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This Article Full Text Full Text (PDF) All Versions of this Article: 577/3/869    most recent jphysiol.2006.118034v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schoffnegger, D. Articles by Sandkühler, J. Search for Related Content PubMed PubMed Citation Articles by Schoffnegger, D. Articles by Sandkühler, J. Related Collections Neuroscience

¹ Center for Brain Research, Medical University Vienna, Vienna, Austria
² Department of Neurology, University of Würzburg, Würzburg, Germany

Aberrant GABAergic inhibition in spinal dorsal horn may underlie some forms of neuropathic pain. Potential, but yet unexplored, mechanisms include reduced excitability, abnormal discharge patterns or altered synaptic input of spinal GABAergic neurons. To test these hypotheses, we quantitatively compared active and passive membrane properties, firing patterns in response to depolarizing current steps and synaptic input of GABAergic neurons in spinal dorsal horn lamina II of neuropathic and of control animals. Transgenic mice were used which expressed enhanced green fluorescent protein (EGFP) controlled by the GAD67 promoter, thereby labelling one-third of all spinal GABAergic neurons. In all neuropathic mice included in this study, chronic constriction injury of one sciatic nerve led to tactile allodynia and thermal hyperalgesia. Control mice were sham-operated. Membrane excitability of GABAergic neurons from neuropathic or sham-treated animals was indistinguishable. The most frequent firing patterns observed in neuropathic and sham-operated animals were the initial burst (neuropathic: 46%, sham-treated: 42%), the gap (neuropathic: 31%, sham-treated: 29%) and the tonic firing pattern (neuropathic: 16%, sham-treated: 24%). The synaptic input from dorsal root afferents was similar in neuropathic and in control animals. Thus, a reduced membrane excitability, altered firing patterns or changes in synaptic input of this group of GABAergic neurons in lamina II of the spinal cord dorsal horn are unlikely causes for neuropathic pain.

(Received 26 July 2006; accepted after revision 10 October 2006; first published online 12 October 2006)
Corresponding author J. Sandkühler: Center for Brain Research, Department of Neurophysiology, Medical University Vienna, Spitalgasse 4, 1090 Vienna, Austria. Email: juergen.sandkuehler{at}meduniwien.ac.at

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