Insulin-like growth factor 2 mitigates depressive behavior in a rat model of chronic stress

Luo, Yanwei; Yang, Xu; Cao, Wenzhi; Zhong, Xiaolin; Duan, Juan; Wang, Xueqin; Hu, Zhao‐Lan; Li, Fang; Zhang, Jianyi; Zhou, Ming; Dai, Renke; Li, Chang-Qi

doi:10.1016/j.neuropharm.2014.10.011

Cited by 65 publications

(35 citation statements)

References 49 publications

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“…Our findings indicated that the rats subjected to CUMS were observed to exhibit obviously poor appetite and significantly slow increase in body weight, the adaptive regression to new environments, the stagnancy to reward stimulation and pleasure, or altered mood switching from irascibility to low spirits throughout the CUMS procedure. The result of the present study is consistent with the current study illustrated that CUMS could induce depressive-like behaviors, effectively imitating the symptoms of depression in the patients [40, 41]. …”

Section: Discussionsupporting

confidence: 92%

Mechanisms Underlying the Antidepressant Response of Acupuncture via PKA/CREB Signaling Pathway

et al. 2017

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Protein kinase A (PKA)/cAMP response element-binding (CREB) protein signaling pathway, contributing to impaired neurogenesis parallel to depressive-like behaviors, has been identified as the crucial factor involved in the antidepressant response of acupuncture. However, the molecular mechanisms associated with antidepressant response of acupuncture, neurogenesis, and depressive-like behaviors ameliorating remain unexplored. The objective was to identify the mechanisms underlying the antidepressant response of acupuncture through PKA signaling pathway in depression rats by employing the PKA signaling pathway inhibitor H89 in in vivo experiments. Our results indicated that the expression of hippocampal PKA-α and p-CREB was significantly downregulated by chronic unpredicted mild stress (CUMS) procedures. Importantly, acupuncture reversed the downregulation of PKA-α and p-CREB. The expression of PKA-α was upregulated by fluoxetine, but not p-CREB. No significant difference was found between Acu and FLX groups on the expression of PKA-α and p-CREB. Interestingly, H89 inhibited the effects of acupuncture or fluoxetine on upregulating the expression of p-CREB, but not PKA-α. There was no significant difference in expression of CREB among the groups. Conclusively, our findings further support the hypothesis that acupuncture could ameliorate depressive-like behaviors by regulating PKA/CREB signaling pathway, which might be mainly mediated by regulating the phosphorylation level of CREB.

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Section: Discussionsupporting

confidence: 92%

Mechanisms Underlying the Antidepressant Response of Acupuncture via PKA/CREB Signaling Pathway

et al. 2017

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“…IGF2, which promotes adult neurogenesis (Bracko et al 2012, Ferrón et al 2015), is downregulated in animals exhibiting depression-like behavior after chronic stress (Luo et al 2014). Remarkably, overexpression of Igf2 in the dentate gyrus reverses these behaviors, but whether this effect is dependent on adult neurogenesis remains to be tested.…”

Section: Functions Of Imprinted Genes In the Postnatal Brainmentioning

confidence: 99%

New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain

Pérez

Rubinstein²,

Dulac

2016

Annu. Rev. Neurosci.

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Mammalian evolution entailed multiple innovations in gene regulation, including the emergence of genomic imprinting, an epigenetic regulation leading to the preferential expression of a gene from its maternal or paternal allele. Genomic imprinting is highly prevalent in the brain, yet, until recently, its central roles in neural processes have not been fully appreciated. Here, we provide a comprehensive survey of adult and developmental brain functions influenced by imprinted genes, from neural development and wiring to synaptic function and plasticity, energy balance, social behaviors, emotions, and cognition. We further review the widespread identification of parental biases alongside monoallelic expression in brain tissues, discuss their potential roles in dosage regulation of key neural pathways, and suggest possible mechanisms underlying the dynamic regulation of imprinting in the brain. This review should help provide a better understanding of the significance of genomic imprinting in the normal and pathological brain of mammals including humans.

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“…Variability in the regulation of IGF2 expression has been associated with depression status in adult monozygotic twins (Córdova-Palomera et al, 2015). In rodents, antidepressant treatments up-regulate IGF2 in the hippocampus (Cline et al, 2012; Lisowski et al, 2013) and other brain regions (Lauterio et al, 1993), and IGF2 is down-regulated in the hippocampus in rodent models exhibiting depression-like behaviors (Andrus et al, 2012; Luo et al, 2015). Hippocampal overexpression of IGF2 ameliorated sucrose consumption and immobility time in the forced swim test displays of depression-like behaviors induced by chronic restraint stress in rats (Luo et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

“…In rodents, antidepressant treatments up-regulate IGF2 in the hippocampus (Cline et al, 2012; Lisowski et al, 2013) and other brain regions (Lauterio et al, 1993), and IGF2 is down-regulated in the hippocampus in rodent models exhibiting depression-like behaviors (Andrus et al, 2012; Luo et al, 2015). Hippocampal overexpression of IGF2 ameliorated sucrose consumption and immobility time in the forced swim test displays of depression-like behaviors induced by chronic restraint stress in rats (Luo et al, 2015). Administration of IGF2 also increased neurogenesis in the hippocampus, a process that may contribute to the action of antidepressants (Bracko et al, 2012; Chen et al, 2007; Ferrón et al, 2015; Kita et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Up-regulation of insulin-like growth factor 2 by ketamine requires glycogen synthase kinase-3 inhibition

Grieco

Cheng

Eldar-Finkelman

et al. 2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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An antidepressant dose of the rapidly-acting ketamine inhibits glycogen synthase kinase-3 (GSK3) in mouse hippocampus, and this inhibition is required for the antidepressant effect of ketamine in learned helplessness depression-like behavior. Here we report that treatment with an antidepressant dose of ketamine (10 mg/kg) increased expression of insulin-like growth factor 2 (IGF2) in mouse hippocampus, an effect that required ketamine-induced inhibition of GSK3. Ketamine also inhibited hippocampal GSK3 and increased expression of hippocampal IGF2 in mice when administered after the induction of learned helplessness. Treatment with the specific GSK3 inhibitor L803-mts was sufficient to up-regulate hippocampal IGF2 expression. Administration of IGF2 siRNA reduced ketamine's antidepressant effect in the learned helplessness paradigm. Mice subjected to the learned helplessness paradigm were separated into two groups, those that were resilient (non-depressed) and those that were susceptible (depressed). Non-depressed resilient mice displayed higher expression of IGF2 than susceptible mice. These results indicate that IGF2 contributes to ketamine's antidepressant effect and that IGF2 may confer resilience to depression-like behavior.

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Insulin-like growth factor 2 mitigates depressive behavior in a rat model of chronic stress

Cited by 65 publications

References 49 publications

Mechanisms Underlying the Antidepressant Response of Acupuncture via PKA/CREB Signaling Pathway

Mechanisms Underlying the Antidepressant Response of Acupuncture via PKA/CREB Signaling Pathway

New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain

Up-regulation of insulin-like growth factor 2 by ketamine requires glycogen synthase kinase-3 inhibition

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