Dahl D, Sarvey J M
Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
Brain Res. 1990 Sep 3;526(2):347-50. doi: 10.1016/0006-8993(90)91245-c.
Isoproterenol induced long-lasting potentiation (LLP) of the medial perforant path-evoked excitatory post-synaptic potential (EPSP) and long-lasting depression (LLD) of the lateral perforant path-evoked EPSP in the absence of perforant path activation. The NMDA receptor antagonist D-(-)-2-amino-5-phosphonovaleric acid [D(-)APV] blocked the induction of LLP and LLD. After wash, a subsequent exposure to isoproterenol induced only LLP of medial perforant path EPSPs; LLD of lateral perforant path-evoked EPSPs did not occur. Our results are consistent with the hypothesis that beta-adrenergic agonist-induced synaptic modifications in the dentate gyrus arise from pre- and postsynaptic events.
在没有穿通通路激活的情况下,异丙肾上腺素可诱导内侧穿通通路诱发的兴奋性突触后电位(EPSP)产生长时程增强(LLP),并使外侧穿通通路诱发的EPSP产生长时程抑制(LLD)。NMDA受体拮抗剂D-(-)-2-氨基-5-磷酸戊酸[D(-)APV]可阻断LLP和LLD的诱导。洗脱后,再次暴露于异丙肾上腺素仅诱导内侧穿通通路EPSP产生LLP;外侧穿通通路诱发的EPSP未出现LLD。我们的结果与以下假设一致,即β-肾上腺素能激动剂诱导的齿状回突触修饰源于突触前和突触后事件。