【摘要】 论文采用离体脑片和膜片箝技术 ,观察了 4 氨基砒啶 ( 4 aminopridine ,4 AP)对海马薛氏侧枝 (Schafferfibers) CA1突触通路活动的影响 .研究结果证明 4 AP可以提高海马CA1区突触传递的效率 ,延长兴奋性突触后电位 (EPSPs)反应的潜伏期 ,并对长时程压抑 (LTD)的幅度有抑制作用更多还原

【Abstract】 Long term potentiation (LTP) and long term depression (LTD), two forms of synaptic plasticity are believed to underlie the mechanisms of learning and memory. It was reported that many kinds of materials could induce LTP or LTD. Potassium is one of them. Changing the concentration of K +in artificial cerebrospinal fluid (ACSF) would affect the amplitude of the EPSPs. 4 amonopridine can inhibit the transient outward potassium current. A reduction in the magnitude of synaptic depression was observed in the presence of 30 μM 4 AP. Application of 4 AP also produced an increase in population spike (PS) amplitude to 46±16.8% above baseline. It was demonstrated that 4 AP affected the magnitude of EPSPs. The present study was carried out with the electrophysiological technique in vitro to investigate the effects of 4 amonopridine (4 AP) on the Schaffer Fibers CA1 pathway in Hippocampus of the rat and patch clamp technique to observe the effects of 4 AP on the transient outward potassium current. The authors observed that addition of 4 AP to the bathing solution produced the following results: (1) The 5 mM 4 AP could selectively inhibit the transient outward potassium current; (2) Input/Output (I/O) curves in 4 AP group tended to be saturated when the stimulus intensity was 0.3 mA, while intensity was 0.9 mA for control group. (3) The latencies of EPSPs in control and 4 AP groups were 1.93±0.048 ms (n=9) and 3.68±0.204 ms (n=10) respectively. The 4 AP induced an increase in latency ((1.57±0.178 ms (P<0.001)); (4) The amplitudes of LTD in 4 AP and control groups were 83.95±2.2% (n=10) and 69.35±0.73% (n=9) respectively. The amplitudes of LTD decreased 14.16 ±2.07% (P<0.001) by 4 AP. The results demonstrated that the 4 AP could increase the synapse efficiency, delay the latency of EPSPs, and inhibit the amplitudes of LTD.更多还原