Because the purpose of the present experiments was to examine
the e¡ects of calcium channel L subunits upon the
recovery from inactivation of K1 subunits, we studied two
K1 subunits, cyCav1 [11], and the human Cav2.3 subunit
[14], that produce robust, rapidly inactivating currents in oocytes
in the absence of coexpressed L subunits. A consistent
e¡ect of L subunit modulation is a leftward shift in the current^
voltage relationship of the K1 subunit. Such a shift was
seen for the cyCav1 subunit in every instance in which a L
subunit was coexpressed (Fig. 1A), demonstrating that each
mammalian L subunit studied can regulate cyCav1. A similar,
though smaller, shift in the hCav2.3 curve was produced by
coexpression of either cyL or the mammalian L subunits (Fig.
1B). The magnitude of the e¡ect is comparable to that previously
reported for the hCav2.3 subunit [14].