Crayfish photoreceptors exhibit a voltage-dependent
potassium conductance, GK, that is
generally similar to the delayed rectifier channel described
in neurons and other arthropod retinular cells.
GK activation (i.e. the apparent threshold,
Vth) occurs near the resting potential and
GK is substantially reduced by 25 mM
extracellular tetraethylammonium (TEA) and by intracellular
Cs+ injections. Light exposure, sufficient to
reduce visual sensitivity 100-fold, increases
Vth (shifts it in the depolarizing
direction) by about 20 mV. The light-dependent change in
Vth does not depend upon the corresponding
increase (depolarization) of the steady-state membrane potential
nor does it depend upon inward calcium currents. Vth
is slightly influenced by fluctuations in Ko
associated with the light-elicited currents. During light
exposure Ko (measured with K+-sensitive
electrodes) increases by 2.1 mM (equivalent to an 8 mV
increase in EK). This increase in
EK makes only a modest contribution
to the light-dependent change in Vth as
determined by perfusion with high potassium salines. Intracellular
calcium injections increase Vth by 10 to 20
mV and reduce visual sensitivity by 5- to 10-fold. The
results imply that during exposure to high levels of illumination,
K+ currents at the steady-state membrane potential
are diminished by a calcium-dependent change in GK
gating and, to a smaller degree, by a reduced K+
concentration gradient. It is notable that Ca2+ appears
to inhibit both GK and the light-elicited
conductance from both inside and outside the plasma membrane. As a
consequence of the light-dependent change in Vth, GK makes only modest contributions to the changes
in sensitivity and speed normally associated with light adaption.
These functions are regulated by the transduction pathway and are
revealed at the resting potential in the time course and magnitude
of the light-elicited currents.