a Department of Pharmacology, College of Medicine , The University of Arizona Health Sciences , Tucson , AZ , USA.
b Department of Anesthesiology , Shenzhen People's Hospital & Second Clinical Medical College of Jinan University , Shenzhen , P.R. China.
Channels (Austin). 2019 Dec;13(1):147-152. doi: 10.1080/19336950.2019.1608129.
Amongst the regulators of voltage-gated ion channels is the collapsin response mediator protein 2 (CRMP2). CRMP2 regulation of the activity and trafficking of NaV1.7 voltage-gated sodium channels as well as the N-type (CaV2.2) voltage-gated calcium channel (VGCC) has been reported. On the other hand, CRMP2 does not appear to regulate L- (CaV1.x), P/Q- (CaV2.1), and R- (CaV2.3) type high VGCCs. Whether CRMP2 regulates low VGCCs remains an open question. Here, we asked if CRMP2 could regulate the low voltage-gated (T-type/CaV3.x) channels in sensory neurons. Reducing CRMP2 protein levels with short interfering RNAs yielded no change in macroscopic currents carried by T-type channels. No change in biophysical properties of the T-type currents was noted. Future studies pursuing CRMP2 druggability in neuropathic pain will benefit from the findings that CRMP2 regulates only the N-type (CaV2.2) calcium channels.
电压门控离子通道的调节剂之一是塌陷反应介质蛋白 2（CRMP2）。已有报道称，CRMP2 调节 NaV1.7 电压门控钠离子通道和 N 型（CaV2.2）电压门控钙通道（VGCC）的活性和运输。另一方面，CRMP2 似乎不调节 L-（CaV1.x）、P/Q-（CaV2.1）和 R-（CaV2.3）型高 VGCC。CRMP2 是否调节低 VGCC 仍然是一个悬而未决的问题。在这里，我们询问 CRMP2 是否可以调节感觉神经元中的低电压门控（T 型/CaV3.x）通道。用短干扰 RNA 降低 CRMP2 蛋白水平不会导致 T 型通道携带的宏观电流发生变化。T 型电流的生理特性没有变化。未来在研究神经性疼痛的 CRMP2 药物靶标时，应注意到 CRMP2 仅调节 N 型（CaV2.2）钙通道这一发现，这将对其产生帮助。
