Paralyzed fairly rapidly at temperatures above 38; adults seem to have a fit before becoming immobile, as opposed to immediately ceasing their movements; increasing times of exposure to high temperature leads to progressively longer times necessary for recovery when temperature is lowered (Jackson et al., 1985); sei1 is recessive for heat-sensitive paralysis (Jackson et al., 1985); sei2 is semi-dominant in this respect, and behavior of hyperploid adults exhibits dose dependence: sei2/sei2/+ flies become paralyzed, at 40, slightly less rapidly than homozygous mutants; sei2/+/+ paralyzed more slowly than sei2/+ but faster than wild-type (Jackson et al., 1985); biochemically, head membrane extracts from sei2 adults exhibit anomalously high Kd of saxitoxin (STX) binding activity, and a different pH dependence of this activity from wild-type; these abnormalities observed when the incubations done at high, but not low, temperatures (Jackson et al., 1984); in flies carrying three sei alleles, apparent reductions in the amounts of STX bound are observed, which are proportional to the relative number of mutant alleles (Jackson et al., 1985); when these kinds of biochemical experiments are performed on head extracts from sei1, Kd values are not appreciably different from wild-type at all assay temperatures, but the concentrations of STX binding activity are lower than wild-type under the influence of this allele, with such reductions being more marked at higher assay temperatures; recovery times, after exposure to high temperature and subsequent return to mild conditions, are shortened when sei2 is combined with napts (Jackson et al., 1985). Recordings of action potentials in the adult giant-fiber pathway reveal no decrement in sei2 at 40 (Nelson and Baird, 1985, Neurosci. Abstr. 11: 313); at temperatures >40, sei2 causes spontaneous activity in recordings from dorsal longitudinal flight muscles, to appear coincidentally with the heat-induced paralysis (Kasbekar et al., 1989); from "tight-seal whole-cell" recordings, using cultured neurons from sei1 embryos, this mutation found to cause sodium current density to be about half-normal; yet, voltage dependence and channel-gating properties were not different from wild type (O'Dowd and Aldrich, 1988); for other aspects of sei-associated defects in physiology, see enhancer of seizure.