Understanding depression: the hippocampus might hold the answer in a CREB ‐regulated transcription coactivator

Schematic of the key findings reported by Niet  al. 2018. Breuillaudet  al. (2012) initially reported that deletion ofCrtc1 results in both decreased BDNF expression in the brain, and behavioral deficits, including depressive ‐like behaviors. Niet  al. (2018) manipulated CRTC1 expression specifically in the hippocampus via knockdown and over ‐expression approaches, and demonstrated the importance of hippocampal CRTC1 in LPS‐induced neuroinflammation and depressive‐like behaviors. This investigation revealed that CRTC1‐mediated increases in the expression of the neuropeptides BDNF and VGF in the hippocampus; and down‐regulation of proinflammatory cytokines (IL‐1β, IL‐6, and TNFα) in the hippocampus, are instrumental in the attenuation of LPS‐induced depressive‐like behaviors. AbstractThe pathophysiology of major depressive disorders is not completely understood. In this issue of Journal of Neurochemistry, Ni and colleagues investigate the role of cyclic adenosine monophosphate response element ‐binding protein (CREB)‐dependent signaling in the hippocampus on depressive‐like behaviors. This editorial highlights the key findings reported by Ni et al., (2018) and how they demonstrated the importance of CREB‐regulated transcription cofactor 1 in LPS‐induced neuroinflammation and dep ressive‐like behaviors.
Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: Editorial Highlight Source Type: research