抄録
Brain-derived neurotrophic factor (BDNF) is known to involved in the development of spinal plasticity underlying inflammation-induced hyperalgesia. An injection of complete Freund adjuvant (CFA) into rat plantar surface produced hyperalgesia, which was significantly attenuated by intraperitoneal administration of anti-BDNF antiserum performed a day before and just after CFA. In vivo patch-clamp recordings from the spinal substantia gelatinosa (SG) neurons of the inflamed rats demonstrated a marked enhancement of excitatory synaptic responses to noxious and non-noxious stimuli, suggesting an increase in the activity-dependent synthesis and release of BDNF in the SG. In the spinal slice preparations, BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically to increase frequency of miniature EPSCs in SG neurons of the inflamed, but not naive rats, through an activation of lidocaine-sensitive, TTX-resistant sodium channels. This effect was observed in slices of the inflamed rat only 2-4 days after CFA injection. On the other hand, the number of monosynaptic A-beta afferent inputs to the SG significantly increased a week after the onset of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum. These findings, taken together, suggest that BDNF, which is considered to be released from the sensitized primary afferents, increases the excitability of SG neurons through its action on the presynaptic terminals, and may thereafter trigger plastic changes in the spinal sensory transmission to develop hyperalgesia/allodynia during inflammation. [J Physiol Sci. 2006;56 Suppl:S50]
