Melatonin attenuates dexamethasone-induced spatial memory impairment and dexamethasone-induced reduction of synaptic protein expressions in the mouse brain

Tongjaroenbuangam, Walaiporn; Ruksee, Nootchanart; Mahanam, Thanutchaporn; Govitrapong, Piyarat

doi:10.1016/j.neuint.2013.08.011

Cited by 43 publications

(25 citation statements)

References 55 publications

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“…Taken together, the levels of SYP and evoked FM®1-43 destaining after treatment with IGF-II suggest a recovery in the mechanisms of synaptic plasticity involved in memory and learning processes. This is in agreement with the neuroprotective mechanism described for other neuroprotective compounds [105], [106].…”

Section: Discussionsupporting

confidence: 92%

IGF-II promotes neuroprotection and neuroplasticity recovery in a long-lasting model of oxidative damage induced by glucocorticoids

et al. 2017

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Insulin-like growth factor-II (IGF-II) is a naturally occurring hormone that exerts neurotrophic and neuroprotective properties in a wide range of neurodegenerative diseases and ageing. Accumulating evidence suggests that the effects of IGF-II in the brain may be explained by its binding to the specific transmembrane receptor, IGFII/M6P receptor (IGF-IIR). However, relatively little is known regarding the role of IGF-II through IGF-IIR in neuroprotection. Here, using adult cortical neuronal cultures, we investigated whether IGF-II exhibits long-term antioxidant effects and neuroprotection at the synaptic level after oxidative damage induced by high and transient levels of corticosterone (CORT). Furthermore, the involvement of the IGF-IIR was also studied to elucidate its role in the neuroprotective actions of IGF-II. We found that neurons treated with IGF-II after CORT incubation showed reduced oxidative stress damage and recovered antioxidant status (normalized total antioxidant status, lipid hydroperoxides and NAD(P) H:quinone oxidoreductase activity). Similar results were obtained when mitochondria function was analysed (cytochrome c oxidase activity, mitochondrial membrane potential and subcellular mitochondrial distribution). Furthermore, neuronal impairment and degeneration were also assessed (synaptophysin and PSD-95 expression, presynaptic function and FluoroJade B® stain). IGF-II was also able to recover the long-lasting neuronal cell damage. Finally, the effects of IGF-II were not blocked by an IGF-IR antagonist, suggesting the involvement of IGF-IIR. Altogether these results suggest that, in or model, IGF-II through IGF-IIR is able to revert the oxidative damage induced by CORT. In accordance with the neuroprotective role of the IGF-II/IGF-IIR reported in our study, pharmacotherapy approaches targeting this pathway may be useful for the treatment of diseases associated with cognitive deficits (i.e., neurodegenerative disorders, depression, etc.).

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Section: Discussionsupporting

confidence: 92%

IGF-II promotes neuroprotection and neuroplasticity recovery in a long-lasting model of oxidative damage induced by glucocorticoids

et al. 2017

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“…The DEX concentration was adapted based on the work of Sigwalt et al (2011), Yao et al (2007 and Li et al (2010) in addition to our own, unpublished findings, which indicate that the doses usually used to induce depressive-like states (0.1-1.5 mg/kg body weight) may cause molecular changes that are too subtle to observe. Furthermore, previous studies have shown that chronic treatment with 60 mg/kg DEX is not lethal (Tongjaroenbuangam et al, 2013;Ruksee et al, 2014). Therefore, the selected dose of 4 mg/kg appeared to be safe.…”

Section: Drug Administrationmentioning

confidence: 86%

Behavioral and molecular alterations in mice resulting from chronic treatment with dexamethasone: Relevance to depression

et al. 2015

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“…Previous studies have documented the protective effect of melatonin on learning and memory deficits induced by a number of pathological or physiological conditions such as Alzheimer's disease [57,58], aging [59], diabetes [60], and head trauma [61]. Additionally, melatonin was shown to prevent cognitive deficits in memory due to administration/ingestion of chemicals and medications such as aromatic thinner solvents [62], pesticides [63], D-galactose [59], and dexamethasone [64].…”

Section: Discussionmentioning

confidence: 99%

Chronic Melatonin Treatment Prevents Memory Impairment Induced by Chronic Sleep Deprivation

et al. 2015

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Sleep deprivation (SD) has been associated with memory impairment through induction of oxidative stress. Melatonin, which promotes the metabolism of many reactive oxygen species (ROS), has antioxidant and neuroprotective properties. In this study, the effect of melatonin on memory impairment induced by 4 weeks of SD was investigated using rat animal model. Animals were sleep deprived using modified multiple platform model. Melatonin was administered via oral gavage (100 mg/kg/day). Spatial learning and memory were assessed using the radial arm water maze (RAWM). Changes in oxidative stress biomarkers in the hippocampus following treatments were measured using ELISA procedure. The result revealed that SD impaired both short- and long-term memory (P < 0.05). Use of melatonin prevented memory impairment induced by SD. Furthermore, melatonin normalized SD-induced reduction in the hippocampus activity of catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD). In addition, melatonin enhanced the ratio of reduced to oxidized glutathione GSH/GSSG in sleep-deprived rats (P < 0.05) without affecting thiobarbituric acid reactive substance (TBARS) levels (P > 0.05). In conclusion, SD induced memory impairment, which was prevented by melatonin. This was correlated with normalizing hippocampus antioxidant mechanisms during chronic SD.

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Melatonin attenuates dexamethasone-induced spatial memory impairment and dexamethasone-induced reduction of synaptic protein expressions in the mouse brain

Cited by 43 publications

References 55 publications

IGF-II promotes neuroprotection and neuroplasticity recovery in a long-lasting model of oxidative damage induced by glucocorticoids

IGF-II promotes neuroprotection and neuroplasticity recovery in a long-lasting model of oxidative damage induced by glucocorticoids

Behavioral and molecular alterations in mice resulting from chronic treatment with dexamethasone: Relevance to depression

Chronic Melatonin Treatment Prevents Memory Impairment Induced by Chronic Sleep Deprivation

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