Rapid cold hardening delays the onset of anoxia-induced coma via an octopaminergic pathway in Locusta migratoria.

Rapid cold hardening (RCH) is a short-term hormesis that occurs in many invertebrate species, especially in insects. Although RCH is best known as enhancing cold tolerance, it can also enhance anoxic tolerance. When exposed to prolonged anoxia, insects enter a reversible coma, which is associated with spreading depolarization (SD) in the central nervous system (CNS). In this study, we investigated the effects of RCH and octopamine (OA) on anoxia-induced SD in L. migratoria. OA is an insect stress hormone that has roles in many physiological processes. Thus, we hypothesized that OA is involved in the mechanism of RCH. First, we found that RCH affects the K sensitivity of the locust blood brain barrier (BBB) in a way similar to the previously described effects of OA. Next, using SD as an indicator of anoxia-induced coma, we took a pharmacological approach to investigate the effects of OA and epinastine (EP), an octopaminergic receptor (OctR) antagonist. We found that OA mimics, whereas EP blocks, the effect of RCH on anoxia-induced SD. This study demonstrates that OA is involved in the mechanism of RCH in delaying the onset of anoxia-induced locust coma and contributes to determining the mechanism of RCH that modulates insect stress tolerances.