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The Journal of Neuroscience, 2001, 21:RC193:1-6

RAPID COMMUNICATION
Thermal Preconditioning and Heat-Shock Protein 72 Preserve Synaptic Transmission during Thermal Stress

Jonathan D. Kelty¹, Peter A. Noseworthy², Martin E. Feder¹, R. Meldrum Robertson², and Jan-Marino Ramirez¹

¹ Department of Organismal Biology and Anatomy, The University of Chicago, Chicago, Illinois 60637, and ² Department of Biology, Queen's University, Kingston, Ontario, Canada, K7L 3N6

As with other tissues, exposing the mammalian CNS to nonlethal heat stress (i.e., thermal preconditioning) increases levels of heat-shock proteins (Hsps) such as Hsp70 and enhances the viability of neurons under subsequent stress. Using a medullary slice preparation from a neonatal mouse, including the site of the neural network that generates respiratory rhythm (the pre-Bötzinger complex), we show that thermal preconditioning has an additional fundamental effect, protection of synaptic function. Relative to 30°C baseline, initial thermal stress (40°C) greatly increased the frequency of synaptic currents recorded without pharmacological manipulation by ~17-fold (p < 0.01) and of miniature postsynaptic currents (mPSCs) elicited by GABA (20-fold) glutamate (10-fold), and glycine (36-fold). Thermal preconditioning (15 min at 40°C) eliminated the increase in frequency of overall synaptic transmission during acute thermal stress and greatly attenuated the frequency increases of GABAergic, glutamatergic, and glycinergic mPSCs (for each, p < 0.05). Moreover, without thermal preconditioning, incubation of slices in solution containing inducible Hsp70 (Hsp72) mimicked the effect of thermal preconditioning on the stress-induced release of neurotransmitter. That preconditioning and exogenous Hsp72 can affect and preserve normal physiological function has important therapeutic implications.

Key words: hyperthermia; heat shock; synaptic transmission; miniature postsynaptic current; GABA; glutamate; glycine

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Copyright © Society for Neuroscience  0270-6474//$05.00/0

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