Abstract 1785
Pulmonary: Control of Breathing Poster Symposium, Tuesday, 5/4
In the adult rat brainstem, NF-κB is activated during hypoxia via phosphorylation of its inhibitory unit IκB by either IκB kinase α or β, and nuclear translocation of the dimeric P50/P65 complex. However, the developmental regulation of these elements is presently unknown. Western blots of neocortical (Neo) and caudal brainstem (CB) lysates revealed decreasing expression of IκB kinase α and stable expression of IκB kinase β with advancing postnatal age in both structures. Immunostaining for the P65 subunit of NF-κB was performed in 30-µ Neo and CB sections from rat pups at 2, 10, and 20 days postnatal age, following either normoxic or hypoxic (3 hrs in 10% O2) exposures. In normoxic animals, P65 immunoreactivity was widely distributed within neurons with occasional expression in glia. In neurons, P65 was primarily circumscribed to the cytosol but exhibited more pronounced nuclear staining in the youngest animals in both Neo and CB. Activation of NF-κB as evidenced by increased P65 nuclear immunoreactivity, was similar during hypoxia at all post-natal ages. We conclude that IκB kinase α expression and NF-κB basal activity are particularly elevated in youngest animals with similar recruitments occurring during mild hypoxic challenges. We postulate that elevated NF-κB nuclear activity may underlie important genomic regulatory processes involved in postnatal neuronal network formation.
