Activity-independent homeostasis in rhythmically active neurons

The shal gene encodes the transient potassium current (I-A) in neurons of the lobster stomatogastric ganglion. Overexpression of Shal by RNA injection into neurons produces a large increase in I-A, but surprisingly little change in the neuron's firing properties. Accompanying the increase in I-A is a dramatic and linearly correlated increase in the hyperpolarization activated inward current (I-h). The enhanced Ih electrophysiologically compensates for the enhanced I-A, since pharmacological blockade of I-h uncovers the physiological effects of the increased I-A. Expression of a nonfunctional mutant Shal also induces a large increase in I-h, demonstrating a novel activity-independent coupling between the Shal protein and I-h enhancement. Since I-A and I-h influence neuronal activity in opposite directions, our results suggest a selective coregulation of these channels as a mechanism for constraining cell activity within appropriate physiological parameters.