Morin F, Beaulieu C, Lacaille J C
Département de physiologie, Centre de recherche en sciences neurologiques, Université de Montréal, QC, Canada.
Epilepsy Res. 1998 Nov;32(3):363-9. doi: 10.1016/s0920-1211(98)00033-3.
The intraventricular injection of kainic acid (KA) in rats produces a loss of dentate hilar neurons and hippocampal CA3 pyramidal cells, and renders the dentate granule cells and the CA1 pyramidal cells hyperexcitable. We have used immunocytochemical detection of glutamic acid decarboxylase (GAD), a marker of gamma-aminobutyric acid (GABA) cells, as well as stereological cell counting techniques, to determine whether inhibitory cell loss was present 2 weeks after KA treatment. In area CA1, we found that the density of GAD-positive cells was reduced by KA, but only in stratum oriens and the alveus. Counts of Nissl-stained neurons were also significantly reduced in this layer. These results demonstrate a loss of GABA cells in the basal dendritic layer of the CA1 region, which may underlie the hyperexcitability of CA1 pyramidal cells following KA treatment.
向大鼠脑室内注射海藻酸(KA)会导致齿状回门区神经元和海马CA3锥体细胞缺失,并使齿状回颗粒细胞和CA1锥体细胞兴奋性增强。我们利用免疫细胞化学方法检测γ-氨基丁酸(GABA)能细胞的标志物谷氨酸脱羧酶(GAD),并结合体视学细胞计数技术,来确定KA处理2周后是否存在抑制性细胞缺失。在CA1区,我们发现KA降低了GAD阳性细胞的密度,但仅在海马下托和脑室下层。该层尼氏染色神经元计数也显著减少。这些结果表明,CA1区基底树突层的GABA能细胞缺失,这可能是KA处理后CA1锥体细胞兴奋性增强的原因。