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Kun Zhang,1 Somayaji Ramamurthy,1 Thomas J Prihoda,2 Maxim S Eckmann1 1Department of Anesthesiology, 2Department of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA Purpose: The current study was designed to examine the antinociceptive effect of intrathecally administered capsaicin, a transient receptor potential vanilloid 1 receptor agonist, in a rat model of neuropathic pain induced by unilateral sciatic nerve chronic constriction injury. Methods: Male adult Sprague Dawley rats were randomly assigned to six groups, and all rats underwent unilateral sciatic nerve chronic constriction injury. Two weeks after injury, five groups received intrathecal administration of either capsaicin in three different dosing regimens or equal volumes of vehicle. The other group received intrathecal capsaicin on the third day after nerve injury. The antinociceptive effect of capsaicin was assessed by measuring the capsaicin-induced change in thermal and mechanical response thresholds. Results: Capsaicin (150–300 µg/100–200 µL), when administered by fast infusion or chronic infusions at 8 µL/hour or 1 µL/hour, attenuated thermal hyperalgesia as indicated by significantly prolonging paw withdrawal latency to noxious thermal stimulation. The antinociceptive effect of capsaicin was more profound in the injured limb compared to that in the uninjured limb. When capsaicin was administered on the third day after nerve injury, it failed to attenuate thermal hyperalgesia. No significant effect on the mechanical response threshold was observed with intrathecally administered capsaicin. Conclusion: Our data suggest that intrathecal capsaicin could significantly attenuate thermal hyperalgesia, depending on the time when the drug is given after nerve injury, and that the antinociceptive efficacy of intrathecal capsaicin positively correlates with the previously reported dynamic profile of spinal transient receptor potential vanilloid 1 activity after nerve injury. Keywords: hyperalgesia, TRPV1, paw withdrawal latency, paw withdrawal threshold

To investigate the extent of genetic damage in the peripheral blood and bone marrow cells of mice exposed to ultra-wideband electromagnetic radiation (UWBR).CF-1 male mice were exposed to UWBR for 15 min at an estimated whole-body average specific absorption rate of 37 mW x kg(-1). Groups of untreated control and positive control mice injected with mitomycin C were also included in the study. After various treatments, half of the mice were killed at 18 h, and the other half at 24 h. Peripheral blood and bone marrow smears were examined to determine the extent of genotoxicity, as assessed by the presence of micronuclei (MN) in polychromatic erythrocytes (PCE).The percentages of PCE and the incidence of MN per 2000 PCE in both tissues in mice killed at 18 h were similar to the frequencies observed in mice terminated at 24 h. There were no significant differences in the percentage of PCE between control and the mice with or without UWBR exposure; the group mean values (+/- standard deviation) were in the range of 3.1+/-0.14 to 3.2+/-0.23 in peripheral blood, and 49.0+/-3.56 to 52.3+/-4.02 in bone marrow. The mean incidence of MN per 2000 PCE in control and in mice with or without UWBR exposure ranged from 7.7+/-2.00 to 9.7+/-2.54 in peripheral blood and 7.4+/-2.32 to 10.0+/-3.27 in bone marrow. Pairwise comparison of the data did not reveal statistically significant differences between the control and mice with or without UWBR exposure groups (excluding positive controls).Under the experimental conditions tested, there was no evidence for excess genotoxicity in peripheral blood or bone marrow cells of mice exposed to UWBR.