Reversal of pathological pain through specific spinal GABAA receptor subtypes

Julia Knabl, Robert Witschi, Katharina Hösl, Heiko Reinold, Ulrike B. Zeilhofer, Seifollah Ahmadi, Johannes Brockhaus, Marina Sergejeva, Andreas Hess, Kay Brune, Jean-Marc Fritschy, Uwe Rudolph, Hanns Möhler and Hanns Ulrich Zeilhofer ()
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Julia Knabl: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Robert Witschi: Institute of Pharmacology and Toxicology, University of Zurich
Katharina Hösl: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Heiko Reinold: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Ulrike B. Zeilhofer: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Seifollah Ahmadi: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Johannes Brockhaus: Institute of Pharmacology and Toxicology, University of Zurich
Marina Sergejeva: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Andreas Hess: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Kay Brune: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg
Jean-Marc Fritschy: Institute of Pharmacology and Toxicology, University of Zurich
Uwe Rudolph: Institute of Pharmacology and Toxicology, University of Zurich
Hanns Möhler: Institute of Pharmacology and Toxicology, University of Zurich
Hanns Ulrich Zeilhofer: Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg

Nature, 2008, vol. 451, issue 7176, 330-334

Abstract: A new target for analgesia The chronic pain that accompanies inflammatory disease and nerve injury is often resistant to conventional analgesics, hence the interest in establishing the mechanisms that induce this pain. Growing evidence points to a loss of synaptic inhibition in the spinal cord as a critical factor in chronic pain. This suggests that a rational therapy should aim at a reversal of this disinhibition. New work using 'knock-in' mice has identified specific GABAA receptor subtypes as keys to this spinal pain. The experimental drug L-838,417, which targets these receptor subtypes, is effective in rat models of inflammatory and neuropathic pain, yet was devoid of sedation, motor impairment and tolerance development expected with less specific GABA agonists.

Date: 2008
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DOI: 10.1038/nature06493

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