Blast exposure causes redistribution of phosphorylated neurofilament subunits in neurons of the adult rat brain

There is little information on threshold levels and critical time factors f or blast exposures, although brain damage after a blast has been establishe d both clinically and experimentally. Moreover, the cellular pathophysiolog y of the brain response is poorly characterized. This study employs a rat m odel for blast exposure to investigate effects on the neuronal cytoskeleton . Exposure in the range of 154 kPa/198 dB or 240 kPa/202 dB has previously been shown neither to cause visual damage to the brain, nor to affect the n euronal populations, as revealed with routine histology. Here, the brains w ere investigated immunohistochemically from 2 h to 21 days after blast expo sure. A monoclonal antibody was used which detects only the phosphorylated epitope of the heavy subunit of the neurofilament proteins (p-NFH). This ep itope is normally restricted to axons, that is, not demonstrable in the per ikarya. Eighteen hours after exposure in the 240-kPa/202-dB range, p-NFH im munoreactivity accumulated in neuronal perikarya in layers II-IV of the tem poral cortex and of the cingulate and the piriform cortices, the dentate gy rus and the CA1 region of the hippocampus. At the same time, the p-NFH immu noreactivity disappeared from the axons and dendrites of cerebral cortex ne urons. The most pronounced immunostaining of neuronal perikarya was found i n the hemisphere, which faced the blast source. The perikaryal accumulation of p-NFH was present also at 7 days but the neuronal perikarya had become negative at 21 days, at which time the axons again displayed p-NFH immunore activity. Exposure in the range of 154 kPa/198 dB caused similar, although less marked accumulation of p-NFH immunoreactivity in the neuronal perikary a. The findings are interpreted to show a dephosphorylation of NFHs in axon s and dendrites and a piling up of p-NFHs in the perikarya due to disturbed axonal transport.