Traumatic brain injury (TBI) frequently causes cardiac autonomic dysfunction (CAD), irrespective of its severity, which is associated with an increased morbidity and mortality in patients. Despite the significance of probing the cellular mechanism underlying TBI-induced CAD, animal studies on this mechanism are lacking. In the current study, we tested whether TBI-induced CAD is associated with functional plasticity in cardiac efferent neurons. In this regard, TBI was induced by a controlled cortical impact in rats. Assessment of heart rate variability and baroreflex sensitivity indicated that CAD was developed in the sub-acute period after moderate and severe TBI. The cell excitability was increased in the stellate ganglion (SG) neurons and decreased in the intracardiac ganglion (ICG) neurons in TBI rats, compared with the sham-operated rats. The transient A-type K⁺ (K_A) currents, but not the delayed rectifying K⁺ currents were significantly decreased in SG neurons in TBI rats, compared with sham-operated rats. Consistent with these electrophysiological data, the transcripts encoding the Kv4 α subunits were significantly downregulated in SG neurons in TBI rats, compared with sham-operated rats. TBI causes downregulation and upregulation of M-type K⁺ (K_M) currents and the KCNQ2 mRNA transcripts, which may contribute to the hyperexcitability of the SG neurons and the hypoexcitability of the ICG neurons, respectively. In conclusion, the key cellular mechanism underlying the TBI-induced CAD may be the functional plasticity of the cardiac efferent neurons, which is caused by the regulation of the K_A and/or K_M currents.

创伤性脑损伤 (TBI) 经常导致心脏自主神经功能障碍 (CAD)，无论其严重程度如何，这与患者的发病率和死亡率增加有关。尽管探索 TBI 诱导的 CAD 的细胞机制具有重要意义，但缺乏对该机制的动物研究。在目前的研究中，我们测试了 TBI 诱导的 CAD 是否与心脏传出神经元的功能可塑性有关。在这方面，TBI 是由大鼠的受控皮质撞击引起的。心率变异性和压力反射敏感性的评估表明，CAD 发生在中度和重度 TBI 后的亚急性期。与假手术大鼠相比，TBI 大鼠星状神经节 (SG) 神经元的细胞兴奋性增加，而心内神经节 (ICG) 神经元的细胞兴奋性降低。与假手术大鼠相比，TBI 大鼠 SG 神经元中的⁺ (K _A ) 电流显着降低，但延迟整流 K ⁺电流没有显着降低。与这些电生理数据一致，与假手术大鼠相比，TBI 大鼠 SG 神经元中编码 Kv4 α 亚基的转录物显着下调。TBI 导致 M 型 K ⁺ (K _M) 电流和 KCNQ2 mRNA 转录本，这可能分别导致 SG 神经元的过度兴奋和 ICG 神经元的低兴奋性。总之，TBI 诱导 CAD 的关键细胞机制可能是心脏传出神经元的功能可塑性，这是由 K _A和/或 K _M电流的调节引起的。