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* To whom correspondence should be addressed. E-mail: song{at}parkercc.edu.
We examined thermal hyperalgesia, excitability of dorsal root ganglion (DRG) neurons and antinociceptive effects of NMDA receptor antagonists in rats with injury to different regions of DRG neurons. The central- or peripheral- branches of axons of DRG neurons were injured by partial dorsal rhizotomy (PDR) and chronic constriction injury of sciatic nerve (CCI), respectively, or the somata injured by chronic compression of DRG (CCD). Thermal hyperalgesia was evidenced by significantly shortened latencies of foot withdrawal to radiant heat stimulation of the plantar surface. Intracellular recordings were obtained in vitro from L4 and/or L5 ganglia. There are four principle findings: (1) PDR as well as CCD and CCI induced thermal hyperalgesia; (2) PDR produced significantly less severe and shorter duration hyperalgesia than CCD and CCI; (3) Intrathecal administration of NMDA receptor antagonists APV and MK-801 inhibited thermal hyperalgesia in PDR-, CCD- and CCI-rats. Pre-treatment of APV and MK-801 delayed the emergence of hyperalgesia for 48-72 h, while post-treatment inhibited hyperalgesia for 24-36 h; (4) CCD and CCI increased excitability of DRG neurons as judged by the significantly lowered threshold currents and action potential voltage thresholds, and increased incidence of repetitive discharges. However, PDR did not alter the excitability of DRG neurons. These findings indicate that injury to the dorsal root, compared to injury to the peripheral nerve or DRG somata has different effects on the development of hyperalgesia. These contributions involve different changes in DRG membrane excitability, but each involves pathways (presumably in the spinal cord) that depend upon NMDA receptors.
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