An ER export signal accelerates the surface expression of shal potassium channels in pyloric neurons of the lobster stomatogastric ganglion.

Abstract

The shal gene encoding the transient potassium current, I(A), plays important roles in shaping the firing properties of neurons in the pyloric network in the stomatogastric ganglion (STG) of the spiny lobster, Panulirus interruptus. However, when we overexpressed the shal protein in pyloric dilator (PD) neurons, the effect of increased I(A )was compensated by a parallel upregulation of the hyperpolarization activated inward current ( I(h)). In an attempt to temporally separate the overexpression of shal from the compensatory up-regulation of I(h) channels, we inserted an endoplasmic reticulum (ER) export signal sequence, FCYENE, into the shal gene. This signal sequence accelerated the surface expression of shal protein in Xenopus oocytes and PD neurons. However, the accelerated expression of shal still did not alter the firing properties of the injected neuron, suggesting that the compensatory upregulation of I(h) occurs simultaneously with the upregulation of I(A).