Tang F R, Lee W L, Yang J, Sim M K, Ling E A
National Neuroscience Institute, 11 Jalan Tan Tock Seng, 308433, Singapore, Singapore.
Epilepsy Res. 2001 Aug;46(2):179-89. doi: 10.1016/s0920-1211(01)00276-5.
The expression of metabotropic glutamate receptor 1alpha was studied in the rat hippocampus after pilocarpine-induced status epilepticus by Western blot and immunocytochemistry at both light and electron microscopic levels. At 1 day after pilocarpine-induced status epilepticus, there was marked decrease in metabotropic glutamate receptor 1alpha immunoreactivity at the border between stratum oriens and alveus in CA1 and CA3, and in the hilus of dentate gyrus. Between 3 and 31 days after pilocarpine-induced status epilepticus, metabotropic glutamate receptor 1alpha-immunoreactive dendrites and cell bodies in the border between stratum oriens and alveus gradually reappeared. Upregulation of metabotropic glutamate receptor 1alpha, however, was observed in the stratum oriens of CA1 at day 1, but returned to baseline by day 7. By electron microscopy, the metabotropic glutamate receptor 1alpha-immunoreactive product was demonstrated only in the post-synaptic elements in the border between the stratum oriens and alveus of CA1 and the hilus of the dentate gyrus in both control and experimental rats. At 1 day after pilocarpine-induced status epilepticus, metabotropic glutamate receptor 1alpha-immunoreactive degenerating neurons were identified in the border between stratum oriens and alveus of CA1 and the hilus of the dentate gyrus. At 7 and 31 days, many degenerating axons were also found. Present results suggest that excitoneurotoxicity mediated through post-synaptic metabotropic glutamate receptor 1alpha may be involved in degeneration and death of interneurons in the hilus of dentate gyrus, and the border between stratum oriens and alveus of CA1 in the early stage after pilocarpine-induced status epilepticus.
通过蛋白质免疫印迹法以及光镜和电镜水平的免疫细胞化学方法,研究了匹罗卡品诱导癫痫持续状态后大鼠海马中代谢型谷氨酸受体1α(mGluR1α)的表达。在匹罗卡品诱导癫痫持续状态后1天,CA1和CA3区的内嗅层与海马槽交界处以及齿状回门区的mGluR1α免疫反应性显著降低。在匹罗卡品诱导癫痫持续状态后3至31天,内嗅层与海马槽交界处的mGluR1α免疫反应性树突和细胞体逐渐重新出现。然而,在第1天观察到CA1区的内嗅层mGluR1α上调,但在第7天恢复到基线水平。电镜观察显示,在对照大鼠和实验大鼠中,mGluR1α免疫反应性产物仅在CA1区的内嗅层与海马槽交界处以及齿状回门区的突触后成分中出现。在匹罗卡品诱导癫痫持续状态后1天,在CA1区的内嗅层与海马槽交界处以及齿状回门区发现了mGluR1α免疫反应性变性神经元。在第7天和第31天,也发现了许多变性轴突。目前的结果表明,在匹罗卡品诱导癫痫持续状态后的早期,通过突触后mGluR1α介导的兴奋性神经毒性可能参与了齿状回门区以及CA1区的内嗅层与海马槽交界处中间神经元的变性和死亡。