ABSTRACT
The transmembrane potential of Drosophila salivary gland cells is largely decreased (by 78% within 120 min) in response to the application of 5 mM-chloramphenicol (CAP), with an initial slope of 0 ·5 mV min−1. This depolarization is reversed immediately after the CAP concentration is reduced to 0 ·06 mM by step-wise dilution with normal medium. At the same concentration, thiamphenicol (TAP) induces only a small reversible depolarization by less than 30% within 120 min. These results are in agreement with the different effects of CAP and TAP on respiration and induction of the heat-shock genes, as known from previous data.
The extent of induced membrane depolarization decreases with the number of repeated applications of CAP to the same cell, alternating with 75-min periods of recovery. Moreover, reduced sensitivity to CAP is also observed in cells recovering from a transient heat shock (30 min, 36°C) 45 min prior to the addition of CAP. This phenomenon is inhibited by cycloheximide (0 ·lmM), which suggests an involvement of heat-induced proteins in the stabilization of certain membrane functions.
