Transient ischemia-induced changes of neurofilament 200 kDa immunoreactivity and protein content in the main olfactory bulb in gerbils.

This study was carried out to investigate alterations of neurofilament 200 kDa (NF-200) and its polyphosphorylation form (RT97) immunoreactivity and protein content in the main olfactory bulb (MOB) after 5 min of transient forebrain ischemia in gerbils. In the sham-operated group, weak NF-200 immunoreactivity was detectable in a few somata of mitral cells, which projected weak NF-200-immunoreactive processes to the external plexiform layer (EPL). At 1-5 days after ischemia, strong NF-200 and RT97 immunoreactivity was shown by the mitral cell processes; however, somata of mitral cells did not show NF-200 immunoreactivity. At this time point, strong NF-200-immunoreactive mitral cell processes ran to the EPL and glomerular layer (GL). Thereafter, NF-200 and RT97 immunoreactivity was decreased up to 30 days after ischemia. In the 15 days post-ischemic group, the distribution pattern of NF-200 and RT97 immunoreactivity was slightly lower than that in the 1-5 days post-ischemic groups. In the 30 days post-ischemic group, moderate NF-200 and RT97 immunoreactivity was found in the mitral cells processes, but the immunoreactivity in the EPL and GL nearly disappeared. A Western blot study showed a pattern of NF-200 and RT97 expression at all post-ischemic time points similar to that of immunohistochemistry after ischemia. This result indicates that NF-200 and RT97 accumulates in injured mitral cell processes a few days after transient ischemia, which suggests that the axonal transport in the MOB may be disturbed during this period after transient ischemia.