vivo. , 2003, Biochemistry.

[28]  D. Craik,et al.  A New Level of Conotoxin Diversity, a Non-native Disulfide Bond Connectivity in α-Conotoxin AuIB Reduces Structural Definition but Increases Biological Activity* , 2002, The Journal of Biological Chemistry.

[29]  T. Yaksh,et al.  Localization of N-type Ca2+ channels in the rat spinal cord following chronic constrictive nerve injury , 2002, Experimental Brain Research.

[30]  T. Tanabe,et al.  Changes in Expression of Voltage-Dependent Ion Channel Subunits in Dorsal Root Ganglia of Rats with Radicular Injury and Pain , 2002, Spine.

[31]  S. Hatakeyama,et al.  Differential nociceptive responses in mice lacking the alpha(1B) subunit of N-type Ca(2+) channels. , 2001, Neuroreport.

[32]  Dong Kwan Kim,et al.  Altered Nociceptive Response in Mice Deficient in the α1B Subunit of the Voltage-Dependent Calcium Channel , 2001, Molecular and Cellular Neuroscience.

[33]  C. Lüscher,et al.  Epilepsy, Hyperalgesia, Impaired Memory, and Loss of Pre- and Postsynaptic GABAB Responses in Mice Lacking GABAB(1) , 2001, Neuron.

[34]  H. Saegusa,et al.  Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N‐type Ca2+ channel , 2001, The EMBO journal.

[35]  M. Capogna,et al.  The effects of GABAB agonists and gabapentin on mechanical hyperalgesia in models of neuropathic and inflammatory pain in the rat , 2001, Pain.

[36]  F. Blyth,et al.  Chronic pain in Australia: a prevalence study , 2001, Pain.

[37]  D. Yoshikami,et al.  α-Conotoxin AuIB Selectively Blocks α3β4 Nicotinic Acetylcholine Receptors and Nicotine-Evoked Norepinephrine Release , 1998, The Journal of Neuroscience.

[38]  J. McIntosh,et al.  Determinants of Specificity for α-Conotoxin MII on α3β2 Neuronal Nicotinic Receptors , 1997 .

[39]  D. Yoshikami,et al.  A New -Conotoxin Which Targets 32 Nicotinic Acetylcholine Receptors (*) , 1996, The Journal of Biological Chemistry.

[40]  R. Egan,et al.  The pharmacology of SCH 50911: a novel, orally-active GABA-beta receptor antagonist. , 1995, The Journal of pharmacology and experimental therapeutics.

[41]  T. Yaksh,et al.  Quantitative assessment of tactile allodynia in the rat paw , 1994, Journal of Neuroscience Methods.

[42]  Ronald Dubner,et al.  A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury , 1990, Pain.

[43]  De-Pei Li,et al.  Modulation of pain transmission by G-protein-coupled receptors. , 2008, Pharmacology & therapeutics.

[44]  D. Keays,et al.  Molecular prospecting for drugs from the sea. Isolating therapeutic peptides and proteins from cone snail venom. , 2005, IEEE engineering in medicine and biology magazine : the quarterly magazine of the Engineering in Medicine & Biology Society.

[45]  B. Olivera,et al.  Conus venoms: a rich source of novel ion channel-targeted peptides. , 2004, Physiological reviews.

[46]  M. Gassmann,et al.  Molecular structure and physiological functions of GABA(B) receptors. , 2004, Physiological reviews.

[47]  D. Craik,et al.  alpha-Conotoxins: nicotinic acetylcholine receptor antagonists as pharmacological tools and potential drug leads. , 2001, Current medicinal chemistry.

[48]  J. McIntosh,et al.  Conus peptides targeted to specific nicotinic acetylcholine receptor subtypes. , 1999, Annual review of biochemistry.

[49]  J. McIntosh,et al.  Determinants of Specificity for a-Conotoxin MII on a 3 b 2 Neuronal Nicotinic Receptors , 1997 .