Eicosanoids mediate control of thermoregulatory sweating in the cicada, Tibicen dealbatus (Insecta: Homoptera)

Cicadas prevent body temperature from exceeding tolerable levels by a combination of behavioral responses and sweating. Sweating is activated when body temperature reaches a critical set-point temperature. We investigated control of sweating in the cicada, Tibicen dealbatus, by chemically manipulating biosynthesis of prostaglandins and other eicosanoids. Injecting prostaglandins in amounts equal to those that induce behavioral fever in scorpions and crustaceans resulted in only a small increase in set-point temperature. Blocking prostaglandin biosynthesis with cyclo-oxygenase inhibitors such as aspirin produced significant changes in set-point temperature, confirming that prostaglandins are involved in control of sweating. However, the effect of cyclo-oxygenase inhibitors was not the opposite of the effect of prostaglandins. Instead, the effect of cyclo-oxygenase inhibitors depended strongly on the value of set-point temperature prior to treatment. Results of biochemical manipulations of other steps in eicosanoid biosynthetic pathways corroborated the results of cyclooxygenase inhibition and indicated that eicosanoids other than prostaglandins may be involved in control of body temperature in normothermic T. dealbatus. The effect of cyclo-oxygenase inhibitors on a given set-point temperature depended on the ambient temperature experienced by cicadas during the experiment. Surprisingly, cicadas exposed to ambient temperatures greater than or equal to 40 degrees C delayed activation of sweating until body temperature exceeded values normally recorded from T. dealbatus in the field. Control of body temperature in normothermic cicadas is thus complex, involving inputs from body temperature sensors, ambient temperature sensors, and at least two cyclo-oxygenase-dependent regulatory pathways.