Long-term potentiation (LTP) and long-term depression (LTD) are considered to be the cellular mechanisms behind the increase or decrease of synaptic strength respectively. Electrophysiologically induced LTP/LTD is associated with the activation of glutamate receptors in the synaptic terminals resulting in the initiation of biochemical processes in the postsynaptic terminals and thus propagation of synaptic activity. Isolated nerve endings i.e. synaptosome preparation was used to study here, the biochemical phenotypes of LTP and LTD, and glutamate treatment in varying concentration for different time was used to induce those biochemical phenomena. Treatment with 200 μM glutamate showed increased GluA1 phosphorylation at serine 831 and activation of CaMKIIα by phosphorylation at threonine 286 like LTP, whereas 100 μM glutamate treatment showed decrease in GluA1 phosphorylation level at both pGluA1(S831) and pGluA1(S845), and activation of GSK3β by de-phosphorylating pGSK3β at serine 9 like LTD. The 200 μM glutamate treatment was associated with an increase in the local translation of Arc, BDNF, CaMKIIα and Homer1, whereas 100 μM glutamate treatments resulted in decrease in the level of the said synaptic proteins and the effect was blocked by the proteasomal inhibitor, Lactasystin. Both, the local translation and local degradation was sensitive to the Ca2+ chellator, Bapta-AM, indicating that both the phenomena were dependent on the rise in intra-synaptosomal Ca2+, like LTP and LTD. Overall the results of the present study suggest that synaptosomal preparations can be a viable alternative to study mechanisms underlying the biochemical activities of LTP/LTD in short term.

中文翻译：

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谷氨酸盐处理模拟可行的突触体制备中的LTP和LTD类生化活性。

长期增强（LTP）和长期抑制（LTD）被认为是分别增加或降低突触强度的细胞机制。电生理诱导的LTP / LTD与突触末端中的谷氨酸受体的活化相关，从而导致突触后末端中生化过程的启动，从而突触活性的传播。在这里研究离体的神经末梢，即突触体的制备，使用LTP和LTD的生化表型，并在不同的时间使用不同浓度的谷氨酸处理来诱发这些生化现象。用200μM谷氨酸盐处理后，丝氨酸831的GluA1磷酸化增强，苏氨酸286的磷酸化（如LTP）激活了CaMKIIα，而100μM谷氨酸盐处理则显示pGluA1（S831）和pGluA1（S845）的GluA1磷酸化水平降低，并且像LTD一样，通过在丝氨酸9上对pGSK3β进行去磷酸化来激活GSK3β。200μM的谷氨酸盐处理与Arc，BDNF，CaMKIIα和Homer1的局部翻译增加有关，而100μM的谷氨酸盐处理导致所述突触蛋白水平降低，并且这种影响被蛋白酶体抑制剂Lactasystin阻断。局部翻译和局部降解都对Ca2 +螯合剂Bapta-AM敏感，表明这两种现象都依赖于突触体内Ca2 +的升高，如LTP和LTD。