Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques

One of the main pathological hallmarks of Alzheimer's disease (AD) is the accumulation of plaques in the cerebral cortex, which may appear either in the neuropil or in direct association with neuronal somata. Since different axonal systems innervate the dendritic (mostly glutamatergic) and peri...

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Detalhes bibliográficos
Autores: Garcia Marin, Virginia, Blazquez Llorca, Lidia, Rodriguez, José Rodrigo, Boluda Casas, Susana, Muntané Medina, Gerard, Ferrer, Isidro (Ferrer Abizanda), DeFelipe, Javier
Tipo de documento: artigo
Estado:Versão publicada
Data de publicação:2009
País:España
Recursos:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositório:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/126816
Acesso em linha:https://hdl.handle.net/2445/126816
Access Level:Acceso aberto
Palavra-chave:Malaltia d'Alzheimer
Epilèpsia
Alzheimer's disease
Epilepsy
Descrição
Resumo:One of the main pathological hallmarks of Alzheimer's disease (AD) is the accumulation of plaques in the cerebral cortex, which may appear either in the neuropil or in direct association with neuronal somata. Since different axonal systems innervate the dendritic (mostly glutamatergic) and perisomatic (mostly GABAergic) regions of neurons, the accumulation of plaques in the neuropil or associated with the soma might produce different alterations to synaptic circuits. We have used a variety of conventional light, confocal and electron microscopy techniques to study their relationship with neuronal somata in the cerebral cortex from AD patients and APP/PS1 transgenic mice. The main finding was that the membrane surfaces of neurons (mainly pyramidal cells) in contact with plaques lack GABAergic perisomatic synapses. Since these perisomatic synapses are thought to exert a strong influence on the output of pyramidal cells, their loss may lead to the hyperactivity of the neurons in contact with plaques. These results suggest that plaques modify circuits in a more selective manner than previously thought.