Abstract
The single-gene mutant shibire (shits) is temperature-sensitive. It causes reversible paralysis at heat pulses greater than 29 degrees C by blocking synaptic transmission. The synapses of these heat-pulsed flies are depleted in vesicles but contain numerous cisternae. We report that such alterations in synaptic physiology and morphology of heat-pulsed flies can be suppressed by internal perfusion of salines with high concentrations (10–18 mM) of the divalent cations Ca2+ or Mg2+. Synaptic morphology in these perfused flies remains normal even when exposed to nonpermissive temperatures (greater than 29 degrees C); in addition, synaptic transmission maintains a high resistance to failure both in frequency and stimulus duration. We also observed many cisternae in close association with extrajunctional as well as with postsynaptic regions of the sarcolemma in heat-pulsed shits flies not perfused with the increased concentrations of divalent cations. Flies perfused with increased amounts of divalent cations lacked such cisternae in the sarcolemma. The evidence suggests that the divalent cations can mitigate an overall membrane defect expressed by the shits gene, perhaps by influencing lipid-phase transition behavior.
