Changes in Membrane Properties of the Drosophila Dorsal Longitudinal Flight Muscle Induced by Sodium Pump Inhibitors Available to Purchase

Drosophila dorsal longitudinal flight muscle fibres made anoxic by passing nitrogen through the tracheal system or treated with 10⁻⁵m ouabain or strophanthidin show a reversible fall in resting membrane potential of 16·5 mV (s.e. 0·96), 13·7 mV (s.e. 0·87), and 17·0 mV (s.e. 2·8), respectively. The reversible depolarization obtained with these sodium pump blockers occurred within 10–15 min.

The depolarization of the muscle fibres was accompanied by a decrease in input resistance of 21·2% (s.e. 3·8) in anoxia, 21·4% in ouabain, and 25·6% (s.e. 6·7) in strophanthidin. The resistance decrease in strophanthidin and ouabain was transient and returned to above the resting level while the muscle fibres were still exposed to these agents.

Recovery of membrane potential in cells exposed to anoxia is biphasic. An initial ‘fast’ phase of recovery occurs within 15 s upon return to air followed by a late ‘slow’ phase lasting several minutes. Recovery of input resistance in cells exposed to N₂ coincided with the ‘fast’ phase of the recovery of resting membrane potential.

Recovery of membrane potential following exposure to strophanthidin is a long, slow process which occurs at conductance values at the resting level or below.

The tendency towards spontaneous action potentials was increased by anoxia and the action potentials occurring in anoxia were elongated into plateau potentials of about 18 s duration.

These results are consistent with the hypothesis that anoxia and cardioactive steroids inhibit a metabolic process, possibly an electrogenic ion pump, that is essential for maintenance of the resting membrane potential in Drosophila flight muscle. Exposure to these agents also results in changes in input resistance. Both of these effects could contribute to the depolarization and affect the excitable properties of the muscle fibre membrane.