Rapid cold hardening (RCH) is a type of phenotypic plasticity that delays the occurrence of chill coma in insects. Chill coma is mediated by a spreading depolarization of neurons and glia in the CNS, triggered by a failure of ion homeostasis. We used biochemical and electrophysiological approaches in the locust, Locusta migratoria, to test the hypothesis that the protection afforded by RCH is mediated by activation of the Na+/K+-ATPase (NKA) in neural tissue. RCH did not affect NKA activity measured in a biochemical assay of homogenized thoracic ganglia. However, RCH hyperpolarized the axon of a visual interneuron (DCMD) and increased the amplitude of an activity-dependent hyperpolarization (ADH) shown previously to be blocked by ouabain. RCH also improved performance of the visual circuitry presynaptic to DCMD to minimize habituation and increase excitability. We conclude that RCH enhances in situ NKA activity in the nervous system but also affects other neuronal properties that promote visual processing in locusts.

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