Transient receptor potential (TRP) channels sense and transduce environmental
stimuli into Ca2+ transients that in turn induce responses essential for cell
function and adaptation. These non-selective channels with variable Ca2+
selectivity are grouped into seven different subfamilies containing 28
subtypes based on differences in amino acid sequence homology. Many of these
subtypes are expressed in the eye on both neuronal and non-neuronal cells
where they affect a host of stress-induced regulatory responses essential for
normal vision maintenance. This article reviews our current knowledge about
the expression, function and regulation of TRPs in different eye tissues. We
also describe how under certain conditions TRP activation can induce responses
that are maladaptive to ocular function. Furthermore, the possibility of an
association between TRP mutations and disease is considered. These findings
contribute to evidence suggesting that drug targeting TRP channels may be of
therapeutic benefit in a clinical setting. We point out issues that must be
more extensively addressed before it will be possible to decide with certainty
that this is a realistic endeavor. Another possible upshot of future studies
is that disease process progression can be better evaluated by profiling
changes in tissue specific functional TRP subtype activity as well as their
gene and protein expression
