Hrabetova S, Sacktor T C
Department of Pharmacology, State University of New York at Brooklyn, 11203, USA.
Neurosci Lett. 1997 Apr 25;226(2):107-10. doi: 10.1016/s0304-3940(97)00252-8.
N-Methyl-D-aspartate (NMDA) receptor activation initiates both homosynaptic long-term depression (LTD) and long-term potentiation (LTP) in the CA1 region of the hippocampus. The mechanism by which two opposing forms of synaptic plasticity can be initiated through the activation of a single receptor is not known. We examined the effects of two competitive antagonists on the induction of LTP and LTD, D-2-amino-5-phosphonovaleric acid (D-AP5), a broad spectrum inhibitor of the NMDA receptor, and 3-((RS)-2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP), an antagonist that binds with high affinity to conventional NMDA receptors subtypes, but not to atypical subtypes that are relatively independent of voltage-dependent Mg2+-blockade. As has previously been reported, LTP, LTD, and depotentiation were all blocked by applications of D-AP5. In contrast, only LTP, but not LTD or depotentiation, was blocked by CPP. These observations suggest that decreases and increases of synaptic strength are mediated by the activation of distinct NMDA receptor subpopulations.
N-甲基-D-天冬氨酸（NMDA）受体激活可引发海马体CA1区的同突触长时程抑制（LTD）和长时程增强（LTP）。通过激活单一受体引发两种相反形式的突触可塑性的机制尚不清楚。我们研究了两种竞争性拮抗剂对LTP和LTD诱导的影响，即D-2-氨基-5-磷酸戊酸（D-AP5），一种NMDA受体的广谱抑制剂，以及3-((RS)-2-羧基哌嗪-4-基)丙基-1-膦酸（CPP），一种与传统NMDA受体亚型高亲和力结合，但不与相对独立于电压依赖性Mg2+阻断的非典型亚型结合的拮抗剂。如先前报道，D-AP5的应用可阻断LTP、LTD和去增强作用。相比之下，CPP仅阻断LTP，而不阻断LTD或去增强作用。这些观察结果表明，突触强度的降低和增加是由不同NMDA受体亚群的激活介导的。
