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The actions of a charged melatonin receptor ligand, TMEPI, and an irreversible MT2 receptor agonist, BMNEP, on mouse hippocampal evoked potentials in vitro

机译:带电的褪黑激素受体配体TMEPI和不可逆的MT2受体激动剂BMNEP在体外对小鼠海马诱发电位的作用

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We have previously determined that melatonin modulates hippocampal synaptic transmission in a biphasic way: an initial depression was followed by a recovery/amplification phase. Here we describe the influence of two novel melatonin receptor ligands, BMNEP (N-bromoacetyl-2-iodo-5-methoxytryptamine) and TMPEI (N[2-(2-Trimethylammoniumethyleneoxy-7-methoxy)ethyl]propionamide iodide), on the population spike (PS) and excitatory postsynaptic potentials (EPSP) recorded from mouse hippocampal slices. BMNEP, which specifically alkylates and constitutively activates the MT2 melatonin receptor, mimicked the first phase of melatonin's action by irreversibly depressing both the PS and EPSP. TMPEI, a charged ligand of plasma membrane melatonin receptors, amplified those potentials in a manner similar to the effect of melatonin observed during the second, recovery phase. Melatonin had no influence on the potentials amplified by the action of TMPEI. Our results suggest that the biphasic, receptor-dependent action of melatonin and its analogs modulates the efficiency of the hippocampal glutamergic synapse and is most likely mediated through two different, sequentially occurring mechanisms. (C) 2004 Elsevier Inc. All rights reserved.
机译:我们先前已经确定褪黑素以双相方式调节海马突触传递:最初的抑郁症之后是恢复/扩增阶段。在这里,我们描述了两种新型褪黑激素受体配体BMNEP(N-溴乙酰基-2-碘-5-甲氧基色胺)和TMPEI(N [2-(2-三甲基铵乙氧基-7-甲氧基)乙基]丙酰胺碘化物)的影响。从小鼠海马切片记录的种群高峰(PS)和兴奋性突触后电位(EPSP)。 BMNEP专门烷基化并组成性激活MT2褪黑激素受体,它通过不可逆转地抑制PS和EPSP来模仿褪黑激素作用的第一阶段。 TMPEI是质膜褪黑激素受体的带电配体,以类似于在第二个恢复阶段观察到的褪黑激素作用的方式放大了这些电位。褪黑激素对通过TMPEI作用放大的电位没有影响。我们的结果表明,褪黑激素及其类似物的双相,受体依赖性作用调节了海马谷氨酸能突触的效率,最有可能是通过两种不同的顺序发生的机制介导的。 (C)2004 Elsevier Inc.保留所有权利。

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