The influence of raising the bath temperature (39°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°C resulted in a depression of field excitatory postsynaptic potential (fEPSP). Application of the selective A1 receptor agonist, 2-chloro-adenosine (2-CADO, 1 μM) reduced the fEPSP and subsequently occluded the raised temperature-induced synaptic depression. On the other hand, the selective adenosine A1 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°C but not at 39°C. The raised temperature-induced block of LTD was mimicked by 2-CADO. Unexpectively, despite the presence of DPCPX, LFS still could not elicit LTD. NMDA receptor-mediated synaptic component (fEPSPNMDA) was decreased when increasing the temperature to 39°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°C than at 39°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.
|Number of pages||8|
|Publication status||Published - 2001 Mar 10|
All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience