Microglial activation and BDNF expression in the phrenic motor nucleus following cervical spinal hemisection

Microglia serve a dual role after spinal cord injury (SCI), contributing both to inflammatory processes that exacerbate the injury and to functional recovery via mechanisms of neuroplasticity. The crossed phrenic phenomenon (CPP) is an example of respiratory neuroplasticity in which C2 hemisection (C2HS) strengthens a normally silent, crossed‐spinal synaptic pathway to phrenic motor neurons ipsilateral to injury. We hypothesized that microglia are activated in the phrenic motor nucleus ipsilateral to C2HS, suggesting their potential for involvement in CPP. We further hypothesized BDNF, a trophic factor critical for phrenic motor plasticity, is produced by microglia after C2HS, again suggesting involvement in CPP. Male Lewis rats were perfused 1 to 14 days after C2HS, and C4‐C5 transverse sections were stained for confocal microscopy. 3 days post‐C2HS: 1) the number and size of OX42 positive microglia increased, and 2) BDNF protein expression increased in OX42 and presumptive phrenic motor neurons (large NeuN positive cells). Thus, microglial activation may play an important role in the CPP. Further studies testing causality between microglial activation, increased BDNF and the CPP are warranted. (Supported by NIH HL69064 and HL07654)