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1 Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan
2 Department of Rehabilitation and Physical Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, 890-8520, Japan
3 Department of Human Physiology and Centre for Neuroscience, Flinders University of South Australia, GPO Box 2100, Adelaide 5001, Australia
4 Pain Research Center, Laboratory of Sensory Plasticity, Department of Anaesthesia, Brigham and Women's Hospital, Harvard Medical School Medical Research Building, Room 60475 Francis Street, Boston, MA 02115, USA
The aim of the current study was to investigate whether, and if so how, brain-derived neurotrophic factor (BDNF) acts to develop the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation induced by complete Freund's adjuvant (CFA), BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically to increase the frequency of excitatory miniature EPSCs in substantia gelatinosa (SG) neurones of the CFA-treated, but not untreated rats, through activation of lidocaine (lignocaine)-sensitive, TTX-resistant Na+ channels. This effect was observed in the spinal cord slices of the CFA-treated rat only 2–4 days after the CFA injection. On the other hand, the number of monosynaptic Aß afferent inputs to the SG significantly increased 1 week after the onset of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum administered 1 day before and just after the CFA injection. In addition, the treatment with anti-BDNF antiserum significantly attenuated the CFA-induced hyperalgesia and/or allodynia. These findings, taken together, suggest that BDNF, which is considered to be released from the sensitized primary afferents, increases the excitability of SG neurones through its action on the presynaptic terminals. BDNF may thereafter induce monosynaptic Aß afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation.
(Received 26 July 2005;
accepted after revision 30 September 2005;
first published online 6 October 2005)
Corresponding author T. Katafuchi: Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan. Email: kataf{at}physiol.med.kyushu-u.ac.jp
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