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Actions of brain‐derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat
Author(s) -
Matayoshi Satoru,
Jiang Nan,
Katafuchi Toshihiko,
Koga Kohei,
Furue Hidemasa,
Yasaka Toshiharu,
Nakatsuka Terumasa,
Zhou XinFu,
Kawasaki Yasuhiko,
Tanaka Nobuyuki,
Yoshimura Megumu
Publication year - 2005
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2005.095331
Subject(s) - hyperalgesia , spinal cord , brain derived neurotrophic factor , nociception , neurotrophic factors , allodynia , medicine , inflammation , nerve growth factor , neuroscience , neurotrophin , anesthesia , endocrinology , psychology , receptor
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 Aβ 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 Aβ afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation.