Download Why do insects enter chill coma? Low temperature and high

Why do insects enter chill coma? Low temperature and high extracellular potassium compromises
muscle function in Locusta migratoria
Anders Findsen1, Thomas Holm Pedersen2, Ole Bækgaard Nielsen2 and Johannes Overgaard1
1
Zoophysiology, Department of Bioscience, Aarhus University
2
Department of Biomedicine - Danish Biomembrane Research Centre, Aarhus University
Many insect species enter a comatose state when their body temperature is lowered to a critical
limit (critical thermal minimum) but the physiological and cellular processes that underlie chill coma
are still unresolved. Several studies have demonstrated that transition into chill-coma involves a
disruption of neuro-muscular performance. It has also been shown that ion homeostasis (particularly
extracellular [K+]) is disrupted during chill coma. Neuro-muscular failure associated with chill coma is
therefore likely to be caused by direct effects of reduced temperature as well as indirect, forcedepressing effects that occur secondary to loss of ion-homeostasis. Using isolated tibial muscle of
the chill susceptible locust we investigated the relationship between tetanic force production,
temperature and extracellular [K+]. Tetanic force was elicited every 10 minutes using 2s trains of 1ms
12-V pulses and a frequency of 60 Hz. To explore to what extent loss of force during cold exposure
reflects loss of muscle function, all experiments were performed both in the presence and absence
of TTX, which selectively inhibits motor nerve function in insects. Maximum tetanic force decreased
approximately 75% when temperature was reduced from 23°C to 0.5°C. Similarly, elevation of
extracellular [K+] from a control value of 10 mM to 30 mM also caused a 50 % reduction of force.
When muscles were simultaneously cooled and exposed to elevated K+, force was reduced to around
1 % of the control. These results suggest that both temperature and ion disruption are of importance
when animals enter chill coma.