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Sodium (Na+) currents are involved in the regulation of the electrical excitability of heart and neurons. Na+ currents in cardiomyocytes are generated by a different set of channel subtypes, that are present in different populations of the heart. Na+ channel subtypes are encoded by different genes and their biophysical properties are also different. The cardiac Na+ channels are activated by a variable voltage and are non-inactivating. In the present study we investigated the subcellular distribution of cardiac Na+ channels (NCX1, NCX2 and NCX3), and their possible role in the excitability of isolated mouse ventricular myocytes. With whole-cell patch-clamp technique we examined the subcellular distribution of the Na+ channels in single cardiomyocytes isolated from WT and Cav1.2(R26S) mice. In WT mouse myocytes the Na+ current distribution was NaV1.5 (functional)>/=hNaV1.7 (tetrodotoxin-insensitive)>/=NaV1.8 (non-functional). Both NaV1.7 and NaV1.
In the mammalian retina, the formation of retinal ganglion cells and the growth of their axons from the eye to the brain are topographically ordered processes. The formation of retinal ganglion cells (RGCs) occurs in two phases (from E14 to P0) in mice. In phase 1 (E14–E16), RGCs originate in the eye and migrate outwards to the optic disc. In phase 2 (E16–P0), they make their final destination in the dorsal midbrain. It is not clear, however, what regulates RGC migration. Pax6 is expressed in RGCs and functions as a key regulator in eye development and in brain pattern formation. Using both genetic and biochemical approaches, we show that Pax6 interacts directly with the translation initiation factor eIF4E and negatively regulates its activity, thus affecting RGC development. Loss of Pax6 function disrupts the organization of brain patterning and results in drastic upregulation of eIF4E. Furthermore, blockage of eIF4E activity resulted in an acceleration of RGC migration. We also show that eIF4E levels are increased during the retinal ganglion cell development of the mammalian optic nerve, suggesting that regulation of translation initiation factor activity is a novel mechanism regulating RGC development.
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