Phinyaphat Srithiphaphirom, PhD Candidate Department of Biology, Robertson Lab, Queens' University Rapid cold hardening and stress-induced spreading depolarization in the central nervous system of Locusta migratoria Rapid cold hardening (RCH) is a short-term hormesis in which brief chilling (minutes to hours) significantly enhances the stress tolerance of an animal. Insects live in varied habitats and thus experience different kinds of environmental stresses. To thrive, insects enter a reversible coma, or hypo-energetic state when they are under stress. This is associated with a sudden loss of ion homeostasis and temporary shutdown in the central nervous system (CNS), which is a hallmark of spreading depolarization (SD). Insectstress tolerance is dependent on the sensitivity of their nervous systems to unfavourable conditions, which can be modulated by RCH. Using pharmacological and electrophysiological approaches, we investigated the mechanism of RCH and its effect on stress-induced SD in locusts, Locusta migratoria. We showed that RCH delays the onset of both chill- and anoxia-induced SD. Octopamine (OA) is an insect stress hormone, and we showed that OA mimics, whereas its antagonist, epinastine (EP), blocks, the effect of RCH on chill- and anoxia-induced SD. Thus, we concluded that OA mediates the RCH-induced delay of the onset of anoxia-induced locust coma. Lastly, we investigated whether RCH affects anoxia-induced SD via one or more of the following homeostatic mechanisms that are involved in maintaining K+ gradients: Na+ /K+ -ATPase (NKA), Na+ /K+ /2Cl- co-transporter (NKCC), and voltage-gated K+ (Kv) channels. We showed that NKA and Kv channels (excluding the Shaker family) modulate SD occurrence and possibly take part in the mechanism of RCH, whereas NKCC is directly involved in the mechanism of RCH. Altogether, we suggested that RCH regulates NKA, NKCC, and Kv channels through an octopaminergic pathway to modulate stress induced SD in locusts.
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