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This Article Full Text Full Text (PDF) All Versions of this Article: 102/1/285    most recent 91174.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Money, T. G. A. Articles by Robertson, R. M. PubMed PubMed Citation Articles by Money, T. G. A. Articles by Robertson, R. M.

Loss of Potassium Homeostasis Underlies Hyperthermic Conduction Failure in Control and Preconditioned Locusts

Department of Biology, Queen's University, Kingston, Ontario, Canada

Submitted 26 October 2008; accepted in final form 13 April 2009

At extreme temperature, neurons cease to function appropriately. Prior exposure to a heat stress (heat shock [HS]) can extend the temperature range for action potential conduction in the axon, but how this occurs is not well understood. Here we use electrophysiological recordings from the axon of a locust visual interneuron, the descending contralateral movement detector (DCMD), to examine what physiological changes result in conduction failure and what modifications allow for the observed plasticity following HS. We show that at high temperature, conduction failure in the DCMD occurred preferentially where the axon passes through the thoracic ganglia rather than in the connective. Although the membrane potential hyperpolarized with increasing temperature, we observed a modest depolarization (3–6 mV) in the period preceding the failure. Prior to the conduction block, action potential amplitude decreased and half-width increased. Both of these failure-associated effects were attenuated following HS. Extracellular potassium concentration ([K⁺]_o) increased sharply at failure and the failure event could be mimicked by the application of high [K⁺]_o. Surges in [K⁺]_o were muted following HS, suggesting that HS may act to stabilize ion distribution. Indeed, experimentally increased [K⁺]_o lowered failure temperature significantly more in control animals than in HS animals and experimentally maintained [K⁺]_o was found to be protective. We suggest that the more attenuated effects of failure on the membrane properties of the DCMD axon in HS animals is consistent with a decrease in the disruptive nature of the [K⁺]_o-dependent failure event following HS and thus represents an adaptive mechanism to cope with thermal stress.