Ferrer I, Ballabriga J, Martí E, Pozas E, Planas A M, Blasi J
Unitat de Neuropatologia, Hospital Princeps d'Espanya, Spain.
J Neuropathol Exp Neurol. 1997 Jul;56(7):790-7.
Delayed cell death of projection cells in the CA1 area of the hippocampus is produced in the adult gerbil following 5 minutes (min) of transient forebrain ischemia. Parvalbumin-immunoreactive local-circuit neurons are resistant to the ischemic insult. Brain-Derived Neurotrophic Factor (BDNF) immunoreactivity is localized in all neurons of the CA1 area in control gerbils. However, TrkB immunoreactivity is observed in a minority of BDNF-immunoreactive neurons in the CA1 area. The number of BDNF-immunoreactive cells in CA1 is dramatically reduced in ischemic gerbils as early as 24 h after ischemia, but the number of TrkB-immunoreactive cells in the CA1 area is maintained following ischemia. Moreover, about 90% of BDNF-immunoreactive cells and about 85% of TrkB-immunoreactive cells in ischemic gerbils co-localize the calcium-binding protein parvalbumin. Finally, BDNF and TrkB are coexpressed in about 95% of CA1 neurons surviving the ischemic insult. These results indicate that a subpopulation of CA1 hippocampal neurons coexpressing TrkB, parvalbumin and BDNF is resistant to transient forebrain ischemia in the gerbil. These results also suggest that a subpopulation of CA1 hippocampal neurons in the gerbil hippocampus is endowed with a putative BDNF/TrkB autocrine regulatory loop that may be involved in both cell survival and synaptic remodeling of the damaged gerbil hippocampus following transient forebrain ischemia.
成年沙鼠在前脑短暂缺血5分钟后，海马CA1区投射细胞会出现延迟性细胞死亡。小白蛋白免疫反应性局部回路神经元对缺血性损伤具有抗性。在对照沙鼠中，脑源性神经营养因子（BDNF）免疫反应性定位于CA1区的所有神经元中。然而，在CA1区少数BDNF免疫反应性神经元中观察到TrkB免疫反应性。早在缺血后24小时，缺血沙鼠CA1区中BDNF免疫反应性细胞的数量就显著减少，但缺血后CA1区TrkB免疫反应性细胞的数量保持不变。此外，缺血沙鼠中约90%的BDNF免疫反应性细胞和约85%的TrkB免疫反应性细胞与钙结合蛋白小白蛋白共定位。最后，在缺血性损伤后存活的约95%的CA1神经元中BDNF和TrkB共表达。这些结果表明，共表达TrkB、小白蛋白和BDNF的CA1海马神经元亚群对沙鼠的短暂性前脑缺血具有抗性。这些结果还表明，沙鼠海马中CA1海马神经元的一个亚群具有假定的BDNF/TrkB自分泌调节环，该调节环可能参与短暂性前脑缺血后受损沙鼠海马的细胞存活和突触重塑。
