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目的 :观察氧糖剥夺引起的MF-CA3通路突触传递的长时程抑制(long-term depression,LTD)现象,并探讨其分子机制。方法:选择出生后2~3周的Sprague Dawley(SD)乳大鼠,制备海马脑片,通过刺激苔藓纤维,采用膜片钳的方法记录突触后电流。氧糖剥夺15 min后,观察突触传递的变化情况。分别采用犬尿喹啉酸阻断α-氨基羟甲基恶唑丙酸(α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid,AMPA)受体、LY341495阻断代谢型谷氨酸受体﹑BAPTA螯合细胞内钙离子,观察对LTD的可能影响。结果:1氧糖剥夺15 min能引起MF-CA3通路AMPA受体介导的突触电流减弱,产生LTD现象;2若氧糖剥夺过程中运用阻断剂阻断AMPA受体的激活,洗脱后并不影响LTD的产生,而阻断代谢型谷氨酸受体可以使AMPA受体电流的LTD现象消失;3除去外液中的钙离子或用BAPTA螯合细胞内的钙离子均能使LTD现象消失。结论:氧糖剥夺引起MF-CA3通路上AMPA受体介导的突触电流持续减弱,呈现LTD现象。这种LTD现象依赖于代谢型谷氨酸受体的激活及胞内外钙离子浓度升高,但不依赖氧糖剥夺过程中AMPA受体的激活。
OBJECTIVE: To observe the phenomenon of long-term depression (LTD) of the MF-CA3 pathway induced by oxy-glucose deprivation and investigate its molecular mechanism. Methods: Sprague Dawley (SD) rats were selected from 2 to 3 weeks after birth to prepare hippocampal slices. The postsynaptic currents were recorded by patch clamp method by stimulating mossy fibers. Oxygen deprivation 15 min after the observation of changes in synaptic transmission. Kynurenine was used to block the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) BAPTA chelated intracellular calcium ions and observed the possible effects on LTD. 1 Oxygen deprivation for 15 min caused AMPA receptor-mediated decrease of synaptic currents at MF-CA3 pathway, resulting in LTD phenomenon. 2 Blockade of AMPA receptor blockade during oxygen deprivation occured And does not affect the production of LTD, while blocking the metabotropic glutamate receptors can AMPA receptor current LTD phenomenon disappeared; 3 to remove the external solution of calcium ions or chelating BAPTA intracellular calcium ions can make LTD phenomenon disappears. CONCLUSION: Oxygen-glucose deprivation causes AMPA receptor-mediated synaptic currents on the MF-CA3 pathway to continue to decrease, exhibiting the LTD phenomenon. This phenomenon of LTD depends on the activation of metabotropic glutamate receptors and the increase of intracellular and extracellular calcium concentration, but not on the activation of AMPA receptors in the process of oxygen sugar deprivation.