Arsenic-containing hydrocarbons (AsHCs) are common constituents of marine organisms and have potential toxicity to human health. This work is to study the effect of AsHCs on long-term potentiation (LTP) for the first time. A multi-electrode array (MEA) system was used to record the field excitatory postsynaptic potential (fEPSP) of CA1 before and after treatment with AsHC 360 in hippocampal slices from infantile male rats. The element content of Na, K, Ca, Mg, Mn, Cu, Zn, and As in the hippocampal slices were analyzed by elemental mass spectrometry after the neurophysiological experiment. The results showed that low AsHC 360 (1.5 μg As L⁻¹) had no effect on the LTP, moderate AsHC 360 (3.75−15 μg As L⁻¹) enhanced the LTP, and high AsHC 360 (45−150 μg As L⁻¹) inhibited the LTP. The enhancement of the LTP by promoting Ca²⁺ influx was proved by a Ca²⁺ gradient experiment. The inhibition of the LTP was likely due to damage of synaptic cell membrane integrity. This study on the neurotoxicity of AsHCs showed that high concentrations have a strong toxic effect on the LTP in hippocampus slices of the infantile male rat, which may lead to a negative effect on the development, learning, and memory.

含砷碳氢化合物 (AsHC) 是海洋生物的常见成分，对人类健康具有潜在毒性。这项工作是首次研究 AsHCs 对长时程增强 (LTP) 的影响。使用多电极阵列 (MEA) 系统记录幼年雄性大鼠海马切片中 CA1 在用 AsHC 360 治疗前后的场兴奋性突触后电位 (fEPSP)。神经生理学实验后,采用元素质谱法分析海马切片中Na、K、Ca、Mg、Mn、Cu、Zn、As的元素含量。结果表明，低 AsHC 360 (1.5 μg As L ^-1 ) 对 LTP 没有影响，中等 AsHC 360 (3.75-15 μg As L ^-1 ) 增强 LTP，高 AsHC 360 (45-150 μg As L ⁻¹) 抑制了 LTP。Ca ²⁺梯度实验证明了通过促进Ca ²⁺流入来增强LTP 。LTP 的抑制可能是由于突触细胞膜完整性的破坏。这项关于 AsHCs 神经毒性的研究表明，高浓度对幼年雄性大鼠海马切片中的 LTP 具有强烈的毒性作用，可能对发育、学习和记忆产生负面影响。