Rapid cold hardening modifies ion regulation to delay anoxia-induced spreading depolarization in the CNS of the locust.

Insects experience different kinds of environmental stresses that can impair neural performance, leading to spreading depolarization (SD) of nerve cells and neural shutdown underlying coma. SD is associated with a sudden loss of ion, notably K, homeostasis in the central nervous system. The sensitivity of an insect's nervous system to stress (e.

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).

Rapid cold hardening and octopamine modulate chill tolerance in Locusta migratoria.

Temperature has profound effects on the neural function and behaviour of insects. When exposed to low temperature, chill-susceptible insects enter chill coma, a reversible state of neuromuscular paralysis. Despite the popularity of studying the effects of low temperature on insects, we know little about the physiological mechanisms controlling the entry to, and recovery from, chill coma.

Chill coma in the locust, Locusta migratoria, is initiated by spreading depolarization in the central nervous system.

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.