Differential GABAergic disinhibition during the development of painful peripheral neuropathy

Janssen, Sofie; Truin, Michiel; Kleef, Maarten van; Joosten, Elbert A.J.

doi:10.1016/j.neuroscience.2011.03.060

Cited by 69 publications

(51 citation statements)

References 43 publications

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“…2 Immunohistochemical staining reveals significantly reduced levels of GABA in laminae I through III early in the development of neuropathic pain, which is followed by dysfunctional GABA release and impaired GABA A R-mediated inhibition in later stages. 9 There is also evidence for some apoptotic cell loss of GABAergic dorsal horn neurons triggered by primary afferent glutamatergic signaling. 10 Application of the GABA A R agonist muscimol to the spinal cord prevents thermal hyperalgesia following peripheral nerve injury, 11 and transplantation of GABAergic neuron precursors into the dorsal horn reduces neuropathic pain.…”

Section: Spinal Gaba/glycinergic System Which Gates Nociceptive Inpumentioning

confidence: 99%

Therapeutic Restoration of Spinal Inhibition via Druggable Enhancement of Potassium-Chloride Cotransporter KCC2–Mediated Chloride Extrusion in Peripheral Neuropathic Pain

et al. 2014

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Section: Spinal Gaba/glycinergic System Which Gates Nociceptive Inpumentioning

confidence: 99%

Therapeutic Restoration of Spinal Inhibition via Druggable Enhancement of Potassium-Chloride Cotransporter KCC2–Mediated Chloride Extrusion in Peripheral Neuropathic Pain

et al. 2014

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“…[37][38][39][40][41] Electrophysiologic studies confirmed that primary afferent-evoked inhibitory postsynaptic currents in the spinal dorsal horn were reduced after nerve injury. 40,42,43 Although controversy exists with regard to the actual loss of GABAergic interneurons, [44][45][46][47] the dysfunction of GABAergic inhibition in the spinal cord likely contributes to neuropathic pain, 48,49 and several lines of evidence suggest that stimulation of the spinal GABAergic system produces analgesia in neuropathic pain.…”

Section: Spinal Ach and Gaba Mechanisms For Donepezil Analgesiamentioning

confidence: 99%

Relief of Hypersensitivity after Nerve Injury from Systemic Donepezil Involves Spinal Cholinergic and γ-Aminobutyric Acid Mechanisms

Kimura¹,

Hayashida²,

Eisenach

et al. 2013

Anesthesiology

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Background: Evoking spinal release of acetylcholine (ACh) produces antinociception in normal animals and reduces hypersensitivity after nerve injury, and some studies suggest that ACh-mediated analgesia relies on γ-aminobutyric acid (GABA)-ergic signaling in the spinal cord. In this study, the authors tested the spinal mechanisms underlying the antihypersensitivity effects of donepezil, a central nervous system-penetrating cholinesterase inhibitor, in a rat model of neuropathic pain. Methods: Male Sprague-Dawley rats were anesthetized, and L5 spinal nerve ligation was performed unilaterally. Withdrawal threshold to a paw pressure test was measured before and after intraperitoneal administration of donepezil, with or without intrathecal antagonists for cholinergic and GABAergic receptors. Microdialysis studies in the ipsilateral dorsal horn of the lumbar spinal cord were also performed to measure extracellular ACh and GABA. Results: Donepezil increased the withdrawal threshold in spinal nerve ligation rats but not in normal rats. The antihypersensitivity effect of donepezil (1 mg/kg) in spinal nerve ligation rats was reduced by intrathecal pretreatment with atropine (30 μg), a muscarinic receptor antagonist; mecamylamine (100 μg), a nicotinic receptor antagonist; bicuculline (0.03 μg), a γ-aminobutyric acid receptor type

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“…In mammals, the family consists of the inward transporters NCC, NKCC1, and NKCC2, the chloride outward transporters KCC1-4, and the chloride transporter-interacting protein CIP1 (10 -12). Furthermore, the orphan transporter CCC9 17), neuropathic pain (18,19), spasticity (20), ischemic insults (21), and brain trauma (22).…”

mentioning

confidence: 99%

A Novel Regulatory Locus of Phosphorylation in the C Terminus of the Potassium Chloride Cotransporter KCC2 That Interferes with N-Ethylmaleimide or Staurosporine-mediated Activation*♦

Weber

Hartmann

Beyer

et al. 2014

Journal of Biological Chemistry

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Differential GABAergic disinhibition during the development of painful peripheral neuropathy

Cited by 69 publications

References 43 publications

Therapeutic Restoration of Spinal Inhibition via Druggable Enhancement of Potassium-Chloride Cotransporter KCC2–Mediated Chloride Extrusion in Peripheral Neuropathic Pain

Therapeutic Restoration of Spinal Inhibition via Druggable Enhancement of Potassium-Chloride Cotransporter KCC2–Mediated Chloride Extrusion in Peripheral Neuropathic Pain

Relief of Hypersensitivity after Nerve Injury from Systemic Donepezil Involves Spinal Cholinergic and γ-Aminobutyric Acid Mechanisms

A Novel Regulatory Locus of Phosphorylation in the C Terminus of the Potassium Chloride Cotransporter KCC2 That Interferes with N-Ethylmaleimide or Staurosporine-mediated Activation*♦

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