Abstract
The ability of chill-sensitive insects to function at low temperatures limits their geographic ranges. They have species-specific temperatures below which movements become uncoordinated prior to entering a reversible state of neuromuscular paralysis. In spite of decades of research, which in recent years has focused on muscle function, the role of neural mechanisms in determining chill coma is unknown. Spreading depolarization (SD) is a phenomenon that causes a shutdown of neural function in the integrating centres of the central nervous system. We investigated the role of SD in the process of entering chill coma in the locust, Locusta migratoria. We used thermolimit respirometry and electromyography in whole animals and extracellular and intracellular recording techniques in semi-intact preparations to characterize neural events during chilling. We show that chill-induced SD in the central nervous system is the mechanism underlying the critical thermal minimum for coordinated movement in locusts. This finding will be important for understanding how insects adapt and acclimate to changing environmental temperatures.
Highlights
When exposed to temperatures below a critical thermal minimum (CTmin)[1], chill-sensitive insects lose neuromuscular coordination and eventually enter a state of complete paralysis at the point of chill coma onset (CCO)[2, 3]
We conclude that Spreading depolarization (SD) is the mechanism for the loss of coordinated movement at CTmin but, because some peripheral neural activity persists after SD, which could cause uncoordinated movements, we conclude that CCO occurs at a lower temperature and is coincident with relaxation of spiracle closer muscles
There were two small peaks (Fig. 1B;
Summary
When exposed to temperatures below a critical thermal minimum (CTmin)[1], chill-sensitive insects lose neuromuscular coordination and eventually enter a state of complete paralysis at the point of chill coma onset (CCO)[2, 3]. Recent research in locusts[15] and Drosophila[16] suggests that shutdown of the central nervous system (CNS) via a spreading depolarization (SD) mechanism could have an important role to play in the entry to chill coma. SD is characterized by a collapse of CNS ion homeostasis resulting in major changes in CNS ion concentrations, neuronal and glial depolarization and a negative DC shift in the extracellular field potential (FP)[23] It appears to be triggered when extracellular potassium ion concentration ([K+]o) surpasses a critical threshold and is dependent on activity levels in the CNS24–26. Subsequent electrophysiological experiments in whole animals and semi-intact preparations showed that bursts of electrical activity in muscles during chilling have a neural origin and that SD in the thoracic ganglia indicates a point at which all neural activity in the central integrative neuropil has terminated, which would prevent coordinated movement. We conclude that SD is the mechanism for the loss of coordinated movement at CTmin but, because some peripheral neural activity persists after SD, which could cause uncoordinated movements, we conclude that CCO occurs at a lower temperature and is coincident with relaxation of spiracle closer muscles
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