Pelletier M R, Kirkby R D, Jones S J, Corcoran M E
Department of Psychology, University of Victoria, B.C., Canada.
Hippocampus. 1994 Apr;4(2):181-8. doi: 10.1002/hipo.450040208.
Previous experiments have described highly specific effects of noradrenergic agonists on synaptic transmission in the dentate gyrus (DG). For example, perfusion of hippocampal slices with the beta-noradrenergic agonist isoproterenol induces a long-lasting potentiation (LLP) of extracellularly recorded responses following stimulation of the medial perforant path (PP), and long-lasting depression (LLD) of responses evoked by stimulation of the lateral PP (Dahl D, Sarvey JM, 1989, Proc Natl Acad Sci USA 86:4776-4780). To examine the possible interactions of LLP, LLD, and long-term potentiation induced by tetanic stimulation (LTP), the authors recorded extracellular field potentials evoked in the DG by stimulation of the lateral or medial perforant path following LTP and LLP or LLD, invoked in different orders. After establishment of LLP or LLD by bath application of isoproterenol, subsequent tetanization of the respective afferents resulted in additional potentiation of the medial PP-evoked response and return of the lateral PP-evoked response to baseline levels. In other slices, application of isoproterenol after establishment of LTP resulted in further potentiation of medial PP-evoked responses but no change in the potentiated response evoked by lateral PP stimulation. Thus the pathway specificity was maintained irrespective of the history of previous potentiation or depression. Experiments using the specific beta 1 antagonist metoprolol further confirmed pathway specificity. Perfusion with 20 microM of metoprolol appeared to reduce LTP evoked by stimulation of the medial but not lateral PP. In a subsequent experiment, metoprolol in the absence of tetanization produced LLD of the medial PP-evoked response and LLP of the lateral PP-evoked response, opposite to the effects of ISO.(ABSTRACT TRUNCATED AT 250 WORDS)
先前的实验已经描述了去甲肾上腺素能激动剂对齿状回(DG)突触传递的高度特异性作用。例如,用β-去甲肾上腺素能激动剂异丙肾上腺素灌注海马切片,会在刺激内侧穿通通路(PP)后诱导细胞外记录反应的长时程增强(LLP),以及刺激外侧PP所诱发反应的长时程抑制(LLD)(达尔D,萨维 JM,1989年,《美国国家科学院院刊》86:4776 - 4780)。为了研究LLP、LLD和强直刺激诱导的长时程增强(LTP)之间可能的相互作用,作者记录了在以不同顺序引发LTP和LLP或LLD后,通过刺激外侧或内侧穿通通路在DG中诱发的细胞外场电位。通过浴用异丙肾上腺素建立LLP或LLD后,随后对相应传入纤维进行强直刺激,导致内侧PP诱发反应进一步增强,外侧PP诱发反应恢复到基线水平。在其他切片中,在建立LTP后应用异丙肾上腺素导致内侧PP诱发反应进一步增强,但外侧PP刺激诱发的增强反应没有变化。因此,无论先前增强或抑制的历史如何,通路特异性都得以维持。使用特异性β1拮抗剂美托洛尔的实验进一步证实了通路特异性。用20微摩尔美托洛尔灌注似乎会降低刺激内侧而非外侧PP所诱发的LTP。在随后的实验中,在没有强直刺激的情况下,美托洛尔产生了内侧PP诱发反应的LLD和外侧PP诱发反应的LLP,与异丙肾上腺素的作用相反。(摘要截短于250字)