Microglial proliferation in the spinal cord of aged rats with a sciatic nerve injury

Nerve injury may lead to chronic neuropathic pain syndromes. We determined whether the extent of central nervous system microglial activation that acc ompanies nerve injury is age dependent and correlated with behavioral manif estations of pain. We used the Bennett and Xie sciatic nerve chronic constr iction injury model (Bennett, G.J., Xie, Y.-K., A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man, P ain, 33 (1998) 87-107) to induce neuropathic pain in three age cohorts of F ischer 344 FBNF1 hybrid rats (4-6, 14-16, and 24-26 months). Rats were asse ssed for thermal sensitivity (hyperalgesia) of their hind paws pre-injury ( day 0) and up to 35 days post injury. On various days post injury, the L4-L 5 levels of their spinal cords were reacted for localization of an antibody to OX-42, a marker for microlgia. OX-42 immunoreactivity (ir) was quantifi ed by use of a Bioquant density analysis system. OX-42 ir was heavy in area s of sciatic nerve primary afferent terminations and in the motor columns o f its neurons. Aging increases OX-42 ir in the absence of injury. After inj ury, OX-42 ir increased further, but the increases over control levels decr eased with age. Ligation-induced analgesia and hyperalgesia were both corre lated with the increases in OX-42 ir, regardless of age. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.