Sloviter R S
Neurology Research Center, Helen Hayes Hospital, New York State Department of Health, West Haverstraw 10993.
Neurosci Lett. 1992 Mar 16;137(1):91-6. doi: 10.1016/0304-3940(92)90306-r.
The hypothesis that lesion-induced hippocampal granule cell axon sprouting causes granule cell hyperexcitability was tested in the rat. Kainic acid damaged dentate hilar neurons, decreased granule cell inhibition, and increased granule cell excitability to afferent stimulation, all before synaptic reorganization occurred. Granule cell recurrent inhibition and relatively normal excitability were unexpectedly restored as granule cell axon sprouting occurred. Anatomical analysis revealed that a dense innervation of inhibitory neurons by aberrant granule cell axons was a consistent feature in each animal. These results indicate that granule cell hyperexcitability precedes dentate synaptic reorganization and is associated with the selective interneuron loss that is the presumed stimulus for axon sprouting. Thus, if granule cell axon sprouting has functional significance, it may be primarily inhibitory, rather than epileptogenic, in nature.
在大鼠中测试了损伤诱导的海马颗粒细胞轴突发芽导致颗粒细胞过度兴奋的假说。在突触重组发生之前， kainic 酸损伤了齿状回门区神经元，降低了颗粒细胞抑制，并增加了颗粒细胞对传入刺激的兴奋性。随着颗粒细胞轴突发芽的发生，颗粒细胞的回返抑制和相对正常的兴奋性意外地恢复了。解剖学分析表明，异常颗粒细胞轴突对抑制性神经元的密集支配是每只动物的一致特征。这些结果表明，颗粒细胞过度兴奋先于齿状回突触重组，并与选择性中间神经元丢失有关，而选择性中间神经元丢失被认为是轴突发芽的刺激因素。因此，如果颗粒细胞轴突发芽具有功能意义，其本质可能主要是抑制性的，而非致痫性的。
