Eliasson S G, Monafo W W
Department of Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110.
J Neurol Sci. 1991 Oct;105(2):175-82. doi: 10.1016/0022-510x(91)90142-t.
The topical application of 4-aminopyridine (4-AP) reverses within 1-3 min the partial conduction block that results from heating 5-mm segments of rat posterior tibial, peroneal and sural nerves to 45 degrees C for several minutes. Nerves previously blocked in vitro or in vivo were incubated in vitro in the presence of [gamma-32P]ATP. The rate of phosphorylation of soluble nerve proteins that had entered the media was determined. Labeled proteins were separated electrophoretically and autoradiograms prepared. We found that 5 mM 4-AP increases the phosphorylation rate in heat-blocked nerve by approximately 50-fold. The process is calcium-dependent and is heat-labile. Soluble proteins with a molecular weight in the 53-55 kDa range are preferentially but not exclusively phosphorylated in the presence of 4-AP at levels effective in restoring conduction. The results suggest that the potassium channel blocker 4-AP may restore conduction by inducing changes in channel proteins.
将4-氨基吡啶（4-AP）局部应用于大鼠胫后神经、腓神经和腓肠神经5毫米节段，加热至45摄氏度几分钟会导致部分传导阻滞，而4-AP可在1至3分钟内逆转这种阻滞。将先前在体外或体内被阻滞的神经在含有[γ-32P]ATP的条件下进行体外孵育。测定进入培养基的可溶性神经蛋白的磷酸化速率。通过电泳分离标记蛋白并制备放射自显影片。我们发现5 mM 4-AP可使热阻滞神经中的磷酸化速率提高约50倍。该过程依赖于钙且对热不稳定。在存在能有效恢复传导的4-AP时，分子量在53 - 55 kDa范围内的可溶性蛋白优先但并非唯一地被磷酸化。结果表明，钾通道阻滞剂4-AP可能通过诱导通道蛋白的变化来恢复传导。
