We have recently found evidence that two smellblind mutants, originally identified as olfactory mutants, define a new class of mutation in the para (paralytic) sodium channel gene (Lilly et al., in press). These two mutants have previously been shown to be heat-sensitive developmental lethals: animals raised at elevated temperatures die as embryos or as young larvae (Lilly and Carlson, 1990, Genetics 124, 293-302). This article shows, surprisingly, that both mutants are not only heat-sensitive lethals, but also cold-sensitive lethals: when raised at reduced temperatures, the mutants develop to the adult stage, but then die prematurely. Moreover, this effect is sexually dimorphic, in that lethality is substantially greater for females than males. The association of cold-sensitivity with mutations of a sodium channel gene has recently been found in the case of a cold-sensitive human muscle disease, paramyotonia congenita, in which sodium channel function is defective (Ptacek et al., 1992, Neuron 8, 891-897). The heat-sensitive and cold-sensitive periods for the two smellblind mutants are determined through a series of reciprocal temperature shift experiments and are found to be different. Most, if not all, of the contribution to the heat-sensitive lethality occurs before metamorphosis, whereas the cold-sensitivity is particularly pronounced after the onset of metamorphosis. These results are discussed in terms of the developmental role of the para sodium channel and the role of electrical activity in Drosophila development.