Pavlides C, Ogawa S, Kimura A, McEwen B S
Rockefeller University, New York, NY 10021, USA.
Brain Res. 1996 Nov 4;738(2):229-35. doi: 10.1016/s0006-8993(96)00776-7.
We previously demonstrated in the dentate gyrus (DG) of anesthetized and freely behaving rats that both acute as well as chronic administration of corticosterone produces a suppression in long-term potentiation (LTP). In subsequent studies we showed, again in the DG, that activation of the two types of adrenal steroid receptors (mineralocorticoid (MR) and glucocorticoid (GR)) produce biphasic effects on synaptic plasticity; activation of MR produces an enhancement while activation of GR produces a suppression in LTP. In a separate study, we further demonstrated in rats administered the specific GR agonist RU 28362 that high-frequency stimulation, which normally produces LTP, instead produced long-term depression (LTD) in these animals. In the present study we investigated the effects of MR and GR activation by adrenal steroids on synaptic plasticity of the hippocampal CA1 field, but we studied this ex vivo, in a slice preparation. The results indicate that, as in our studies in the DG, adrenal steroids produce biphasic effects: in ADX rats, aldosterone (a specific MR agonist) enhanced while RU 28362 suppressed synaptic plasticity. Unlike the in vivo preparation, however, rarely was LTD observed in the animals receiving RU 28362. Also, ADX itself did not produce noticeable effects on synaptic plasticity. The present results are in agreement with previous studies showing that elevations in corticosterone or an acute episode of experimentally induced stress in vivo causes a suppression in LTP in the hippocampal CA1 field, in vitro.
我们先前在麻醉和自由活动的大鼠齿状回（DG）中证明，急性和慢性给予皮质酮均会抑制长时程增强（LTP）。在随后的研究中，我们再次在DG中表明，两种肾上腺类固醇受体（盐皮质激素受体（MR）和糖皮质激素受体（GR））的激活对突触可塑性产生双相效应；MR的激活会增强LTP，而GR的激活则会抑制LTP。在另一项研究中，我们进一步在给予特异性GR激动剂RU 28362的大鼠中证明，通常会产生LTP的高频刺激在这些动物中反而产生了长时程抑制（LTD）。在本研究中，我们研究了肾上腺类固醇激活MR和GR对海马CA1区突触可塑性的影响，但我们是在离体脑片制备中进行研究的。结果表明，与我们在DG中的研究一样，肾上腺类固醇产生双相效应：在肾上腺切除（ADX）大鼠中，醛固酮（一种特异性MR激动剂）增强了突触可塑性，而RU 28362则抑制了突触可塑性。然而，与体内实验不同的是，接受RU 28362的动物中很少观察到LTD。此外，ADX本身对突触可塑性没有明显影响。目前的结果与先前的研究一致，先前的研究表明，体内皮质酮升高或实验性诱导的急性应激会导致体外海马CA1区长时程增强的抑制。
