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

• Main Authors: Ming- Zen Luo, 羅明仁
• Other Authors: Po-Wu Gean
• Format: Others
• Language: zh-TW
• Published: 2000
• Online Access: http://ndltd.ncl.edu.tw/handle/68846269199250924420

碩士 === 國立成功大學 === 藥理學研究所 === 89 === The average core temperature of a rat is between 37 and 38 oC. The brain temperature rose during fever, which is the most common manifestation of acute inflammation and is used by nearly all vertebrates as part of acute-phase reaction to immune challenge. It is orchestrated by the hypothalamus and involves a wide range of endocrine, autonomic and behavioral responses. With fever, we shiver, have chills, become anorexic, sleepy and feel malaise. The general activity and response to stimuli become slow or dull, not to mention learning or attention.. Furthermore, not only during fever but also under more physiological conditions such as physical exercise or behavioral exploration, may increase of brain temperature to 39 oC occur in intact animals. The influence of raising bath temperature (39oC) on synaptic transmission and neuronal plasticity was studied in CA1 region of the rat hippocampus using extracellular recording technique. Increasing the bath temperature from 32 0C to 39 0C resulted in a depression of field excitatory postsynaptic potential (fEPSP). Application of the selective A1 receptor agonist, 2-chloro-adenosine (2-CADO, 1 M) reduced the fEPSP and subsequently occluded the raising 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 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 0C but not at 39 0C. The raising temperature-induced block of LTD was mimicked by 2-CADO. Unexpectedly, despite in the presence of DPCPX, LFS still could not elicit LTD. NMDA receptor-mediated synaptic component (fEPSPNMDA) was decreased when increasing the temperature to 39 0C 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 0C than at 39 0C. These results suggest that, by increasing the sensitivity of Mg++ block, increase in temperature modulates NMDA responses and thereby inhibits the induction of LTD.