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Biophys J, June 2000, p. 2959-2972, Vol. 78, No. 6
2
Subunit Interferes
with Prepulse Facilitation in Cardiac L-type Calcium Channels
§¶
§ and
Departments of *Anesthesiology, Physiology and
Biological Chemistry, and §Brain Research;
¶Molecular Biology Institutes, UCLA School of
Medicine, Los Angeles, California 90095-7115; and #INFM UdR
Ferrara, Dipartimento di Biologia, Università di Ferrara, 441000 Ferrara, Italy
We investigated the role of the accessory
2
subunit on the voltage-dependent facilitation of
cardiac L-type Ca2+ channels (1C).
1C Channels were coexpressed in Xenopus
oocytes with 
3 and 2 calcium channel
subunits. In 1C + 3, the amplitude of the ionic current (measured during pulses to 10 mV) was in average
~1.9-fold larger after the application of a 200-ms prepulse to +80
mV. This phenomenon, commonly referred to as voltage-dependent facilitation, was not observed when 2 was coexpressed
with 1C + 3. In 1C + 3, the prepulse produced a left shift (~40 mV) of the
activation curve. Instead, the activation curve for 1C + 3 + 2 was minimally affected by the
prepulse and had a voltage dependence very similar to the
G-V curve of the 1C + 3
channel facilitated by the prepulse. Coexpression of
2 with 1C + 3 seems to
mimic the prepulse effect by shifting the activation curve toward more
negative potentials, leaving little room for facilitation. The
facilitation of 1C + 3 was associated
with an increase of the charge movement. In the presence of
2, the charge remained unaffected after the prepulse.
Coexpression of 2 seems to set all the channels in a
conformational state from where the open state can be easily reached,
even without prepulse.
Biophys J, June 2000, p. 2959-2972, Vol. 78, No. 6
© 2000 by the Biophysical Society 0006-3495/00/06/2959/14 $2.00
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