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Fig. 5 | BMC Neuroscience

Fig. 5

From: Effects of escitalopram and paroxetine on mTORC1 signaling in the rat hippocampus under chronic restraint stress

Fig. 5

Possible mechanisms underlying antidepressant-induced molecular changes related to antidepressant effects. Antidepressants increase BDNF [please spell out] expression. The release of BDNF and the stimulation of associated signaling cascades (PI3 K/Akt and MEK/ERK) activate mTORC1 signaling and translation which, in turn, increases synaptic protein levels and synaptogenesis. These effects contribute to the sustained antidepressant actions of antidepressants. TrkB tyrosine-related kinase B, PI3 K phosphoinositide 3-kinase, MEK MAP/ERK kinase, ERK extracellular signal-regulated kinases, GSK-3, glycogen synthase kinase-3, mTORC1 mammalian target of rapamycin complex 1, 4E-BP-1 4E-binding protein 1, p70S6 K p70ribosomal protein S6 kinase, eEF2 eukaryotic elongation factor 2, eIF4E eukaryotic translation initiation factor 4E, S6 small ribosomal protein 6, eIF4B eukaryotic translation initiation factor 4B, PSD-95 post-synaptic density 95, GluA1 glutamate ionotropic receptor AMPA type subunit 1, BDNF brain-derived neurotrophic factor. The molecular pathways shown in red illustrate novel observations from the present study while those in black are generally accepted signaling pathways involved in antidepressant action

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