The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neuronsThe contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
Faculty of Medicine and Health Sciences
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Molecular biophysics, physiology and pharmacology
Neurochemistry and behaviour
4(2016):6, 13 p.
University of Antwerp
Delayed rectifier voltage‐gated K+ (Kv) channels play an important role in the regulation of the electrophysiological properties of neurons. In mouse dorsal root ganglion (DRG) neurons, a large fraction of the delayed rectifier current is carried by both homotetrameric Kv2 channels and heterotetrameric channels consisting of Kv2 and silent Kv (KvS) subunits (i.e., Kv5‐Kv6 and Kv8‐Kv9). However, little is known about the contribution of Kv2‐mediated currents during the postnatal development of DRG neurons. Here, we report that the Stromatoxin‐1 (ScTx)‐sensitive fraction of the total outward K+ current (IK) from mouse DRG neurons gradually decreased (~13%, P < 0.05) during the first month of postnatal development. Because ScTx inhibits both Kv2.1‐ and Kv2.2‐mediated currents, this gradual decrease may reflect a decrease in currents containing either subunit. However, the fraction of Kv2.1 antibody‐sensitive current that only reflects the Kv2.1‐mediated currents remained constant during that same period. These results suggested that the fractional contribution of Kv2.2‐mediated currents relative to IK decreased with postnatal age. Semiquantitative RT‐PCR analysis indicated that this decrease can be attributed to developmental changes in Kv2.2 expression as the mRNA levels of the Kv2.2 subunit decreased gradually between 1 and 4 weeks of age. In addition, we observed age‐dependent fluctuations in the mRNA levels of the Kv6.3, Kv8.1, Kv9.1, and Kv9.3 subunits. These results support an important role of both Kv2 and KvS subunits in the postnatal maturation of DRG neurons.