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首页> 外文期刊>The European Journal of Neuroscience >Exposure to interferon-gamma during synaptogenesis increases inhibitory activity after a latent period in cultured rat hippocampal neurons.
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Exposure to interferon-gamma during synaptogenesis increases inhibitory activity after a latent period in cultured rat hippocampal neurons.

机译：突触形成过程中暴露于干扰素-γ增加潜伏期后培养的大鼠海马神经元中的抑制活性。

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Certain disorders of the nervous system may have their origin in disturbances in the development of synaptic connections and network structure that may not become overt until later in life. As inflammatory cytokines can influence synaptic activity in neuronal cultures, we analysed whether cytokine exposure during synaptogenesis can lead to imbalances in a neuronal network. Short-term application of interferon-gamma (IFN-gamma), but not tumour necrosis factor-alpha, during peak synaptogenesis (but not before or after) in Sprague-Dawley rat hippocampal cultures, caused both a decrease in the frequency of spontaneous excitatory postsynaptic currents (EPSCs) and an increase in the frequency of spontaneous inhibitory postsynaptic currents (IPSCs). These effects were only detected in recordings made weeks later. This was not due to a depression of glutamatergic synapses or to a change in the relative number of neurons containing glutamic acid decarboxylase (GAD). There was an increase in the average amplitude of miniature IPSCs, and in GAD-expressing neurons the amplitude of miniature EPSCs were larger as well as the responses to glutamate. This indicates that IFN-gamma-treatment induced increased inhibition via postsynaptic changes. These effects of IFN-gamma treatment were not observed when neuronal nitric oxide synthase was inhibited. Our study therefore shows that exposure to IFN-gamma during a restricted period of development, which coincides with the peak of excitatory synaptogenesis, can cause progressive changes in synaptic activity in the network. Thus, cytokine exposure at a critical period of development may constitute a 'hit-and-run' mechanism for certain nervous system disorders that become manifest after a latency period.
机译：神经系统的某些疾病可能源于突触连接和网络结构发育的障碍，这些障碍直到晚年才变得明显。由于炎性细胞因子可影响神经元培养物中的突触活性，因此我们分析了突触发生过程中细胞因子的暴露是否会导致神经元网络失衡。在Sprague-Dawley大鼠海马培养物的突触形成高峰期（但不是之前或之后）短期应用干扰素-γ（IFN-γ）而非肿瘤坏死因子-α导致自发兴奋性频率降低突触后电流（EPSC）和自发抑制性突触后电流（IPSC）的频率增加。这些效果仅在几周后的录音中被检测到。这不是由于谷氨酸能突触的抑制或由于含有谷氨酸脱羧酶（GAD）的神经元的相对数目的变化。微型IPSC的平均幅度增加，在表达GAD的神经元中，微型EPSC的幅度以及对谷氨酸的响应都更大。这表明IFN-γ治疗通过突触后变化诱导了增加的抑制作用。当神经元一氧化氮合酶被抑制时，未观察到IFN-γ治疗的这些作用。因此，我们的研究表明，在发育受限的时期内（与兴奋性突触形成的高峰相吻合）暴露于IFN-γ可以引起网络中突触活性的逐步改变。因此，在发育的关键时期暴露于细胞因子可能构成某些神经系统疾病的“一击即逃”机制，这些潜伏期后变得明显。

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