Résumé
The association between the
β
1 subunit and the
α subunit of the sodium channel from rat brain was studied in hippocampus during postnatal development and in cultures of fetal rat forebrain neurons and cerebellar granule cells, using an anti-
β
1 antipeptide antibody to specifically immunoprecipitate
α
β
1 complexes labeled with [
3H]saxitoxin. In the hippocampus, the increase in
β
1 RNA expression during development was accompanied by an increase in immunoprecipitated
α
β
1 complexes. Most of the
α
β
1 complexes were constituted during the first 3 postnatal weeks, with the steepest rise between postnatal days 5 and 12. In cultured fetal neurons, the amount of
β
1 RNA and of
α
β
1 complexes was ≈3–4% of that found in the adult, whereas it reached 60–70% in cultured cerebellar granule cells. We had previously described a neurotoxin-induced internalization of sodium channels which occurred in immature neurons but not in adult tissue. Internalization decreased during development in neurotoxin-treated hippocampal slices, and resistance of plasma membrane sodium channels to internalization followed the same time course than the appearance of
α
β
1 complexes. Similarly, neurotoxin activation resulted in sodium channel internalization in fetal neurons, while cerebellar granule cells, which express high levels of
β
1 RNA and of
α
β
1 complexes, did not internalize their [
3H]saxitoxin receptors in that same conditions. These data suggested that the association of the
β
1 subunit with the
α subunit could provide a suitable marker for the stabilization and anchoring of sodium channels in discrete membrane domains which occur during neuronal development.