The neuronal insulin sensitizer dicholine succinate reduces stress-induced depressive traits and memory deficit: possible role of insulin-like growth factor 2

Cline, Brandon H.; Steinbusch, Harry W.M.; Malin, Dmitry; Revishchin, A. V.; Pavlova, Galia V; Cespuglio, Raymond; Strekalova, Tatyana

doi:10.1186/1471-2202-13-110

Cited by 65 publications

(74 citation statements)

References 77 publications

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“…Although elevation of hippocampal IGF-2 is closely related to the reduced anxiety scores in stressed rats (Cline et al, 2012), the role of IGF-2 in the pathogenesis of anxiety is obscure. In the present study, hippocampal IGF-2 expression was downregulated, accompanied by the dendritic retraction in the offspring of morphine-exposed groups.…”

Section: Discussionmentioning

confidence: 99%

Development of Anxiety-Like Behavior via Hippocampal IGF-2 Signaling in the Offspring of Parental Morphine Exposure: Effect of Enriched Environment

Luo

Cui

et al. 2014

Neuropsychopharmacol

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Opioid addiction is a major social, economic, and medical problem worldwide. Long-term adverse consequences of chronic opiate exposure not only involve the individuals themselves but also their offspring. Adolescent maternal morphine exposure results in behavior and morphologic changes in the brain of their adult offspring. However, few studies investigate the effect of adult opiate exposure on their offspring. Furthermore, the underlying molecular signals regulating the intergenerational effects of morphine exposure are still elusive. We report here that morphine exposure of adult male and female rats resulted in anxiety-like behavior and dendritic retraction in the dentate gyrus (DG) region of the hippocampus in their adult offspring. The behavior and morphologic changes were concomitant with the downregulation of insulin-like growth factor (IGF)-2 signaling in the granular zone of DG. Overexpression of hippocampal IGF-2 by bilateral intra-DG injection of lentivirus encoding the IGF-2 gene prevented anxiety-like behaviors in the offspring. Furthermore, exposure to an enriched environment during adolescence corrected the reduction of hippocampal IGF-2 expression, normalized anxietylike behavior and reversed dendritic retraction in the adult offspring. Thus, parental morphine exposure can lead to the downregulation of hippocampal IGF-2, which contributed to the anxiety and hippocampal dendritic retraction in their offspring. An adolescent-enriched environment experience prevented the behavior and morphologic changes in their offspring through hippocampal IGF-2 signaling. IGF-2 and an enriched environment may be a potential intervention to prevention of anxiety and brain atrophy in the offspring of parental opioid exposure.

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Section: Discussionmentioning

confidence: 99%

Development of Anxiety-Like Behavior via Hippocampal IGF-2 Signaling in the Offspring of Parental Morphine Exposure: Effect of Enriched Environment

Luo

Cui

et al. 2014

Neuropsychopharmacol

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“…Given that insulin does not bind to IGF2 receptors (Jones and Clemmons 1995) and the different temporal profile of IGF2 and insulin effects, we propose that the memory-enhancing effects mediated by IGF2 and insulin occur through distinct mechanisms. We suggest that while insulin acts mainly through glucose metabolism, the IGF2-mediated memory-enhancing mechanisms target activity or plasticity mechanisms, and perhaps in addition to, as suggested by previous literature, acetylcholine modulation (Napoli et al 2008;Cline et al 2012;Kita et al 2013), GABA modulation (Amritraj et al 2010), and vesicle-and/or receptor trafficking (Alberini and Chen 2012).…”

Section: Discussionmentioning

confidence: 99%

The effect of insulin and insulin-like growth factors on hippocampus- and amygdala-dependent long-term memory formation

2014

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Recent work has reported that the insulin-like growth factor 2 (IGF2) promotes memory enhancement. Furthermore, impaired insulin or IGF1 functions have been suggested to play a role in the pathogenesis of neurodegeneration and cognitive impairments, hence implicating the insulin/IGF system as an important target for cognitive enhancement and/or the development of novel treatments against cognitive disorders. Here, we tested the effect of intracerebral injections of IGF1, IGF2, or insulin on memory consolidation and persistence in rats. We found that a bilateral injection of insulin into the dorsal hippocampus transiently enhances hippocampal-dependent memory and an injection of IGF1 has no effect. None of the three peptides injected into the amygdala affected memories critically engaging this region. Together with previous data on IGF2, these results indicate that IGF2 produces the most potent and persistent effect as a memory enhancer on hippocampal-dependent memories. We suggest that the memory-enhancing effects of insulin and IGF2 are likely mediated by distinct mechanisms.

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“…In support of this notion, converging findings reveal dysfunctions of insulin signaling pathway in different neurological or neuropsychiatric disorders (Blazquez et al, 2014;Ghasemi et al, 2013b;Yates et al, 2012). A number of epidemiological studies also point to an association between medical conditions defined by insulin resistance and depression (Cline et al, 2012;Kan et al, 2013;Pomytkin et al, 2015). In addition, insulin resistance displayed by obese db/db mice in brain areas with high density of insulin receptors, such as the hippocampus and cortex, is associated with emotional alterations Kim et al, 2011).…”

Section: Role Of Insulin Resistancementioning

confidence: 97%

“…In addition, insulin resistance displayed by obese db/db mice in brain areas with high density of insulin receptors, such as the hippocampus and cortex, is associated with emotional alterations Kim et al, 2011). Conversely, compounds enhancing neuronal insulin receptor-mediated transmission in the hippocampus show antidepressant-like effects in preclinical paradigms of depression (Cline et al, 2012;Cline et al, 2015). In line with these findings, recent pharmacological studies highlight the antidepressant properties of several antidiabetic drugs, which may involve, beyond improvement of hyperglycemia, positive impact on inflammation and neuronal activity Pomytkin et al, 2015).…”

Section: Role Of Insulin Resistancementioning

confidence: 99%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

136

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Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

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The neuronal insulin sensitizer dicholine succinate reduces stress-induced depressive traits and memory deficit: possible role of insulin-like growth factor 2

Cited by 65 publications

References 77 publications

Development of Anxiety-Like Behavior via Hippocampal IGF-2 Signaling in the Offspring of Parental Morphine Exposure: Effect of Enriched Environment

Development of Anxiety-Like Behavior via Hippocampal IGF-2 Signaling in the Offspring of Parental Morphine Exposure: Effect of Enriched Environment

The effect of insulin and insulin-like growth factors on hippocampus- and amygdala-dependent long-term memory formation

Role of Adiposity-Driven Inflammation in Depressive Morbidity

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