Abstract
SummaryNeuron electrical properties are critical to function and generally subtype specific, as are patterns of axonal and dendritic projections. Specification of motoneuron morphology and axon pathfinding has been studied extensively, implicating the combinatorial action of Lim-homeodomain transcription factors. However, the specification of electrical properties is not understood. Here, we address the key issues of whether the same transcription factors that specify morphology also determine subtype specific electrical properties. We show that Drosophila motoneuron subtypes express different K+ currents and that these are regulated by the conserved Lim-homeodomain transcription factor Islet. Specifically, Islet is sufficient to repress a Shaker-mediated A-type K+ current, most likely due to a direct transcriptional effect. A reduction in Shaker increases the frequency of action potential firing. Our results demonstrate the deterministic role of Islet on the excitability patterns characteristic of motoneuron subtypes.
Highlights
Diversity in neuronal signaling is critical for emergence of appropriate behavior
This diversity is reflected in dendrite morphology, axon pathfinding, choice of synaptic partners, transmitter phenotype, and cocktail of ion channels expressed by individual neurons
We show that Islet is sufficient to repress expression of a Sh-mediated K+ current
Summary
Diversity in neuronal signaling is critical for emergence of appropriate behavior This diversity is reflected in dendrite morphology, axon pathfinding, choice of synaptic partners, transmitter phenotype, and cocktail of ion channels expressed by individual neurons. Neurons grown in culture often express their normal complement of both voltage- and ligand-gated ion channels (O’Dowd et al, 1988; Ribera and Spitzer, 1990; Spitzer, 1994) This suggests a significant degree of cell autonomy in the determination of electrical properties that presumably facilitates initial network formation. As a result, predetermined electrical properties are modified by a variety of well-described mechanisms (Davis and Bezprozvanny, 2001; Spitzer et al, 2002) Such tuning ensures consistency of network output in response to potentially destabilizing activity resulting from Hebbian-based synaptic plasticity (Turrigiano and Nelson, 2004). Key to understanding how intrinsic and extrinsic mechanisms are integrated will be the identification of factors that regulate predetermination
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