Loss of Leptin-Induced Modulation of Hippocampal Synaptic Trasmission and Signal Transduction in High-Fat Diet-Fed Mice

Mainardi, Marco; Spinelli, Matteo; Scala, Federico; Mattera, Andrea; Fusco, Salvatore; D’Ascenzo, Marcello; Grassi, Claudio

doi:10.3389/fncel.2017.00225

Cited by 37 publications

(28 citation statements)

References 59 publications

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“…Leptin enhances LTP and decreases LTD, increasing the efficacy of excitatory synaptic transmission (Shanley et al, 2001; Wayner et al, 2004; Moult and Harvey, 2011; McGregor and Harvey, 2018b; McGregor et al, 2018). Moreover, leptin resistance is determinant for hippocampal dysfunction (Mainardi et al, 2017). In AD models, leptin prevents the anomalous effects of Aβ on hippocampal LTP and LTD, restoring normal hippocampal synaptic function (Doherty et al, 2013), and also increasing the synaptic density and rescuing memory deficits (Perez-Gonzalez et al, 2014).…”

Section: The Role Of Leptin In Admentioning

confidence: 99%

Obesity as a Risk Factor for Alzheimer’s Disease: Implication of Leptin and Glutamate

et al. 2019

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Obesity is known to induce leptin and insulin resistance. Leptin is a peptide hormone synthesized in adipose tissue that mainly regulates food intake. It has been shown that insulin stimulates the production of leptin when adipocytes are exposed to glucose to encourage satiety; while leptin, via a negative feedback, decreases the insulin release and enhances tissue sensitivity to it, leading to glucose uptake for energy utilization or storage. Therefore, resistance to insulin is closely related to leptin resistance. Obesity in middle age has also been related to Alzheimer’s disease (AD). In recent years, the relation between impaired leptin signaling pathway and the onset of AD has been studied. In all this context the role of the blood brain barrier (BBB) is crucial. Slow excitotoxicity happens in AD due to an excess of the neurotransmitter glutamate. Since leptin has been shown to regulate N -methyl- D -aspartate (NMDA) receptors, we want to review the link between these pathological pathways, and how they are affected by other AD triggering factors and its role in the onset of AD.

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Section: The Role Of Leptin In Admentioning

confidence: 99%

Obesity as a Risk Factor for Alzheimer’s Disease: Implication of Leptin and Glutamate

et al. 2019

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“…Moreover, severe mood disorders such as MDD and bipolar affective disorder have been characterized by dysregulation of neurotrophic signaling. Both GDNF and leptin exert neurotrophin-like actions in the hippocampus (Mainardi et al, 2017), and disturbances in the availability and function of either effector has been implicated in the development of mood disorders. Recent evidence supports the hypothesis that GDNF is critical to hippocampal dendrite development and results from in vitro and in vivo experiments show that GDNF and its receptor are required for the proper growth and morphology of dendritic arbors and spines (Irala et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Dietary Exposure to Excess Saturated Fat During Early Life Alters Hippocampal Gene Expression and Increases Risk for Behavioral Disorders in Adulthood

Page

Anday

2020

Front. Neurosci.

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Purpose: Maternal and postnatal diets result in long-term changes in offspring brain and behavior; however, the key mediators of these developmental changes are not welldefined. In this study, we investigated the impact of maternal and post-weaning high-fat diets on gene expression of key components mediating hippocampal synaptic efficacy. In addition, we evaluated the risk for impaired stress-coping and anxiety-like behaviors in adult offspring exposed to obesogenic diets during early life. Methods: Dams were fed a control (C) or high-fat (HF) diet prior to mating, pregnancy, and lactation. Male offspring from control chow and high-fat fed dams were weaned to control chow or HF diets. The forced swim test (FST) and the elevated-plus maze (EPM) were used to detect stress-coping and anxiety-like behavior, respectively. Real-time RT-PCR and ELISA were used to analyze hippocampal expression of genes mediating synaptic function. Results: Animals fed a HF diet post-weaning spent more time immobile in the FST. Swimming time was reduced in response to both maternal and post-weaning HF diets. Both maternal and post-weaning HF diets contributed to anxiety-like behavior in animals exposed to the EPM. Maternal and post-weaning HF diets were associated with a significant decrease in mRNA and protein expression for hippocampal GDNF, MAP2, SNAP25, and synaptophysin. Hippocampal mRNA expression of key serotonergic and glutamatergic receptors also exhibited differential responses to maternal and postweaning HF diets. Hippocampal serotonergic receptor 5HT1A mRNA was reduced in response to both the maternal and post-weaning diet, whereas, 5HT2A receptor mRNA expression was increased in response to the maternal HF diet. The glutamate AMPA receptor subunit, GluA1, mRNA expression was significantly reduced in response to both diets, whereas no change was detected in GluA2 subunit mRNA expression. Conclusion: These data demonstrate that the expression of genes mediating synaptic function are differentially affected by maternal and post-weaning high-fat diets. The postweaning high-fat diet clearly disturbs both behavior and gene expression. In addition,

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“…ulation of hippocampal synaptic transmission is attenuated under the same conditions (Mainardi et al 2017). HFD can also increase glutamatergic signaling within the hippocampus through altered regulation of astroglial GLT-1 activity and the inhibition of glutamine synthesis (Cano et al 2014;Valladolid-Acebes et al 2012).…”

Section: Amygdala and Hippocampusmentioning

confidence: 99%

Role of astroglia in diet-induced central neuroplasticity

Clyburn

Browning

2019

Journal of Neurophysiology

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Obesity, characterized by increased adiposity that develops when energy intake outweighs expenditure, is rapidly becoming a serious health crisis that affects millions of people worldwide and is associated with severe comorbid disorders including hypertension, cardiovascular disease, and type II diabetes. Obesity is also associated with the dysregulation of central neurocircuits involved in the control of autonomic, metabolic, and cognitive functions. Systemic inflammation associated with diet-induced obesity (DIO) has been proposed to be responsible for the development of these comorbidities as well as the dysregulation of central neurocircuits. A growing body of evidence suggests, however, that exposure to a high-fat diet (HFD) may cause neuroinflammation and astroglial activation even before systemic inflammation develops, which may be sufficient to cause dysregulation of central neurocircuits involved in energy homeostasis before the development of obesity. The purpose of this review is to summarize the current literature exploring astroglial-dependent modulation of central circuits following exposure to HFD and DIO, including not only dysregulation of neurocircuits involved in energy homeostasis and feeding behavior, but also the dysregulation of learning, memory, mood, and reward pathways.

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Loss of Leptin-Induced Modulation of Hippocampal Synaptic Trasmission and Signal Transduction in High-Fat Diet-Fed Mice

Cited by 37 publications

References 59 publications

Obesity as a Risk Factor for Alzheimer’s Disease: Implication of Leptin and Glutamate

Obesity as a Risk Factor for Alzheimer’s Disease: Implication of Leptin and Glutamate

Dietary Exposure to Excess Saturated Fat During Early Life Alters Hippocampal Gene Expression and Increases Risk for Behavioral Disorders in Adulthood

Role of astroglia in diet-induced central neuroplasticity

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