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Updated: Jun 13, 2025

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慢性Pb2+暴露导致海马网络超同步,缺席发作和感官运动缺陷

Nathan W Schultheiss, Jennifer L McGlothan, Tomás R Guilarte

bioRxiv : the preprint server for biology

|June 12, 2025

概括

早期的暴露扰乱了海马网络节奏,并损害了成年雄性大鼠的前脉冲抑制. 这些发现联系了领先的领导.

科学领域:

神经科学是一个神经科学.
环境健康环境健康
神经毒理学神经毒理学

背景情况:

慢性早年 (Pb2+) 暴露与认知缺陷,行为问题和成人精神病理有关.
Pb2+作为N-甲基-D-酸盐受体 (NMDAR) 抗剂,影响神经发育,包括海马 (HC) 内神经元和突触功能.
Pb2+对HC网络动态的影响,对于将细胞变化与认知结果联系起来至关重要,仍然不太了解.

研究的目的:

为了研究早期慢性Pb²⁺暴露对自由行为大鼠HC网络动态的影响.
评估Pb²⁺诱导的网络变化的功能后果,对声波震惊反射 (PPI) 的前脉冲抑制.

主要方法:

在早期慢性暴露于Pb2+的老鼠中记录了HC局部场潜力 (LFP).
分析了theta和gamma频段的同步及其行为调制.
在暴露于Pb2+的成年雄性和雌性大鼠中评估PPI,检查性别特异性影响.

主要成果:

在HC中,Pb²⁺暴露诱导了乙太节律超同步和放大了快速马同步.
和的行为调节被破坏,缺席发作 (频SWD) 被加剧.
成年男性,但不是女性或青少年男性,表现出降低的PPI,反映了精神分裂症中观察到的性别差异.

结论:

慢性早期生活中的Pb2+暴露失调了HC网络节律协调.
这些网络变化与感官门障碍 (PPI) 相关,可能是认知缺陷的基础.
这些发现突出了Pb2+诱导的神经发育毒性及其与精神疾病相关性的发现.

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