Transient degradation of myelin basic protein in the rat hippocampus following acute carbon monoxide poisoning.

Abstract The neurotoxicity of carbon monoxide (CO) poisoning is a significant clinical problem, but its mechanisms remain unclear. Previous studies of CO-exposed rats showed spatial memory disturbances and degradation of myelin basic protein (MBP) in the brain; however, regional localization of the degradation was not analyzed. In the present study, we histologically determined the foci of CO effects in the hippocampus. Wistar rats were exposed to CO for 60 min (1000 ppm for 40 min + 3000 ppm for 20 min) and returned into room air. For histological evaluation, the animals were sacrificed 90 min, 1, 7 and 14 days after CO exposure and the brain tissue was analyzed with hematoxylin–eosin (HE), Nissl and Gallyas myelin staining as well as immunohistochemistry for MBP and phosphorylated or nonphosphorylated neurofilament. No histological changes were observed on HE, Nissl or Gallyas staining. In contrast, we detected MBP reduction at 90 min after CO exposure in the dentate gyrus and CA3, and the recovery of MBP was observed after 14 days. The immunoreactivity of neurofilament also changed after CO exposure. Nevertheless, water maze test showed no significant effects of CO exposure on spatial memory. Our findings demonstrate that CO poisoning causes transient degradation of MBP and axonal injury in the hippocampus even though the animals showed no neurological disturbances.