Rapid cold hardening and stress-induced spreading depolarization in the central nervous system of Locusta migratoria

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Srithiphaphirom, Phinyaphat
Keyword
Locust , Insect , Rapid cold hardening , Spreading depolarization , RCH , SD , Chill coma , Anoxic coma , CNS , Potassium , Stress , Octopamine , DC potential
Abstract
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). Insect stress tolerance is dependent on the sensitivity of their nervous systems to unfavourable conditions, which can be modulated by RCH. In my thesis, I used pharmacological and electrophysiological approaches to investigate the mechanism of RCH and its effect on stress-induced SD in locusts, Locusta migratoria. I show that RCH delays the onset of both chill- and anoxia-induced SD. Octopamine (OA) is an insect stress hormone and I show that OA mimics, whereas epinastine (EP; octopamine receptor antagonist) blocks, the effect of RCH on chill coma (intact locust) and anoxia-induced SD (semi-intact preparation). Additionally, I show that RCH affects the K+ sensitivity of the locust blood brain barrier (BBB) similarly to the previously described effects of OA. Thus, I conclude that OA mediates the RCH-induced delay of the onset of anoxia-induced locust coma at least partially by modulating the K+ sensitivity of the BBB. Lastly, I 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. I show that NKA and Kv channels (excluding the Shaker family) are involved in SD occurrence and possibly take part in the mechanism of RCH, whereas NKCC is directly involved in the mechanism of RCH. These findings suggest that RCH regulates NKA, NKCC, and Kv channels through an octopaminergic pathway to modulate stress-induced SD in locusts.
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