Galantamine increases hippocampal insulin-like growth factor 2 expression via α7 nicotinic acetylcholine receptors in mice

Kita, Yuki; Ago, Yukio; Takano, Erika; Fukada, Akio; Takuma, Kazuhiro; Matsuda, Takehisa

doi:10.1007/s00213-012-2841-7

Cited by 39 publications

(32 citation statements)

References 46 publications

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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: Discussionsupporting

confidence: 58%

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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Section: Discussionsupporting

confidence: 58%

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

2014

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“…Evidence suggests that antidepressant-like effects of dicholine succinate might be mediated via up-regulation of hippocampal expression of IGF2 (Cline et al, 2012). Another study shows that galantamine increases hippocampal IGF2 levels, producing a neurotrophic effect (Kita et al, 2013). Other reports suggest that IGF2 may improve behavioral performance by promoting adult neurogenesis in the hippocampal dentate gyrus (Bracko et al, 2012).…”

Section: Discussionmentioning

confidence: 96%

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

et al. 2015

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“…Real-time quantitative PCR was performed similarly to that previously reported [27]. In brief, total RNA was isolated from primary cortical neurons, and the concentration of RNA was determined using a Nano-Drop ® ND-1000 spectrophotometer (Thermo Scientific, Wilmington, DE, USA).…”

Section: Real-time Quantitative Pcrmentioning

confidence: 99%

Prenatal Exposure to Histone Deacetylase Inhibitors Affects Gene Expression of Autism-Related Molecules and Delays Neuronal Maturation

et al. 2016

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Valproic acid (VPA) is a multi-target drug and an inhibitor of histone deacetylase (HDAC). We have previously demonstrated that prenatal exposure to VPA at embryonic day 12.5 (E12.5), but not at E14.5, causes autism-like behavioral abnormalities in male mouse offspring. We have also found that prenatal VPA exposure causes transient histone hyperacetylation in the embryonic brain, followed by decreased neuronal cell numbers in the prefrontal and somatosensory cortices after birth. In the present study, we examined whether prenatal HDAC inhibition affects neuronal maturation in primary mouse cortical neurons. Pregnant mice were injected intraperitoneally with VPA (500 mg/kg) and the more selective HDAC inhibitor trichostatin A (TSA; 500 µg/kg) at E12.5 or E14.5, and primary neuronal cultures were prepared from the cerebral cortices of their embryos. Prenatal exposure to VPA at E12.5, but not at E14.5, decreased total number, total length, and complexity of neuronal dendrites at 14 days in vitro (DIV). The effects of VPA weakened at 21 DIV. Exposure to TSA at E12.5, but not at E14.5, also delayed maturation of cortical neurons. In addition, real-time quantitative PCR revealed that the prenatal exposure to TSA decreased neuroligin-1 (Nlgn1), Shank2, and Shank3 mRNA levels and increased contactin-associated protein-like 2 mRNA level. The delay in neuronal maturation was also observed in Nlgn1-knockdown cells, which were transfected with Nlgn1 siRNA. These findings suggest that prenatal HDAC inhibition causes changes in gene expression of autism-related molecules linked to a delay of neuronal maturation.

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Galantamine increases hippocampal insulin-like growth factor 2 expression via α7 nicotinic acetylcholine receptors in mice

Abstract: These findings suggest that galantamine increases hippocampal IGF2 levels via α7 nAChR activation in mice and imply that the effect may contribute to its neuroprotection or neurogenesis.

Cited by 39 publications

References 46 publications

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

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

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

Prenatal Exposure to Histone Deacetylase Inhibitors Affects Gene Expression of Autism-Related Molecules and Delays Neuronal Maturation

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