Mechanism of modulation of single sodium channels from skeletal muscle by the β₁-subunit from rat brain

We studied the molecular mechanism of the rat skeletal muscle α-subunit (α_μI) gating kinetics modulation by the brain β₁-subunit by heterologous expression of single sodium channels from α_μI and β₁ in Xenopus laevis oocytes. Coexpression of β₁ reduced mean open time at -10 mV to ∼21% when compared to channels expressed by α_μI alone. Channels formed by α_μI exerted multiple openings per depolarization, which occurred in bursts, in contrast to the channels formed by the α_μI/β₁ complex that opened in average only once per depolarizing voltage pulse. Macroscopic current decay (mcd), as evidenced by reconstructed open probability vs. time {Mathematical expression}, was greatly accelerated by β₁, closely resembling mcd of sodium currents from native skeletal muscle. Generally {Mathematical expression} was larger for channels expressed from the pure α_μI subunit. From our single channel data we conclude that β₁ accelerates the inactivation process of the sodium channel complex.