Exposure to noise produces cognitive and emotional disorders, and recent studies have shown that auditory stimulation or deprivation affects hippocampal function. Previously, we showed that exposure to high-intensity sound (110 dB, 1 min) strongly inhibits Schaffer-CA1 long-term potentiation (LTP). Here we investigated possible mechanisms involved in this effect. We found that exposure to 110 dB sound activates c-fos expression in hippocampal CA1 and CA3 neurons. Although sound stimulation did not affect glutamatergic or GABAergic neurotransmission in CA1, it did depress the level of brain-derived neurotrophic factor (BDNF), which is involved in promoting hippocampal synaptic plasticity. Moreover, perfusion of slices with BDNF rescued LTP in animals exposed to sound stimulation, whereas BDNF did not affect LTP in sham-stimulated rats. Furthermore, LM22A4, a TrkB receptor agonist, also rescued LTP from sound-stimulated animals. Our results indicate that depression of hippocampal BDNF mediates the inhibition of LTP produced by high-intensity sound stimulation.

中文翻译：

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脑源性神经营养因子的丧失介导高强度声音对海马长期增强的抑制。


暴露于噪音会导致认知和情绪障碍，最近的研究表明听觉刺激或剥夺会影响海马功能。之前，我们发现暴露于高强度声音（110 dB，1 分钟）会强烈抑制 Schaffer-CA1 长时程增强（LTP）。在这里，我们研究了这种效应所涉及的可能机制。我们发现暴露于 110 dB 声音会激活海马 CA1 和 CA3 神经元中的 c-fos 表达。虽然声音刺激不会影响 CA1 区的谷氨酸能或 GABA 能神经传递，但它确实会降低脑源性神经营养因子 (BDNF) 的水平，而脑源性神经营养因子与促进海马突触可塑性有关。此外，在暴露于声音刺激的动物中，用BDNF灌注切片可以挽救LTP，而BDNF并不影响假刺激大鼠的LTP。此外，LM22A4（一种 TrkB 受体激动剂）也可以从声音刺激的动物中拯救 LTP。我们的结果表明，海马 BDNF 的抑制介导了高强度声音刺激产生的 LTP 的抑制。