Is abundant L-type calcium channel Ca ( v ) 1.3 ( alpha1D ) subunit mRNA detected in rod photoreceptors of the mouse retina via in situ hybridization?
Our finding of expression of the L-type calcium channel Ca(v)1.3 (alpha1D) subunit mRNA in rods substantiates the possibility that this pore-forming subunit may be a competent component of channels mediating the residual photoreceptor responses observed in mutant mice lacking functional Ca(v)1.4 (alpha1F) subunits and in humans with CSNB2. Furthermore, the combined observations of abundant expression of Ca(v)1.3 (alpha1D) mRNA in wild type rods and the large reduction in the transmission of photoreceptor responses in mice lacking Ca(v)1.4 (alpha1F) raises the possibility that Ca(v)1.3 (alpha1D) protein expression levels, localization, or functioning might be concomitantly altered by disruption of the Ca(v)1.4 (alpha1F) subunit in rods. To date, no studies of Ca(v)1.3 (alpha1D) mRNA nor protein expression levels or localization in cacna1f mutant mice or humans with CSNB2 have been published. Our findings warrant such studies to address the abovementioned possibilities. Finally, the observation of Ca(v)1.3 (alpha1D) mRNA expression in multiple retinal cell types suggests the potential for a broader role for this L-type calcium channel subunit in overall functioning of the normal retina than previously appreciated. We therefore suggest that lesions in either the gene encoding the L-type calcium channel Ca(v)1.3 (alpha1D) subunit or other molecules that interact with and regulate it may underlie one or more retinopathies with currently unidentified molecular etiologies.
It is clear from these results that, while alertness may successfully "predict" variations in some measures of performance capability, and especially those of simple perceptual motor speed, care should be exercised in extrapolating to other performance measures.