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

Previous studies have shown that increasing the temperature of rat hippocampal brain slices from 32.5 to 38.5 degrees C initiates a profound, adenosine-mediated decrease in excitatory synaptic transmission in the CA1 region. Here we found that upon lowering the temperature back to 32.5 degrees C, the amplitude of the field excitatory postsynaptic potential often recovers to a level that is significantly potentiated with respect to the initial baseline. This potentiation is rapid in onset (< 5min following return to 32.5 degrees C) and long lasting (>60min following the termination of the increase in temperature). Similar effects could not be induced by superfusion with adenosine alone, and adenosine receptor antagonists did not block the potentiation. Therefore, although an adenosine-mediated decrease in excitatory synaptic transmission occurs during the temperature increase, it is unrelated to the potentiation. Likewise, N-methyl-D-aspartate receptor activation is not required, as N-methyl-D-aspartate receptor antagonists do not influence 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, and may provide a paradigm to elucidate additional cellular mechanisms involved in functional plasticity.