A transient increase in temperature induces persistent potentiation of synaptic transmission in rat hippocampal slices

Previous studies have shown that increasing the temperature of rat hippocam pal brain slices from 32.5 to 38.5 degreesC initiates a profound, adenosine -mediated decrease in excitatory synaptic transmission in the CAI region. H ere we found that upon lowering the temperature back to 32.5 degreesC, the amplitude of the field excitatory postsynaptic potential often recovers to a level that is significantly potentiated with respect to the initial basel ine. This potentiation is rapid in onset (< 5 min following return to 32.5< degrees>C) and long lasting (>60 min following the termination of the incre ase in temperature). Similar effects could not be induced by superfusion wi th adenosine alone, and adenosine receptor antagonists did not block the po tentiation. Therefore, although an adenosine-mediated decrease in excitator y synaptic transmission occurs during the temperature increase, it is unrel ated to the potentiation. Likewise, N-methyl-D-aspartate receptor activatio n is not required, as N-methyl-D-aspartate receptor antagonists do not infl uence this form of potentiation. In summary, we propose that transiently increasing brain slice temperature represents a novel way to induce synaptic plasticity in the hippocampus, an d may provide a paradigm to elucidate additional cellular mechanisms involv ed in functional plasticity. (C) 2000 IBRO. Published by Elsevier Science L td. All rights reserved.