Résumé
Mitogen-activated protein kinase (MAPK) signaling influences a variety of neuronal properties, including structural characteristics such as spine density, and physiological features like long-term potentiation. Spatiotemporal control of MAPK signaling is crucial to generate specific changes in neuronal physiology. However, while many studies have concentrated on the activation of MAPK signaling by trophic factors such as BDNF and neuronal activity, the mechanisms that lead to its termination have not been well described. Two recent reports begin to address this question by focusing on the role of the MAPK phosphatase, MKP-1, in neuronal function. The first study provides a cellular mechanism underlying MKP-1 action in the brain.1 The second study describes potential roles of MKP-1 during stress and major depression.2