Hauss-Wegrzyniak B, Lynch M A, Vraniak P D, Wenk G L
Arizona Research Laboratories, Division of Neural Systems, Memory & Aging, University of Arizona, Tucson 85724, USA.
Exp Neurol. 2002 Aug;176(2):336-41. doi: 10.1006/exnr.2002.7966.
Alzheimer's disease (AD) is characterized by chronic neuroinflammation, significant temporal lobe cell loss, and dementia. We investigated the influence of chronic neuroinflammation produced by chronic infusion of lipopolysaccharide (LPS) into the fourth ventricle for 4 weeks upon the induction and maintenance of long-term potentiation (LTP) in the dentate gyrus of the hippocampus, a well-characterized model of cellular synaptic plasticity. We also examined for pyramidal cell loss within the entorhinal cortex an area of the brain that contains the cell bodies of the perforant path. The results demonstrate that chronic neuroinflammation results in the loss of pyramidal cells within layers II and III of the entorhinal cortex and a significant attenuation of LTP within the dentate gyrus. Similar changes may underlie the temporal lobe pathology and dementia associated with AD.
阿尔茨海默病（AD）的特征是慢性神经炎症、显著的颞叶细胞丢失和痴呆。我们研究了通过向第四脑室慢性注入脂多糖（LPS）4周所产生的慢性神经炎症对海马齿状回长期增强（LTP）的诱导和维持的影响，海马齿状回是一个具有明确特征的细胞突触可塑性模型。我们还检查了内嗅皮质（大脑中包含穿通通路细胞体的一个区域）内锥体细胞的丢失情况。结果表明，慢性神经炎症导致内嗅皮质第II层和第III层内的锥体细胞丢失，以及齿状回内LTP的显著减弱。类似的变化可能是与AD相关的颞叶病理学和痴呆的基础。
