Changes in sodium channel function during postnatal brain development reflect increases in the level of channel sialidation.

Developmental changes of forebrain sodium channels were studied at three postnatal ages: P0, P15 and adult (P30/P180). Electrophysiological analysis determined that the midpoint potential of activation was -64, -75 and -81 mV for P0, P15 and adult channels, respectively. At negative potentials, gating state changes were observed in all channels; at positive potentials they were observed in most P0 (72%) and to a lower extent in older channels (25%). A long non-conductive state was displayed with a higher frequency in P0 than in older channels. Immunoblot analysis determined that the apparent molecular weight was approximately 227, approximately 241 and approximately 246 kDa for P0, P15 and adult channels, respectively. Upon neuraminidase treatment, which cleaves sialic acids, these differences in molecular weight were abolished. The data suggest that these developmental changes in the function of forebrain sodium channels correlate with changes in the channel's sialidation level.