Alpha1T Encoded CaV3 Type Calcium Channels Regulate Neuronal Excitability in Adult Drosophila Brain

Voltage gated calcium channels mediate calcium influx that influences a wide variety of cellular processes including excitability and chemical synaptic transmission in the nervous system. In Drosophila, there are three genes, Dmca1D, cac, and alpha1T encoding Cav1, Cav2 and Cav3-type channels respectively (Smith et al. 1996; Zheng et al. 1995; Littleton and Ganetzky 2000; King 2007). Null alleles in each of these genes result in embryonic lethality, demonstrating that they are not functionally redundant, but rather each plays a unique role in the organism (Eberl et al., 1998). Whole cell recordings from antennal lobe projection neurons (PNs) in adult brains reveal calcium currents with two components, a rapidly decaying transient current and a slowly decaying sustained current. In a previous study we showed that cac encodes channels underlying the sustained calcium current. Here we demonstrate the transient component is sensitive to prepulse inactivation and is blocked by amiloride, a vertebrate Cav3 channel blocker, in a dose dependent manner. RNAi knockdown of the alpha1T gene specifically in PNs caused a dramatic reduction in the fast inactivating current without altering the sustained current. These data demonstrate that the a1T gene encodes the voltage gated calcium channels underlying the amiloride sensitive fast-inactivating current. PN’s display altered firing properties in the alpha1T knockdowns indicating the CaV3 type calcium current is important in regulating neuronal excitability.