Pharmacological characterization of sodium channels in the primary culture of individual Drosophila embryos: neurons of a mutant deficient in a putative sodium channel gene.

Sodium channels in Drosophila embryonic neurons were characterized pharmacologically in the primary culture of individual gastrulae. In normal cultures, presence of sodium channels was demonstrated by neuronal degeneration in the presence of veratridine and ouabain, which was inhibited by tetrodotoxin. Embryonic neurons of Df(2R)M-c33a homozygotes that lack a putative sodium channel gene at 60E region showed normal neurotoxin sensitivity. Therefore, sodium channel genes other than 60E must be functional at this developmental stage. We also examined para(ts1) and nap(ts) mutants and found that they were also sensitive to the neurotoxins. To determine the genotypes of single embryo cultures by histochemical staining, we utilized a special chromosome bearing a hsp70-lacZ fusion gene. The lacZ expression in the culture was studied in detail.