Genetic alteration of nerve membrane excitability in temperature-sensitive paralytic mutants of Drosophila melanogaster

Abstract

Single mutations that disrupt basic physiological processes such as axonal conduction and synaptic transmission provide one means to study the membrane components and mechanisms that underlie these processes^1,8. Temperature-sensitive paralytic mutants of Drosophila melanogaster which behave normally at a permissive temperature (23–25 °C) but become paralysed at a restrictive temperature (usually 29–37 °C) have been utilized in such studies. An example is nap^ts (no action potential, temperature-sensitive), a recessive second-chromosome mutation that causes paralysis of larvae and adults at 37 °C. Electrophysiological recordings have demonstrated that nap^ts specifically affects a component of axonal membranes⁵. Here we show that axonal conduction in nap^ts larvae is abnormally sensitive to tetrodotoxin (TTX), a specific blocker of voltage-sensitive sodium channels⁹, and that the refractory period of action potentials differs from wild type, consistent with the idea that nap^ts alters the function of sodium channels. It is further shown that para^ts (paralysed, temperature-sensitive), a recessive X-linked mutation¹, also specifically disrupts axonal conduction and that the two mutations affect functionally related membrane components. Identification of other mutants defective in associated components of nerve membranes is made feasible by using techniques described here.