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Abstract
<p class="first" id="P1">Calcium plays important roles in the function and survival
of rod and cone photoreceptor
cells. Rapid regulation of calcium in the outer segments of photoreceptors is required
for the modulation of phototransduction that drives the termination of the flash response
as well as light adaptation in rods and cones. On a slower time scale, maintaining
proper calcium homeostasis is critical for the health and survival of photoreceptors.
Decades of work have established that the level of calcium in the outer segments of
rods and cones is regulated by a dynamic equilibrium between influx via the transduction
cGMP-gated channels and extrusion via rod- and cone-specific Na
<sup>+</sup>/Ca
<sup>2+</sup>, K
<sup>+</sup> exchangers (NCKXs). It had been widely accepted that the only mechanism
for extrusion
of calcium from rod outer segments is via the rod-specific NCKX1, while extrusion
from cone outer segments is driven exclusively by the cone-specific NCKX2. However,
recent evidence from mice lacking NCKX1 and NCKX2 have challenged that notion and
have revealed a more complex picture, including a NCKX-independent mechanism in rods
and two separate NCKX-dependent mechanisms in cones. This review will focus on recent
findings on the molecular mechanisms of extrusion of calcium from the outer segments
of rod and cone photoreceptors, and the functional and structural changes in photoreceptors
when normal extrusion is disrupted.
</p>