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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Inhibition of hippocampal LTP by ginkgolide B is mediated by its blocking action on PAF rather than glycine receptors.
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Inhibition of hippocampal LTP by ginkgolide B is mediated by its blocking action on PAF rather than glycine receptors.

机译：银杏内酯B对海马LTP的抑制作用是由其对PAF而非甘氨酸受体的阻滞作用介导的。

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摘要

Platelet-activating factor (PAF), a biologically active lipid (1-O-alkyl-2-acetyl-sn-glycero-3-phosphoholine), is identified in different regions of brain, including hippocampus. Specific PAF-activated receptors (PAFRs) are expressed in corresponding brain areas. PAF has been proposed to be a retrograde messenger of long-term potentiation (LTP): the antagonist of PAFRs, ginkgolide B (or BN52021) prevents induction of LTP. Recently it has been found that ginkgolide B is also an efficient blocker of the glycine receptor (GlyR) operated chloride channels (IC(50)=270+/-10 nM in hippocampal pyramidal neurons). The question is as follows: is the alteration of LTP by BN52021 due to the PAF antagonism or to the inhibition of glycine-gated chloride channels? We have studied the effects of ginkgolides B and J on LTP induced in the CA1 area of rat hippocampus. Ginkgolide J which is the weakest blocker of PAFR (IC(50)=54 microM, as compared to IC(50)=2.5 microM for ginkgolide B) inhibits GlyR-operated channels with IC(50)=2.0 microM. This assures a convenient concentration window which allows to inhibit GlyR-operated channels without affecting PAFRs. An amount of 5 microM of ginkgolide J did not prevent the induction of LTP, while ginkgolide B (5 microM) completely inhibited this phenomenon. The effect of ginkgolide B on LTP did not alter considerably if GlyRs were blocked by strychnine (2 microM). Strychnine itself had no significant effect on the induction of LTP. Both ginkgolides and strychnine significantly facilitated short-term potentiation (STP). Our data support a hypothesis according to which ginkgolides affect LTP by inhibiting PAFRs.
机译：血小板活化因子（PAF）是一种生物活性脂质（1-O-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱），在大脑的不同区域（包括海马区）均已鉴定。特定的PAF激活受体（PAFRs）在相应的大脑区域表达。有人提出PAF是长期增强（LTP）的逆向信使：PAFR的拮抗剂银杏内酯B（或BN52021）可防止LTP的诱导。最近发现银杏内酯B也是甘氨酸受体（GlyR）操纵的氯离子通道的有效阻滞剂（海马锥体神经元中的IC（50）= 270 +/- 10 nM）。问题如下：BN52021对LTP的改变是由于PAF拮抗作用还是由于甘氨酸门控氯离子通道的抑制？我们已经研究了银杏内酯B和J对大鼠海马CA1区诱导的LTP的影响。银杏内酯J是PAFR的最弱阻滞剂（与银杏内酯B的IC（50）= 2.5 microM相比，IC（50）= 54 microM）抑制了IC（50）= 2.0 microM的GlyR操作通道。这确保了方便的浓度窗口，该窗口允许抑制GlyR操作的通道而不会影响PAFR。 5μM银杏内酯J不能阻止LTP的诱导，而银杏内酯B（5 microM）则完全抑制了这种现象。如果GlyRs被士的宁（2 microM）阻断，银杏内酯B对LTP的作用不会显着改变。士的宁本身对LTP的诱导没有明显影响。银杏内酯和士的宁都大大促进了短期增强作用（STP）。我们的数据支持一种假设，即银杏内酯通过抑制PAFRs影响LTP。

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