A new neuronal target for beta-amyloid peptide in the rat hippocampus

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• 作者：Vincent Villette^a ; ^{vincent.villette@inserm.fr} ; Fré ; dé ; rique Poindessous-Jazat^a ; Brice Bellessort^a ; Elodie Roullot^b ; Yvan Peterschmitt^c ; Jacques Epelbaum^a ; Aline Sté ; phan^c ; Patrick Dutar^a ; ^{patrick.dutar@inserm.fr}
• 关键词：Septohippocampal network ; Hippocamposeptal neurons ; Calbindin ; Somatostatin ; Theta oscillation ; Alzheimer's disease ; Rat model
• 刊名：Neurobiology of Aging
• 出版年：2012
• 期刊代码：202_01974580
• 类别：med
• 出版时间：June, 2012
• 卷：33
• 期：6
• 页码：1126.e1-1126.e14
• 文件大小：2741 K

摘要

In Alzheimer's disease, amyloid beta peptide (A尾) accumulation is associated with hippocampal network dysfunction. Intrahippocampal injections of A尾 induce aberrant inhibitory septohippocampal (SH) network activity in vivo and impairment of memory processing. In the present study, we observed, after hippocampal A尾 treatment, a selective loss of neurons projecting to the medial septum (MS) and containing calbindin (CB) and/or somatostatin (SOM). Other GABAergic neuronal subpopulations were not altered. Thus, the present study identifies hippocamposeptal neuron populations as specific targets for A尾 deposits. We observed that in A尾-treated rats but not in controls, glutamate agonist application induced rhythmic bursting in 55%of the slow-firing neurons in the medial septum. This suggests that hippocampal A尾 can trigger modifications of the septohippocampal pathway via the alteration of a specific neuronal population. Long-range hippocamposeptal GABA/calbindin neurons, targets of hippocampal amyloid deposits, are implicated in supporting network synchronization. By identifying this target, we contribute to the understanding of the mechanisms underlying deleterious effects of A尾, one of the main agents of dementia in Alzheimer's disease.