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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.