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首页> 外文期刊>Neuron >β-Amyloid inhibits E-S potentiation through suppression of cannabinoid receptor 1-dependent synaptic disinhibition
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β-Amyloid inhibits E-S potentiation through suppression of cannabinoid receptor 1-dependent synaptic disinhibition

机译：β-淀粉样蛋白通过抑制大麻素受体1依赖性突触抑制作用来抑制E-S增强

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摘要

It has been widely reported that β-amyloid peptide (Aβ) blocks long-term potentiation (LTP) of hippocampal synapses. Here, we show evidence that Aβ more potently blocks the potentiation of excitatory postsynaptic potential (EPSP)-spike coupling (E-S potentiation). This occurs, not by direct effect on excitatory synapses or postsynaptic neurons, but rather through an indirect mechanism: reduction of endocannabinoid-mediated peritetanic disinhibition. During high-frequency (tetanic) stimulation, somatic synaptic inhibition is suppressed by endocannabinoids. We find that Aβ prevents this endocannabinoid-mediated disinhibition, thus leaving synaptic inhibition more intact during tetanic stimulation. This intact inhibition opposes the normal depolarization of hippocampal pyramidal neurons that occurs during tetanus, thus opposing the induction of synaptic plasticity. Thus, a pathway through which Aβ can act to modulate neural activity is identified, relevant to learning and memory and how it may mediate aspects of the cognitive decline seen in Alzheimer's disease.
机译：广泛报道β-淀粉样肽（Aβ）阻断海马突触的长期增强（LTP）。在这里，我们显示出证据表明Aβ更有效地阻断了兴奋性突触后电位（EPSP）-突触偶联的增强作用（E-S增强作用）。发生这种情况，不是通过对兴奋性突触或突触后神经元的直接影响，而是通过间接机制发生：减少内源性大麻素介导的腹膜白斑抑制。在高频（强直）刺激过程中，内源性大麻素抑制了突触的抑制。我们发现，Aβ阻止了这种由内源性大麻素介导的去抑制作用，从而在强直性刺激过程中使突触抑制作用更加完整。这种完整的抑制作用与破伤风期间发生的海马锥体神经元的正常去极化相反，因此与诱导突触可塑性相反。因此，确定了Aβ可以通过其调节神经活动的途径，该途径与学习和记忆有关，以及它如何介导阿尔茨海默氏病中认知能力下降的方面。

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