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Article Dans Une Revue Nature Neuroscience Année : 2006

Deletion of the background potassium channel TREK-1 results in a depression-resistant phenotype

Résumé

Depression is a devastating illness with a lifetime prevalence of up to 20%. The neurotransmitter serotonin or 5-hydroxytryptamine (5-HT) is involved in the pathophysiology of depression and in the effects of antidepressant treatments. However, molecular alterations that underlie the pathology or treatment of depression are still poorly understood. The TREK-1 protein is a background K+ channel regulated by various neurotransmitters including 5-HT. In mice, the deletion of its gene (Kcnk2, also called TREK-1) led to animals with an increased efficacy of 5-HT neurotransmission and a resistance to depression in five different models and a substantially reduced elevation of corticosterone levels under stress. TREK-1–deficient (Kcnk2−/−) mice showed behavior similar to that of naive animals treated with classical antidepressants such as fluoxetine. Our results indicate that alterations in the functioning, regulation or both of the TREK-1 channel may alter mood, and that this particular K+ channel may be a potential target for new antidepressants.
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Dates et versions

hal-00091223 , version 1 (05-09-2006)

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Citer

C. Heurteaux, G. Lucas, N. Guy, Malika El Yacoubi, S. Thümmler, et al.. Deletion of the background potassium channel TREK-1 results in a depression-resistant phenotype. Nature Neuroscience, 2006, 9, pp.1134-1141. ⟨10.1038/nn1749⟩. ⟨hal-00091223⟩
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