Armstrong D L, Garcia E A, Ma T, Quinones B, Wayner M J
Division of Life Sciences, University of Texas at San Antonio 78249-0662, USA.
Peptides. 1996;17(4):689-93. doi: 10.1016/0196-9781(96)00030-7.
Field recordings of evoked excitatory postsynaptic potentials (pEPSPs) were carried out in the granule cell stratum moleculare following stimulation of the perforant path in rat hippocampal slices. Under control conditions tetanic stimulation produced long-term potentiation (LTP) as measured by an increase in the initial slope of the pEPSPs that lasted for at least 1 h. LTP experiments were repeated with 0.5, 5.0, 50, or 500 nM angiotensin II (AII) present in the bath at the time of tetanization. Induction of LTP was blocked by 50 nM AII; however, normal baseline responses were not affected. At the highest dose tested, 500 nM, a decrease in the amplitude and slope of baseline pEPSPs was observed. When the AII AT1 receptor antagonist losartan was present in the bath AII inhibition of LTP was blocked. The application of losartan alone had no effect on LTP expression. These findings support previous results from in vivo studies demonstrating that activation of AT1 receptors in the dentate gyrus blocks the induction of LTP at the perforant path-granule cell synapse.
在大鼠海马切片中，对穿通通路进行刺激后，在颗粒细胞分子层进行诱发兴奋性突触后电位（pEPSP）的场记录。在对照条件下，强直刺激产生长时程增强（LTP），通过pEPSP初始斜率的增加来测量，这种增加持续至少1小时。在强直刺激时，分别在浴槽中加入0.5、5.0、50或500 nM血管紧张素II（AII）重复进行LTP实验。50 nM的AII可阻断LTP的诱导；然而，正常的基线反应不受影响。在测试的最高剂量500 nM时，观察到基线pEPSP的幅度和斜率降低。当浴槽中存在AII AT1受体拮抗剂氯沙坦时，AII对LTP的抑制作用被阻断。单独应用氯沙坦对LTP的表达没有影响。这些发现支持了先前体内研究的结果，表明齿状回中AT1受体的激活会阻断穿通通路-颗粒细胞突触处LTP的诱导。
