References
- Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: an evidence based proposal. Pain 118(3), 289–305 (2005).
- Freynhagen R, Strojek K, Griesing T, Whalen E, Balkenohl M. Efficacy of pregabalin in neuropathic pain evaluated in a 12-week, randomised, double-blind, multicentre, placebo-controlled trial of flexible- and fixed-dose regimens. Pain 115(3), 254–263 (2005).
- Ferrini F, Trang T, Mattioli TA et al. Morphine hyperalgesia gated through microglia-mediated disruption of neuronal Cl- homeostasis. Nat. Neurosci. 16(2), 183–192 (2013).
- Garber K. Fate of novel painkiller mAbs hangs in balance (Erratum). Nat. Biotechnol. 29(3), 173–174 (2011).
- Berger JV, Knaepen L, Janssen SP et al. Cellular and molecular insights into neuropathy-induced pain hypersensitivity for mechanism-based treatment approaches. Brain Res. Rev. 67(1–2), 282–310 (2011).
- Labrakakis C, Ferrini F, De Koninck Y. Mechanisms of plasticity of inhibition in chronic pain conditions. In: Inhibitory Synaptic Plasticity. Springer, 91–105 (2011).
- Coull JA, Boudreau D, Bachand K et al. Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain. Nature 424(6951), 938–942 (2003).
- Lu Y, Zheng J, Xiong L, Zimmermann M, Yang J. Spinal cord injury-induced attenuation of GABAergic inhibition in spinal dorsal horn circuits is associated with down-regulation of the chloride transporter KCC2 in rat. J. Physiol. (Lond.) 586(Pt 23), 5701–5715 (2008).
- Zhang W, Liu LY, Xu TL. Reduced potassium–chloride cotransporter expression in spinal cord dorsal horn neurons contributes to inflammatory pain hypersensitivity in rats. Neuroscience 152(2), 502–510 (2008).
- Jolivalt CG, Lee CA, Ramos KM, Calcutt NA. Allodynia and hyperalgesia in diabetic rats are mediated by GABA and depletion of spinal potassium-chloride cotransporters. Pain 140(1), 48–57 (2008).
- Wei B, Kumada T, Furukawa T et al. Pre- and post-synaptic switches of GABA actions associated with Cl- homeostatic changes are induced in the spinal nucleus of the trigeminal nerve in a rat model of trigeminal neuropathic pain. Neuroscience 228, 334–348 (2013).
- Coull JA, Beggs S, Boudreau D et al. BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain. Nature 438(7070), 1017–1021 (2005).
- Ulmann L, Hatcher JP, Hughes JP et al. Up-regulation of P2X4 receptors in spinal microglia after peripheral nerve injury mediates BDNF release and neuropathic pain. J. Neurosci. 28(44), 11263–11268 (2008).
- Zhao J, Seereeram A, Nassar MA et al.; London Pain Consortium. Nociceptor-derived brain-derived neurotrophic factor regulates acute and inflammatory but not neuropathic pain. Mol. Cell. Neurosci. 31(3), 539–548 (2006).
- Tsuda M, Shigemoto-Mogami Y, Koizumi S et al. P2X4 receptors induced in spinal microglia gate tactile allodynia after nerve injury. Nature 424(6950), 778–783 (2003).
- Prescott SA, Sejnowski TJ, De Koninck Y. Reduction of anion reversal potential subverts the inhibitory control of firing rate in spinal lamina I neurons: towards a biophysical basis for neuropathic pain. Mol. Pain 2, 32 (2006).
- Asiedu M, Ossipov MH, Kaila K, Price TJ. Acetazolamide and midazolam act synergistically to inhibit neuropathic pain. Pain 148(2), 302–308 (2010).
- Doyon N, Prescott SA, Castonguay A, Godin AG, Kröger H, De Koninck Y. Efficacy of synaptic inhibition depends on multiple, dynamically interacting mechanisms implicated in chloride homeostasis. PLoS Comput. Biol. 7(9), e1002149 (2011).
- Cordero-Erausquin M, Coull JAM, Boudreau D, Rolland M, De Koninck Y. Differential maturation of GABA action and anion reversal potential in spinal lamina I neurons: impact of chloride extrusion capacity (Erratum). J. Neurosci. 25(42), 9613–9623 (2005).
- Hewitt SA, Wamsteeker JI, Kurz EU, Bains JS. Altered chloride homeostasis removes synaptic inhibitory constraint of the stress axis. Nat. Neurosci. 12(4), 438–443 (2009).
- Kaila K. Ionic basis of GABAA receptor channel function in the nervous system. Prog. Neurobiol. 42(4), 489–537 (1994).
- Buzsáki G, Kaila K, Raichle M. Inhibition and brain work. Neuron 56(5), 771–783 (2007).
- Blaesse P, Guillemin I, Schindler J et al. Oligomerization of KCC2 correlates with development of inhibitory neurotransmission. J. Neurosci. 26(41), 10407–10419 (2006).
- Coull JA, Gagnon M. The manipulation of cation-chloride cotransporters as a novel means to treat persistent pain, epilepsy and other neurological disorders. Curr. Opin. Investig. Drugs 10(1), 56–61 (2009).
- Bos R, Sadlaoud K, Boulenguez P et al. Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2. Proc. Natl Acad. Sci. USA 110(1), 348–353 (2013).
- Rivera C, Voipio J, Payne JA et al. The K+/Cl- cotransporter KCC2 renders GABA hyperpolarizing during neuronal maturation. Nature 397(6716), 251–255 (1999).
- Arion D, Lewis DA. Altered expression of regulators of the cortical chloride transporters NKCC1 and KCC2 in schizophrenia. Arch. Gen. Psychiatry 68(1), 21–31 (2011).
- Boulenguez P, Liabeuf S, Bos R et al. Down-regulation of the potassium-chloride cotransporter KCC2 contributes to spasticity after spinal cord injury. Nat. Med. 16(3), 302–307 (2010).
- Huberfeld G, Wittner L, Clemenceau S et al. Perturbed chloride homeostasis and GABAergic signaling in human temporal lobe epilepsy. J. Neurosci. 27(37), 9866–9873 (2007).
- Hyde TM, Lipska BK, Ali T et al. Expression of GABA signaling molecules KCC2, NKCC1, and GAD1 in cortical development and schizophrenia. J. Neurosci. 31(30), 11088–11095 (2011).
Website
- NeurogesX/Astellas: Qutenza failure opens pathway for NGX-1998, Datamonitor, 2012. http://tinyurl.com/Qutenza-HIVpain (Accessed 4 March 2013)