Differential alterations of synaptic plasticity in dentate gyrus and CA1 hippocampal area of Calbindin-D28K knockout mice

Westerink, Remco H.S.; Beekwilder, J.P.; Wadman, Wytse J.

doi:10.1016/j.brainres.2012.02.036

Cited by 34 publications

(27 citation statements)

References 37 publications

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“…Additionally, we also determined neuronal activity in the brains of these transgenic mice via the detection of c-Fos 18, showing miR-196a transgenic mice had increased intensity of c-Fos signals in the brains using immunohistochemical staining and Western blotting (Figure 1F, 1G, 1H and 1I). We also examined the expression profiling of Calbindin D-28k , a marker related to neuronal activity and synaptic plasticity 19, and found higher expression levels of Calbindin D-28k in miR-196a transgenic mice (Supplementary Figure 4). Most importantly, electrophysiology was applied to determine the long-term potentiation (LTP) of CA1 in these mice, and we did observe the trend of stronger LTP in miR-196a transgenic mice (P=0.09; Figure 1J).…”

Section: Resultsmentioning

confidence: 99%

miR-196a Enhances Neuronal Morphology through Suppressing RANBP10 to Provide Neuroprotection in Huntington's Disease

Her¹,

Mao²,

Chang³

et al. 2017

Theranostics

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MicroRNAs (miRNAs) play important roles in several neurobiological processes, including the development and progression of diseases. Previously, we identified that one specific miRNA, miR-196a, provides neuroprotective effects on Huntington's disease (HD), although the detailed mechanism is still unclear. Based on our bioinformatic analyses, we hypothesize miR-196a might offer neuroprotective functions through improving cytoskeletons of brain cells. Here, we show that miR-196a could enhance neuronal morphology, further ameliorating intracellular transport, synaptic plasticity, neuronal activity, and learning and memory abilities. Additionally, we found that miR-196a could suppress the expression of RAN binding protein 10 (RANBP10) through binding to its 3' untranslated region, and higher expression of RANBP10 exacerbates neuronal morphology and intracellular transport. Furthermore, miR-196a enhances neuronal morphology through suppressing RANBP10 and increasing the ability of β-tubulin polymerization. Most importantly, we observed higher expression of RANBP10 in the brains of HD transgenic mice, and higher expression of RANBP10 might exacerbate the pathological aggregates in HD. Taken together, we provide evidence that enhancement of neuronal morphology through RANBP10 is one of the neuroprotective mechanisms for miR-196a. Since miR-196a has also been reported in other neuronal diseases, this study might offer insights with regard to the therapeutic use of miR-196a in other neuronal diseases.

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Section: Resultsmentioning

confidence: 99%

miR-196a Enhances Neuronal Morphology through Suppressing RANBP10 to Provide Neuroprotection in Huntington's Disease

Her¹,

Mao²,

Chang³

et al. 2017

Theranostics

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show abstract

“…Calbindin-D28k is one of the major calcium-binding proteins in the brain, and plays a role in neuronal survival as well as synaptic plasticity [44,45]. Calbindin D-28k undergoes reduced expression in the rat hippocampus with aging [46,47].…”

Section: Alterations In Calbindin-d28k and Map2 Immunoreactivitymentioning

confidence: 99%

Detrimental effects of a high fat/high cholesterol diet on memory and hippocampal markers in aged rats

Ledreux

Wang

Schultzberg

et al. 2016

Behavioural Brain Research

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High fat diets have detrimental effects on cognitive performance, and can increase oxidative stress and inflammation in the brain. The aging brain provides a vulnerable environment to which a high fat diet could cause more damage. We investigated the effects of a high fat/high cholesterol (HFHC) diet on cognitive performance, neuroinflammation markers, and phosphorylated Tau (p-Tau) pathological markers in the hippocampus of Young (4-month old) versus Aged (14-month old) male rats. Young and Aged male Fisher 344 rats were fed a HFHC diet or a normal control diet for 6 months. All animals underwent cognitive testing for 12days in a water radial arm maze to assess spatial and working reference memory. Hippocampal tissue was analyzed by immunohistochemistry for structural changes and inflammation, and Western blot analysis. Young and Aged rats fed the HFHC diet exhibited worse performance on a spatial working memory task. They also exhibited significant reduction of NeuN and calbindin-D28k immunoreactivity as well as an increased activation of microglial cells in the hippocampal formation. Western blot analysis of the hippocampus showed higher levels of p-Tau S202/T205 and T231 in Aged HFHC rats, suggesting abnormal phosphorylation of Tau protein following the HFHC diet exposure. This work demonstrates HFHC diet-induced cognitive impairment with aging and a link between high fat diet consumption and pathological markers of Alzheimer's disease.

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“…(127, 128); see figure 5 by Rakic (2)]. The identification of the telencephalic origin of local circuit neurons in cerebral cortex of mammals is of capital importance to understand mechanisms operating during primate brain evolution (2, 129, 130) and the pathogenesis of congenital and acquired neurological disorders, such as ASD, related to defects of separate classes of local circuit neurons (131, 132). …”

Section: Critical Issues Of Cerebral Cortex Developmentmentioning

confidence: 99%

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

2014

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The morphological alterations of cortical lamination observed in mouse models of developmental hypothyroidism prompted the recognition that these experimental changes resembled the brain lesions of children with autism; this led to recent studies showing that maternal thyroid hormone deficiency increases fourfold the risk of autism spectrum disorders (ASD), offering for the first time the possibility of prevention of some forms of ASD. For ethical reasons, the role of thyroid hormones on brain development is currently studied using animal models, usually mice and rats. Although mammals have in common many basic developmental principles regulating brain development, as well as fundamental basic mechanisms that are controlled by similar metabolic pathway activated genes, there are also important differences. For instance, the rodent cerebral cortex is basically a primary cortex, whereas the primary sensory areas in humans account for a very small surface in the cerebral cortex when compared to the associative and frontal areas that are more extensive. Associative and frontal areas in humans are involved in many neurological disorders, including ASD, attention deficit-hyperactive disorder, and dyslexia, among others. Therefore, an evo-devo approach to neocortical evolution among species is fundamental to understand not only the role of thyroid hormones and environmental thyroid disruptors on evolution, development, and organization of the cerebral cortex in mammals but also their role in neurological diseases associated to thyroid dysfunction.

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Differential alterations of synaptic plasticity in dentate gyrus and CA1 hippocampal area of Calbindin-D28K knockout mice

Cited by 34 publications

References 37 publications

miR-196a Enhances Neuronal Morphology through Suppressing RANBP10 to Provide Neuroprotection in Huntington's Disease

miR-196a Enhances Neuronal Morphology through Suppressing RANBP10 to Provide Neuroprotection in Huntington's Disease

Detrimental effects of a high fat/high cholesterol diet on memory and hippocampal markers in aged rats

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

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