Large conductance of Ca²⁺-activated K⁺ channel (KCa1.1) plays an inhibitory role in neuroexcitation. However, the expression of KCNMB4/β4-subunit in the nodose ganglia (NG) and nucleus tractus solitarius (NTS), and its effect and regulation on baroreflex afferent function at post-transcriptional level of female rats remains unknown. Here, we demonstrated that the expression of β4-subunit encoded by KCNMB4 was significantly lower in females vs. males and ovariectomized (OVX) rats in the NG. Although all baroreceptor neurons (BRNs) expressed β4-subunit, altered discharge characteristics were only observed in Ah-type neurons after ovariectomy. Notably, the decreased excitability of Ah-types was restored by paxilline and further enhanced by iberiotoxin. The consistent changes were observed in excitatory post-synaptic currents. The level of miR-504 was higher in females, which was predicted to bind to the 3′UTR of KCNMB4. In consistent, an inverse expression pattern between miR-504 and KCNMB4 was observed in baroreflex afferents. The paxilline-sensitive β4-subunits is less in Ah-types and up-regulated by ovariectomy. These data indicated that KCa1.1 β4-subunit is the key regulator in neuroexcitation of Ah-types and sexual-dimorphism in baroreflex afferent function through estrogen-dependent inhibition of KCNMB4 expression via miR-504.

^{Ca 2+}激活的 K ⁺的大电导通道（KCa1.1）在神经兴奋中起抑制作用。然而，KCNMB4/β4-亚基在结节神经节（NG）和孤束核（NTS）中的表达，及其对雌性大鼠转录后水平压力反射传入功能的影响和调节仍不清楚。在这里，我们证明了由 KCNMB4 编码的 β4 亚基的表达在 NG 中的雌性与雄性和去卵巢 (OVX) 大鼠中显着降低。尽管所有压力感受器神经元 (BRN) 都表达 β4 亚基，但仅在卵巢切除术后 Ah 型神经元中观察到放电特性的改变。值得注意的是，Ah 型兴奋性降低被 paxilline 恢复，并被 iberiotoxin 进一步增强。在兴奋性突触后电流中观察到一致的变化。miR-504 水平在女性中较高，预计将与 KCNMB4 的 3'UTR 结合。一致地，在压力反射传入神经中观察到 miR-504 和 KCNMB4 之间的反向表达模式。对 paxilline 敏感的 β4 亚基在 Ah 型中较少，并且通过卵巢切除术上调。这些数据表明，KCa1.1 β4 亚基通过 miR-504 雌激素依赖性抑制 KCNMB4 表达，是 Ah 型神经兴奋和压力反射传入功能中的性二态性的关键调节因子。