Dipartimento di Medicina Interna, Sezione di Fisiologia Umana, Università di Perugia, Via del Giochetto, I-06126 Perugia, Italy.
Neuroscience. 2011 Sep 29;192:67-73. doi: 10.1016/j.neuroscience.2011.06.078. Epub 2011 Jul 1.
In the hippocampal formation many neuromodulators are possibly implied in the synaptic plasticity such as the long-term potentiation (LTP) induced by high-frequency stimulation (HFS) of afferent fibers. We investigated the involvement of locally synthesized neural 17β-estradiol (nE(2)) in the induction of HFS-LTP in hippocampal slices from male rats by stimulating the Schaffer collateral fibers and recording the evoked field excitatory postsynaptic potential (fEPSP) in the CA1 region. We demonstrated that either the blockade of nE(2) synthesis by the aromatase inhibitor letrozole, or the antagonism of E(2) receptors (ERs) by ICI 182,780 did not prevent the induction of HFS-LTP, but reduced its amplitude by ∼60%, without influencing its maintenance. Moreover, letrozole and ICI 182,780 did not affect the first short-term post-tetanic component of LTP and the paired-pulse facilitation (PPF). These findings demonstrate that nE(2) plays an important role in the induction phase of HFS-dependent LTP. Since the basal responses were not affected by the blocking agents, we suggest that the synthesis of nE(2) is induced or enhanced by HFS through aromatase activation. In this context, the local production of nE(2) seems to be a very effective mechanism to modulate the amplitude of LTP.
在海马结构中，许多神经调质可能参与突触可塑性，例如传入纤维高频刺激（HFS）诱导的长时程增强（LTP）。我们通过刺激 Schaffer 侧支纤维并记录 CA1 区诱发的场兴奋性突触后电位（fEPSP），研究了局部合成的神经 17β-雌二醇（nE（2））在雄性大鼠海马切片中诱导 HFS-LTP 中的作用。我们证明，通过芳香酶抑制剂来曲唑阻断 nE（2）的合成，或通过 ICI 182,780 拮抗 E（2）受体（ERs），均不能阻止 HFS-LTP 的诱导，但会将其幅度降低约 60%，而不影响其维持。此外，来曲唑和 ICI 182,780 并不影响 LTP 的第一个短期强直后成分和成对脉冲易化（PPF）。这些发现表明，nE（2）在 HFS 依赖性 LTP 的诱导相中发挥重要作用。由于基础反应不受阻断剂的影响，我们推测 nE（2）的合成是通过芳香酶的激活被 HFS 诱导或增强的。在这种情况下，nE（2）的局部产生似乎是调节 LTP 幅度的非常有效的机制。
