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Voltage-dependent calcium channels play a role in many cellular phenomena. Very little is known about Ca2+ channels in Drosophila, especially those in muscles. Existing literature on neuronal Ca2+ channels of Drosophila suggests that their pharmacology may be distinct from that of vertebrate Ca2+ channels. This raises questions on the pharmacology and diversity of Ca2+ channels in Drosophila muscles. Here we show that the Ca2+ channel current in the body-wall muscles of Drosophila larvae consists of two main components. One component is sensitive to 1,4-dihydropyridines and diltiazem, which block vertebrate L-type Ca2+ channels. The second component is sensitive to amiloride, which blocks vertebrate T-type Ca2+ channels. In contrast to Drosophila brain membrane preparations in which a majority of the Ca2+ channels are phenylalkylamine-sensitive but dihydropyridine-insensitive, the major current in the muscles was dihydropyridine-sensitive but relatively less sensitive to verapamil. This might indicate an underlying tissue specific distribution of distinct subtypes of dihydropyridine/phenylalkylamine-sensitive Ca2+ channels in Drosophila. Low verapamil sensitivity of the dihydropyridine-sensitive current of Drosophila muscles also set it apart from the vertebrate L-type channels which are sensitive to 1,4-dihydropyridines, benzothiazepines as well as phenylalkylamines. The dihydropyridine-sensitive current in Drosophila muscles activated in a similar voltage range as the vertebrate L-type current. As with the vertebrate current, blockade by dihydropyridines was voltage dependent.

Resolution and pharmacological analysis of the voltage-dependent calcium channels of Drosophila larval muscles