Purpose. To detect the presence of voltage-gated Ca2+ channels in the plasm
a membranes of freshly isolated Muller glial cells from the human retina an
d their modulation by GABA(B) receptor agonists.
Methods. Whole cell voltage-clamp recordings were made to study Ca2+, Ba2+,
and Na+ currents through voltage-gated Ca2+ channels.
Results. The vast majority of the investigated cells displayed no resolvabl
e currents through Ca2+ channels when Ca2+ ions (2 mM) were present in the
extracellular solution. Small-amplitude inwardly directed currents (similar
to 0.6 pA/pF) were detected when Ba2+ ions (20 mM) were used as charge car
rier. However, when Na+ ions were used as charge carrier in divalent cation
-free external solution, currents of large amplitudes (similar to 7.5 pA/pF
) through voltage-gated Ca2+ channels were detected. Human Muller cells dis
played currents through both transient, low voltage-activated Ca2+ channels
and long-lasting, high voltage-activated channels. The Na+ fluxes through
low voltage-activated Ca2+ channels were inhibited in a voltage-independent
manner in the presence of GABA(B) receptor agonists.
Conclusions. Human Muller glial cells express different kinds of voltage-ga
ted Ca2+ channels in their plasma membranes that can be activated only unde
r certain physiological or pathophysiological conditions. The record of Na fluxes in divalent cation-free solutions may be a technique to detect the
presence of "hidden" voltage-gated Ca2+ channels in Muller glial cells.