The strength and quality of the signal propagated by the glutamate synapse (Glu) depend, among other things, on the structure of the postsynaptic part and the quality of adhesion between the interacting components of the synapse. Postsynaptic density protein 95 (PSD95), mammalian target of rapamycin (mTOR), and Down syndrome cell adhesion molecule (DSCAM) are components of the proper functioning of an excitatory synapse. PSD95 is a member of the membrane-associated guanylate kinases protein family, mainly located at the postsynaptic density of the excitatory synapse. PSD95, via direct interaction, regulates the clustering and functionality of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptors at a synapse. Here, the effects of treatment with an antagonist of mGluR5 (MTEP) and NS398 (cyclooxygenase-2, COX-2 inhibitor) on PSD95, mTOR, and DSCAM in the hippocampus (HC) of C57B1/6 J mice using Western blots in the context of learning were examined. Moreover, the sensitivity of selected proteins to lipopolysaccharide (LPS) was monitored. MTEP injected for seven days induced upregulation of PSD95 in HC of mice. The observed effect was regulated by a COX-2 inhibitor and concurrently by LPS. Accompanying alterations in DSCAM protein were found, suggesting changes in adhesion strength after modulation of glutamatergic (Glu) synapse via tested compounds.

谷氨酸突触 (Glu) 传播的信号的强度和质量尤其取决于突触后部分的结构以及突触相互作用组件之间的粘附质量。突触后密度蛋白 95 (PSD95)、哺乳动物雷帕霉素靶蛋白 (mTOR) 和唐氏综合症细胞粘附分子 (DSCAM) 是兴奋性突触正常功能的组成部分。PSD95 是膜相关鸟苷酸激酶蛋白家族的成员，主要位于兴奋性突触的突触后密度处。PSD95 通过直接相互作用调节 α-氨基-3-羟基-5-甲基-4-异恶唑丙酸 (AMPA) 和N的聚类和功能突触处的-甲基-D-天冬氨酸 (NMDA) 受体。此处，使用蛋白质印迹法观察 mGluR5 拮抗剂 (MTEP) 和 NS398（环氧合酶-2、COX-2 抑制剂）治疗对 C57B1/6 J 小鼠海马 (HC) 中 PSD95、mTOR 和 DSCAM 的影响。检查了学习背景。此外，还监测了所选蛋白质对脂多糖（LPS）的敏感性。注射 7 天的 MTEP 诱导 HC 小鼠 PSD95 上调。观察到的效果受到 COX-2 抑制剂的调节，同时受到 LPS 的调节。DSCAM 蛋白也随之发生变化，表明通过测试化合物调节谷氨酸 (Glu) 突触后粘附强度发生变化。