Ec. Toolson et al., EICOSANOIDS MEDIATE CONTROL OF THERMOREGULATORY SWEATING IN THE CICADA, TIBICEN DEALBATUS (INSECTA, HOMOPTERA), Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 164(4), 1994, pp. 278-285
Cicadas prevent body temperature from exceeding tolerable levels by a
combination of behavioral responses and sweating. Sweating is activate
d when body temperature reaches a critical set-point temperature. We i
nvestigated control of sweating in the cicada, Tibicen dealbatus, by c
hemically manipulating biosynthesis of prostaglandins and other eicosa
noids. 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 biosynthesi
s 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-oxygenas
e inhibitors was not the opposite of the effect of prostaglandins. Ins
tead, the effect of cyclo-oxygenase inhibitors depended strongly on th
e value of setpoint temperature prior to treatment. Results of biochem
ical manipulations of other steps in eicosanoid biosynthetic pathways
corroborated the results of cyclo-oxygenase inhibition and indicated t
hat eicosanoids other than prostaglandins may be involved in control o
f body temperature in normothermic T. dealbatus. The effect of cyclo-o
xygenase inhibitors on a given set-point temperature depended on the a
mbient temperature experienced by cicadas during the experiment. Surpr
isingly, 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. Con
trol of body temperature in normothermic cicadas is thus complex, invo
lving inputs from body temperature sensors, ambient temperature sensor
s, and at least two cyclo-oxygenase-dependent regulatory pathways.