The hypoalgesia-specific sensory impairment in MeHg-exposed rats is not associated with peripheral neural degeneration

Abstract

Methylmercury (MeHg) is the causative substrate for Minamata disease, and it is known to induce sensory impairment. The neurotoxicological mechanism of MeHg has been widely studied in the central nervous system, but not as much in the peripheral nervous system. It has been reported that the number of neurons in the rat dorsal root ganglion (DRG) decreased 14 days after MeHg exposure (Day14). In addition, from behavioral analysis, only hypoalgesia was observed during Day11 to 48 and then, recovered to control level. However, the histological background for hypoalgesia-specificity remain unclear. In this study, we investigated the possibility that hypoalgesia originates in the peripheral nervous system. MeHgCl (6.7 mg/kg/day) was orally administered into 9-week male Wistar rats for 5 days, followed by 2 days without administration, and this cycle was repeated once. Seven, 14, 28, 42, 56, and 70 days after the beginning of MeHg exposure, frozen sections from L4-5 DRG were prepared and immunostained by nociceptive and mechanoreceptive cell markers. DNA microarray analysis for Day14 was also performed. Histological analysis showed that the number of mechanoreceptive and nociceptive cells have both decreased around Day14 and recovered afterwards. Microarray data also did not show specific cell death of nociceptor cells. These data suggest that the hypoalgesia-specificity may be caused by the impairment of central but not peripheral nervous system.