Kokoris G J, Silverman A J, Zimmerman E A, Perlow M J, Gibson M J
Neuroscience. 1987 Jul;22(1):159-67. doi: 10.1016/0306-4522(87)90206-5.
Transplantation of fetal preoptic area tissue containing gonadotropin-releasing hormone neurons into the third ventricle of male hypogonadal mice resulted in an elevation of pituitary gonadotropin levels and correction of hypogonadism. This reversal of the neuroendocrine deficit was correlated with innervation of the median eminence by gonadotropin-releasing hormone axons. The specificity of fiber outgrowth suggested that local neuromodulatory factors might guide these axons to the nearby median eminence. To test this hypothesis, 14 adult hypogonadal males received unilateral fetal preoptic area grafts into the lateral ventricle, a site distant from the median eminence. After four months, healthy grafts containing numerous gonadotropin-releasing hormone neurons were seen in 9 hosts. However, none of these grafts corrected the hypogonadism of the host and there was no gonadotropin-releasing hormone innervation of the median eminence in any of these animals, thus demonstrating that the presence of gonadotropin-releasing hormone neurons in the ventricular space is itself not sufficient to stimulate the pituitary-gonadal axis. Instead, gonadotropin-releasing hormone axons coursed in the host fimbria, fornix, corpus callosum, and stria terminalis. These fibers could be traced into the anterior hippocampal area, medial and lateral septum, and the anterior hypothalamus. The distribution of these fibers included a number of regions which receive gonadotropin-releasing hormone fiber input in the normal mouse. These findings show that gonadotropin-releasing hormone neurons transplanted into the lateral ventricle can survive and extend processes into the host brain, often projecting to sites of normal gonadotropin-releasing hormone innervation. Their success in contacting these sites suggests that gonadotropin-releasing hormone fiber outgrowth may be influenced by regionally specified trophic and/or guidance factors.
将含有促性腺激素释放激素神经元的胎儿视前区组织移植到雄性性腺功能减退小鼠的第三脑室，可导致垂体促性腺激素水平升高并纠正性腺功能减退。这种神经内分泌缺陷的逆转与促性腺激素释放激素轴突对正中隆起的神经支配有关。纤维生长的特异性表明，局部神经调节因子可能引导这些轴突到达附近的正中隆起。为了验证这一假设，14只成年性腺功能减退雄性小鼠接受了将单侧胎儿视前区移植到侧脑室的手术，侧脑室是一个远离正中隆起的部位。四个月后，在9只宿主中发现了含有大量促性腺激素释放激素神经元的健康移植物。然而，这些移植物均未纠正宿主的性腺功能减退，且这些动物中没有一只的正中隆起有促性腺激素释放激素神经支配，因此表明脑室空间中促性腺激素释放激素神经元的存在本身不足以刺激垂体-性腺轴。相反，促性腺激素释放激素轴突在宿主的海马伞、穹窿、胼胝体和终纹中走行。这些纤维可以追踪到前海马区、内侧和外侧隔以及下丘脑前部。这些纤维的分布包括正常小鼠中接受促性腺激素释放激素纤维输入的一些区域。这些发现表明，移植到侧脑室的促性腺激素释放激素神经元能够存活并将突起延伸到宿主大脑中，通常投射到促性腺激素释放激素正常神经支配的部位。它们成功接触这些部位表明，促性腺激素释放激素纤维的生长可能受区域特异性营养和/或导向因子的影响。
