Verdi J M, Anderson D J
Division of Biology, California Institute of Technology, Pasadena 91125.
Neuron. 1994 Dec;13(6):1359-72. doi: 10.1016/0896-6273(94)90421-9.
We have examined the mechanisms controlling the induction of the two NGF receptors, trkA and p75, in proliferating neuroblasts immuno-isolated from thoracolumbar embryonic sympathetic ganglia. Contrary to prior studies, we find that induction of p75 follows rather than precedes that of trkA; this late induction is consistent with the fact that p75 functions at relatively late stages of sympathetic development. trkA induction is apparently not controlled by a cell-intrinsic mechanism. Rather, this receptor is induced by environmental signals including NT-3, which also acts as an interim survival factor for these neuroblasts. trkA induction by NT-3 is consequent to its promotion of mitotic arrest, as anti-mitotic drugs also efficiently induce trkA. p75 expression is induced in trkA-expressing cells by NGF. Thus, the development of sympathetic neurons involves sequential actions of different neurotrophins, which also regulate the expression of their own and each other's receptors.
我们研究了从胸腰段胚胎交感神经节免疫分离出的增殖神经母细胞中，控制两种神经生长因子（NGF）受体trkA和p75诱导的机制。与先前的研究相反，我们发现p75的诱导发生在trkA之后而非之前；这种后期诱导与p75在交感神经发育相对后期起作用的事实一致。trkA的诱导显然不受细胞内在机制的控制。相反，该受体由包括NT-3在内的环境信号诱导，NT-3对这些神经母细胞也起临时存活因子的作用。NT-3诱导trkA是因其促进有丝分裂停滞，因为抗有丝分裂药物也能有效诱导trkA。p75的表达由NGF在表达trkA的细胞中诱导。因此，交感神经元的发育涉及不同神经营养因子的顺序作用，这些因子也调节它们自身以及彼此受体的表达。
