Mutant flies show increased sensitivity to lack of O₂ compared to wild type; the mean recovery time from stupor induced by 5 minutes of anoxia is more than double that of wild-type flies (615.8 +/- 23.5 seconds versus 321.1 +/- 7 seconds). In addition, mutant flies lose motor control on exposure to anoxia at a significantly faster rate than wild-type flies. Mutant flies have limited locomotor ability, although they can jump and more around in the culture vial. O₂ consumption in the mutant is similar to that in wild-type flies in both normal and low-O₂ environments. Mutant flies are significantly more sensitive to heat shock compared to wild-type flies; the duration of heat shock that causes 50% death is significantly shorter in the mutant flies than in wild type (3.15 hours versus 4.26 hours). At 25^oC, mutant flies have a shorter lifespan than wild-type flies. Mutant 35 day old adults show degeneration in cortical neurons of the medulla and lobula complex as well as in the lamina (this degeneration is not seen in 3 day old mutant flies or in 3 or 35 day old wild-type flies). The membrane potential of cultured mutant neurons is significantly lower than in wild-type cultured neurons. However, the Na⁺-channel current density, or peak Na⁺-current normalised to capacitance, is significantly higher in the mutant than in the wild-type neurons.

Mutants take twice as long a wild type to recover from anoxia. Mutants have enhanced sensitivity to low oxygen and they lose motor control faster than wild-type flies when exposed to anoxia. Electrophysiological studies reveal the mutation has a profound effect on synaptic transmission in the central nervous system.