Thermal preconditioning and heat-shock protein 72 preserve synaptic transmission during thermal stress.

摘要: 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 viability neurons under subsequent stress. Using a medullary slice preparation from neonatal mouse, including site neural network that generates respiratory rhythm (the pre-Botzinger complex), we show preconditioning has an additional fundamental effect, protection synaptic function. Relative 30 degrees C baseline, initial (40 C) greatly increased frequency currents recorded without pharmacological manipulation by approximately 17-fold (p < 0.01) miniature postsynaptic (mPSCs) elicited GABA (20-fold) glutamate (10-fold), glycine (36-fold). Thermal (15 min at 40 eliminated increase in overall transmission during acute attenuated GABAergic, glutamatergic, glycinergic mPSCs (for each, p 0.05). Moreover, preconditioning, incubation slices solution containing inducible (Hsp72) mimicked effect on stress-induced release neurotransmitter. That exogenous Hsp72 can affect preserve normal physiological function important therapeutic implications.