Traumatic brain injury (TBI) is associated with epileptiform activity in the hippocampus; however, the underlying mechanisms have not been fully determined. The goal was to understand what changes take place in intrinsic neuronal physiology in the hippocampus after blunt force trauma to the cortex. In this context, hyperpolarization‐activated cation current (I_h) currents may have a critical role in modulating the neuronal intrinsic membrane excitability; therefore, its contribution to the TBI‐induced hyperexcitability was assessed. In a model of TBI caused by controlled cortical impact (CCI), the intrinsic electrophysiological properties of pyramidal neurons were examined 1 week after TBI induction in rats. Whole‐cell patch‐clamp recordings were performed under current‐ and voltage‐clamp conditions following ionotropic receptors blockade. Induction of TBI caused changes in the intrinsic excitability of pyramidal neurons, as shown by a significant increase and decrease in firing frequency and in the rheobase current, respectively (p < .05). The evoked firing rate and the action potential time to peak were also significantly increased and decreased, respectively (p < .05). In the TBI group, the amplitude of instantaneous and steady‐state I_h currents was both significantly smaller than those in the control group (p < .05). The I_h current density was also significantly decreased (p < .001). Findings indicated that TBI led to an increase in the intrinsic excitability in CA1 pyramidal neurons and changes in I_h current could be, in part, one of the underlying mechanisms involved in this hyperexcitability.

中文翻译：

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创伤性脑损伤大鼠模型中海马 CA1 神经元中超极化激活的阳离子电流 (Ih) 降低介导的内在神经元兴奋性增强

创伤性脑损伤 (TBI) 与海马的癫痫样活动有关；然而，潜在的机制尚未完全确定。目的是了解大脑皮层受到钝力创伤后海马体内在神经元生理发生了哪些变化。在这种情况下，超极化激活的阳离子电流（I _h) 电流可能在调节神经元内在膜兴奋性中起关键作用；因此，评估了它对 TBI 引起的过度兴奋的贡献。在由受控皮质冲击 (CCI) 引起的 TBI 模型中，在大鼠 TBI 诱导后 1 周检查了锥体神经元的内在电生理特性。在离子型受体阻断后，在电流和电压钳条件下进行全细胞膜片钳记录。TBI 的诱导引起锥体神经元内在兴奋性的变化，分别表现为放电频率和 rheobase 电流的显着增加和减少 ( p < .05)。诱发放电率和动作电位达峰时间也分别显着增加和减少（p < .05)。TBI 组的瞬时和稳态 I _h电流幅度均显着小于对照组 ( p < .05)。I _h电流密度也显着降低（p < .001）。研究结果表明，TBI 导致 CA1 锥体神经元的内在兴奋性增加，并且 I _h电流的变化可能部分是这种过度兴奋性所涉及的潜在机制之一。