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Spreading depression (SD) is associated with large changes in extracellular ion concentrations and can be induced by impairing mechanisms of K+ ion homeostasis. We tested activity dependence of SD in the locust model of ouabain-induced SD in the metathoracic ganglion. Wind activation of thoracic circuitry resulted in small increases of K+ concentration that took 5--10 s to be cleared from the extracellular space. In the presence of the Na+/K+-ATPase inhibitor ouabain, wind stimulation every 30 s halved the latency to the first SD event and increased its duration.Wind stimulation was able to trigger the first event, suggesting that local activity could determine the origin of successive SD events. Perfusion with calcium-free saline blocked neural activity in the ganglion and prevented the occurrence of ouabain-induced SD.We conclude that ouabain-induced SD in the locust CNS is strongly dependent on the existing level of neural activity. [ABSTRACT FROM AUTHOR]

The sensitivity of insect nervous systems to anoxia can be modulated genetically and pharmacologically, but the cellular mechanisms responsible are poorly understood. We examined the effect of a heat shock pretreatment (HS) on the sensitivity of the locust (Locusta migratoria) nervous system to anoxia induced by water immersion. Prior HS made locusts more resistant to anoxia by increasing the time taken to enter a coma and by reducing the time taken to recover the ability to stand. Anoxic comas were accompanied by surges of extracellular potassium ions in the neuropile of the metathoracic ganglion, and HS reduced the time taken for clearance of excess extracellular potassium ions. This could not be attributed to a decrease in the activity of protein kinase G, which was increased by HS. In homogenates of the metathoracic ganglion, HS had only a mild effect on the activity of Na+-K+-ATPase. However, we demonstrated that HS caused a threefold increase in the immunofluorescent localization of the α-subunit of Na+-K+-ATPase in metathoracic neuronal plasma membranes relative to background labeling of the nucleus.We conclude that HS induced trafficking of Na+-K+-ATPase into neuronal plasma membranes and suggest that this was at least partially responsible for the increased resistance to anoxia and the increased rate of recovery of neural function after a disturbance of K+ homeostasis. [ABSTRACT FROM AUTHOR]

Reviews of the article "Defense strategies against hypoxia and hypothermia" by Peter Hochachka, "Sensing and surviving hypoxia in vertebrates" by M. G. Jonz, and "Mechanisms of spreading depolarization in vertebrate and insect central nervous systems" by K. E. Spong, are presented.

Abstract: Environmental temperature is one of the most important abiotic factors affecting insect behaviour; virtually all physiological processes, including those which regulate nervous system function, are affected. At both low and high temperature extremes insects enter a coma during which individuals do not display behaviour and are unresponsive to stimulation. We investigated neurophysiological correlates of chill and hyperthermic coma in Drosophila melanogaster. Coma resulting from anoxia causes a profound loss of K+ homeostasis characterized by a surge in extracellular K+ concentration ([K+]o) in the brain. We recorded [K+]o in the brain during exposure to both low and high temperatures and observed a similar surge in [K+]o which recovered to baseline concentrations following return to room temperature. We also found that rapid cold hardening (RCH) using a cold pretreatment (4°C for 2h; 2h recovery at room temperature) increased the peak brain [K+]o reached during a subsequent chill coma and increased the rates of accumulation and clearance of [K+]o. We conclude that RCH preserves K+ homeostasis in the fly brain during exposure to cold by reducing the temperature sensitivity of the rates of homeostatic processes. [Copyright &y& Elsevier]

We investigated the effects of heat shock on the temperature sensitivity of synaptic transmission in the motor circuit for flight in Locusta migratoria. In heat shocked animals synaptic transmission failed at 5-6 degrees C higher than in control animals and recovery of transmission was more than three times faster upon return to room temperature. We also found that synaptic delay was rendered insensitive to increases in temperature by heat shock. Thus we have shown in the locust that heat shock has important protective effects on synaptic transmission, thereby extending the upper temperature limit for the motor patterns that generate flight. This is the first description of an effect of heat shock that preserves neuronal communication under subsequent stressful conditions.