Metabolic rate in diapause and nondiapause brown locust eggs correlated with embryonic development

Insects use dormancy to survive adverse conditions. Brown locust Locustana pardalina (Walk.) eggs offer a convenient model to study dormancy (diapause and quiescence), which contributes to their survival under arid conditions. The metabolic rates of developing nondiapause, diapause and quiescent eggs are compared in the present study using closed‐system respirometry. The embryo becomes committed to continue development and hatch or to enter diapause 6 days after the eggs are placed on moist soil. The metabolic rate of nondiapause eggs increases exponentially until hatching, whereas that of diapause eggs is low and stable. The metabolic rate of diapause laboratory eggs (1.9 ± 0.6 µL CO₂ mg^?1 h^?1) is significantly higher than that of field eggs (0.5 ± 0.3 µL CO₂ mg^?1 h^?1), although the ranges of metabolic rate overlap and the embryos are all in late anatrepsis. The metabolic rate of quiescent eggs is similar to that of diapause eggs but decreases with time. Low metabolic rates during arrested development allow eggs to persist over long periods before hatching.     

Ionic Permeability of Insect Epithelia

In general, ionic regulation will depend on active transportby epithelia and also on the permeability properties of thesetissues. Passive permeability has recently been studied in thehindgut of the desert locust Schistocerca gregaria using electrophysiologicaland radiotracer techniques. Although locust rectum has low electricalresistance, cell membranes provide the major route for transepithelialionic diffusion; i.e., the locust rectum is a tight epithelium.Potassium permeability (P_K) is apparently regulated by luminalK and osmotic concentrations (local control), and also by thepeptide hormone CTSH (chloride transport-stimulating hormone).Transepithelial resistance declines when isolated recta areexposed to CTSH or its "second-messenger" cAMP (adenosine 3':5'-cyclicmonophosphate). Cyclic-AMP also stimulates K diffusion acrossrecta by 400%. Intracellular cable analysis indicatesthat cAMPlowers apical and basal membrane resistances (R_a and R_b, respectively)by {small tilde}80%; however different ionic permeabilitiesare affected at thelumen- and hemolymph-facing membranes: ThecAMP-induced decline in R_a, requires potassium whereas R_b isCl-dependent. The actions of cAMP on active transport and passivepermeability are complementary and would allow remarkably efficientcontrol over KC1 absorption in vivo. One hypothesis is as follows:CTSH elevates intracellular cAMP concentration by stimulatingadenyl cyclase. Cyclic-AMP enhances transepithelial Cl absorptionby stimulating a Cl pump in the apical membrane and also byincreasing the Cl permeability of the basal membrane. PassiveK absorption would also increase during cAMP stimulation sinceCl transport results in a more positive luminal potential, andbecause cAMP elevates transrectal P_K. The mechanisms by whichmembrane permeability is regulated in insects have not yet beenstudied, but these might involve the modulation of ion channelsby cAMP- or calmodulin-dependent phosphorylation, Ca or calmodulinbinding, methylation, or insertion of new channels into themembrane.