2016
DOI: 10.1016/j.neuint.2016.04.017
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Effects of novel small compounds targeting TrkB on neuronal cell survival and depression-like behavior

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Cited by 13 publications
(8 citation statements)
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“…some researchers to suggest that mere regulation of any of these effectors leads to rapid and sustained antidepressant responses. Although this idea has turned out to be promising in some rodent studies (Shirayama et al, 2002;Chen et al, 2012;Fukuda et al, 2016;Hasegawa et al, 2019), it essentially ignores how these molecular events are part of activity-dependent synaptic plasticity (Changeux and Danchin, 1976;Thoenen, 1995;Hensch, 2005;Park and Poo, 2013) (see Introduction). Moreover, such molecular perspectives fail to appreciate the temporal distribution of the effects of ketamine on cortical excitation and plasticity as well as the prolonged influence on depressive symptoms (Fig.…”
Section: Examining Rapid Antidepressant Effects Through Encodingmentioning
confidence: 99%
“…some researchers to suggest that mere regulation of any of these effectors leads to rapid and sustained antidepressant responses. Although this idea has turned out to be promising in some rodent studies (Shirayama et al, 2002;Chen et al, 2012;Fukuda et al, 2016;Hasegawa et al, 2019), it essentially ignores how these molecular events are part of activity-dependent synaptic plasticity (Changeux and Danchin, 1976;Thoenen, 1995;Hensch, 2005;Park and Poo, 2013) (see Introduction). Moreover, such molecular perspectives fail to appreciate the temporal distribution of the effects of ketamine on cortical excitation and plasticity as well as the prolonged influence on depressive symptoms (Fig.…”
Section: Examining Rapid Antidepressant Effects Through Encodingmentioning
confidence: 99%
“…Activated AKT mediated anti-anoikis and apoptosis via mitochondrion-driven apoptotic pathway, rendering cancer cells survival, chemoresistance and invasiveness [ 15 ]. Previous studies have shown that the activation of TrkB by BDNF could mediate the anoikis suppression and metastasis by activating PI3K/AKT pathway [ 16 ]. The overexpression of TrkB has been reported in different malignant tumors, such as neuroblastoma, pancreatic cancer, breast cancer, lung cancer, prostate cancer and myeloma [ 12 ].…”
Section: Introductionmentioning
confidence: 99%
“…Synaptic transmission depends on the functional Trk B receptor. The lack of BDNF-TrkB signal due to the inhibitation of TrkB will reduce the antidepressant effect (25), which suggests that the BDNF-Trk B signaling pathway will participate in the antidepressant process. Kozono et al (26) reported that 5-HT4 receptor coupled with Gs protein can promote dendritic formation in hippocampal neurons, and increased expression of BDNF can induce 5-HT4 receptor to play a role by Trk B signal transduction.…”
Section: Discussionmentioning
confidence: 99%