Poirier J, Hess M, May P C, Finch C E
McGill Center For Studies In Aging, Montreal General Hospital, Que., Canada.
Brain Res Mol Brain Res. 1991 Sep;11(2):97-106. doi: 10.1016/0169-328x(91)90111-a.
Entorhinal cortex lesions (ECL) that damage the perforant path to the hippocampus induce rapid increases of apolipoprotein E (apo E) mRNA in the hippocampus. Apo E mRNA was localized in astrocytes by in situ hybridization in combination with immunocytochemistry for glial fibrillary acidic protein (GFAP). Unilateral ECL also increased hippocampal GFAP mRNA, with increases preceding those of apo E mRNA. The apo E mRNA and GFAP mRNA responses were transiently bilateral in non-denervated zones. The timing of response in apo E mRNA to deafferentation supports suggestions that apo E has roles in membrane remodelling during responses to neuron injury.
损伤通往海马体的穿通通路的内嗅皮质损伤（ECL）会导致海马体中载脂蛋白E（apo E）mRNA迅速增加。通过原位杂交结合胶质纤维酸性蛋白（GFAP）免疫细胞化学，将apo E mRNA定位在星形胶质细胞中。单侧ECL也会增加海马体GFAP mRNA，其增加先于apo E mRNA。apo E mRNA和GFAP mRNA的反应在非去神经支配区域短暂地双侧出现。apo E mRNA对去传入神经反应的时间支持了apo E在神经元损伤反应中参与膜重塑的观点。
