The effects of chronic stress on hippocampal adult neurogenesis and dendritic plasticity are reversed by selective MAO-A inhibition

被引:61
作者
Morais, Monica [1 ,2 ,3 ]
Santos, Paulo A. R. [1 ,2 ]
Mateus-Pinheiro, Antonio [1 ,2 ,3 ]
Patricio, Patricia [1 ,2 ,3 ]
Pinto, Luisa [1 ,2 ,3 ]
Sousa, Nuno [1 ,2 ,3 ]
Pedroso, Pedro [4 ]
Almeida, Susana [4 ]
Filipe, Augusto [4 ]
Bessa, Joao M. [1 ,2 ,3 ]
机构
[1] Univ Minho, Life & Hlth Sci Res Inst ICVS, Sch Hlth Sci, P-4710057 Braga, Portugal
[2] ICVS 3Bs PT Govt Associate Lab, Braga, Portugal
[3] Behav & Mol Lab, BnML, Braga, Portugal
[4] Dept Med, Grp Tecnimede, Sintra, Portugal
关键词
Depression; pirlindole; fluoxetine; stress; neuroplasticity; hippocampus; neurogenesis; PIRLINDOLE;
D O I
10.1177/0269881114553646
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
There is accumulating evidence that adult neurogenesis and dendritic plasticity in the hippocampus are neuroplastic phenomena, highly sensitive to the effects of chronic stress and treatment with most classes of antidepressant drugs, being involved in the onset and recovery from depression. However, the effects of antidepressants that act through the selective inhibition of monoamine oxidase subtype A (MAO-A) in these phenomena are still largely unknown. In the present study, adult neurogenesis and neuronal morphology were examined in the hippocampus of rats exposed to chronic mild stress (CMS) and treated with the selective reversible MAO-A inhibitor (RIMA) drug, pirlindole and the selective serotonin reuptake inhibitor (SSRI), fluoxetine. The results provide the first demonstration that selective MAO-A inhibition with pirlindole is able to revert the behavioural effects of stress exposure while promoting hippocampal adult neurogenesis and rescuing the stress-induced dendritic atrophy of granule neurons.
引用
收藏
页码:1178 / 1183
页数:6
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