Cameron J S, Lhuillier L, Subramony P, Dryer S E
Department of Biology and Biochemistry, University of Houston, Texas 77204, USA.
Neuron. 1998 Nov;21(5):1045-53. doi: 10.1016/s0896-6273(00)80622-4.
The functional expression of Ca2+-activated K+ channels (KCa) in developing chick ciliary ganglion (CG) neurons requires interactions with target tissues and preganglionic innervation. Here, we show that the stimulatory effects of target tissues are mediated by an isoform of TGFbeta. Exposure of cultured CG neurons to TGFbeta1, but not TGFbeta2 or TGFbeta3, caused robust stimulation of KCa. The KCa stimulatory effects of target tissue extracts were blocked by a neutralizing pan-TGFbeta antiserum but not by specific TGFbeta2 or TGFbeta3 antisera. Intraocular injection of TGFbeta1 caused robust stimulation of KCa, whereas intraocular injection of pan-TGFbeta antiserum inhibited expression of KCa in CG neurons developing in vivo. The effects of TGFbeta1 were potentiated by beta-neuregulin-1, a differentiation factor expressed in preganglionic neurons.
发育中的鸡睫状神经节（CG）神经元中钙激活钾通道（KCa）的功能表达需要与靶组织和节前神经支配相互作用。在此，我们表明靶组织的刺激作用是由转化生长因子β（TGFβ）的一种亚型介导的。将培养的CG神经元暴露于TGFβ1，而非TGFβ2或TGFβ3，会强烈刺激KCa。靶组织提取物对KCa的刺激作用被一种中和性泛TGFβ抗血清阻断，但未被特异性TGFβ2或TGFβ3抗血清阻断。眼内注射TGFβ1会强烈刺激KCa，而眼内注射泛TGFβ抗血清则会抑制体内发育的CG神经元中KCa的表达。TGFβ1的作用被β-神经调节蛋白-1增强，β-神经调节蛋白-1是节前神经元中表达的一种分化因子。
