Dissociation between synaptic depression and block of long-term depression induced by raising the temperature in rat hippocampal slices

The influence of raising the bath temperature (39 degrees C) on synaptic transmission and neuronal plasticity was studied in the CA1 region of the rat hippocampus using an extracellular recording technique. Increasing the bath temperature from 32 to 39 degrees C resulted in a depression of field excitatory postsynaptic potential (fEPSP). Application of the selective A(1) receptor agonist, 2-chloro-adenosine (2-CADO, 1 microM) reduced the fEPSP and subsequently occluded the raised temperature-induced synaptic depression. On the other hand, the selective adenosine A(1) receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX) blocked depression of fEPSP produced by raising the temperature. These results suggest that raising temperature-induced synaptic depression is due to an alteration of extracellular adenosine concentration. Long-term depression (LTD) could be reliably induced by the standard low-frequency stimulation (LFS, 1 Hz for 15 min) protocol at 32 degrees C but not at 39 degrees C. The raised temperature-induced block of LTD was mimicked by 2-CADO. Unexpectedly, despite the presence of DPCPX, LFS still could not elicit LTD. NMDA receptor-mediated synaptic component (fEPSP(NMDA)) was decreased when increasing the temperature to 39 degrees C and DPCPX failed to reverse such a depression. The increase in the NMDA response in 0.1 mM Mg(++) compared with 1 mM Mg(++) was significantly greater at 32 degrees C than at 39 degrees C. These results suggest that, by increasing the sensitivity of Mg(++) block, an increase in temperature modulates NMDA responses and thereby inhibits the induction of LTD.