Arginine vasopressin (AVP) neurons play essential roles in sensing the change in systemic osmolarity and regulating AVP release from their neuronal terminals to maintain the plasma osmolarity. AVP exocytosis depends on the Ca²⁺ entry via voltage-gated Ca²⁺ channels (VGCCs) in AVP neurons. In this study, suppression by siRNA-mediated knockdown and pharmacological sensitivity of VGCC currents evidenced molecular and functional expression of N-type Cav2.2 and T-type Cav3.1 in AVP neurons under normotonic conditions. Also, both the Cav2.2 and Cav3.1 currents were found to be sensitive to flufenamic acid (FFA). TTX-insensitive spontaneous action potentials were suppressed by FFA and T-type VGCC blocker Ni²⁺. However, Cav2.2-selective ω-conotoxin GVIA failed to suppress the firing activity. Taken together, it is concluded that Cav2.2 and Cav3.1 are molecularly and functionally expressed and both are sensitive to FFA in unstimulated rat AVP neurons. Also, it is suggested that Cav3.1 is primarily involved in their action potential generation.

中文翻译：

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正常张力条件下大鼠加压素神经元N型Cav2.2和T型Cav3.1通道的表达和功能


精氨酸加压素 (AVP) 神经元在感知全身渗透压变化和调节神经元末梢释放 AVP 以维持血浆渗透压方面发挥着重要作用。 AVP 胞吐作用取决于 AVP 神经元中通过电压门控 Ca ²⁺通道 (VGCC) 的 Ca ²⁺进入。在这项研究中，通过 siRNA 介导的敲低和 VGCC 电流的药理敏感性抑制，证明了正常张力条件下 AVP 神经元中 N 型 Cav2.2 和 T 型 Cav3.1 的分子和功能表达。此外，发现 Cav2.2 和 Cav3.1 电流都对氟芬那酸 (FFA) 敏感。 TTX 不敏感的自发动作电位被 FFA 和 T 型 VGCC 阻滞剂 Ni ²⁺抑制。然而，Cav2.2-选择性ω-芋螺毒素GVIA未能抑制放电活性。综上所述，得出的结论是，Cav2.2 和 Cav3.1 在分子和功能上都有表达，并且在未刺激的大鼠 AVP 神经元中都对 FFA 敏感。此外，还表明 Cav3.1 主要参与其动作电位的产生。