Adiponectin modulates synaptic plasticity in hippocampal dentate gyrus

Pousti, Farideh; Ahmadi, Rahim; Mirahmadi, Fatemeh; Hosseinmardi, Narges; Rohampour, Kambiz

doi:10.1016/j.neulet.2017.10.042

Cited by 31 publications

(21 citation statements)

References 27 publications

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“…Adiponectin functions in the brain are highly diversified. It has been shown to act locally in the brain to control key processes of brain physiology including neuronal excitability and synaptic plasticity, neuroprotection, neurogenesis and regulation of glial cells activation (Yau et al, 2014; Chabry et al, 2015; Song et al, 2015; Nicolas et al, 2017; Shah et al, 2017; Pousti et al, 2018). More recently, adiponectin was found to modulate glucose metabolism in hippocampal neurons, increasing glucose uptake, glycolysis and ATP production rates (Cisternas et al, 2018).…”

Section: Adiponectinmentioning

confidence: 99%

“…Intracerebroventricular administration of adiponectin in anesthetized rats potentiates high frequency stimulation (HFS)-induced LTP and suppresses low-frequency stimulation (LFS)-induced LTD. Furthermore, adiponectin administration alone induced a chemical LTP, independent of presynaptic stimulus (Pousti et al, 2018). Osmotin, a plant-derived homolog of adiponectin capable of activate AdipoRs, improves LTP impairment and ameliorates memory deficits in a mouse model of AD (Shah et al, 2017).…”

Section: Adiponectinmentioning

confidence: 99%

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The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

2019

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Cross-talk between adipose tissue and central nervous system (CNS) underlies the increased risk of obese people to develop brain diseases such as cognitive and mood disorders. Detailed mechanisms for how peripheral changes caused by adipose tissue accumulation in obesity impact the CNS to cause brain dysfunction are poorly understood. Adipokines are a large group of substances secreted by the white adipose tissue to regulate a wide range of homeostatic processes including, but not limited to, energy metabolism and immunity. Obesity is characterized by a generalized change in the levels of circulating adipokines due to abnormal accumulation and dysfunction of adipose tissue. Altered adipokine levels underlie complications of obesity as well as the increased risk for the development of obesity-related comorbidities such as type 2 diabetes, cardiovascular and neurodegenerative diseases. Here, we review the literature for the role of adipokines as key mediators of the communication between periphery and CNS in health and disease. We will focus on the actions of leptin and adiponectin, two of the most abundant and well studied adipokines, in the brain, with particular emphasis on how altered signaling of these adipokines in obesity may lead to cognitive dysfunction and augmented risk for Alzheimer’s disease. A better understanding of adipokine biology in brain disorders may prove of major relevance to diagnostic, prevention and therapy.

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Section: Adiponectinmentioning

confidence: 99%

Section: Adiponectinmentioning

confidence: 99%

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

2019

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“…Adiponectin may also influence cognition by directly affecting hippocampal synaptic plasticity. Adiponectin injection in the DG of the hippocampus leads to a chemical long-term potentiation (LTP) characterized by a 20% increase in excitatory post-synaptic potential slope [ 111 ], indicating that adiponectin may have a beneficial effect on memory. Furthermore, adiponectin applied 10 minutes prior to stimulation protocols potentiates LTP via high-frequency stimulation and prevents induction of long-term depression (LTD) via low-frequency stimulation, suggesting that adiponectin may play a role in both LTP and LTD.…”

Section: Adiponectin and Alzheimer's Diseasementioning

confidence: 99%

Role of Adiponectin in Central Nervous System Disorders

et al. 2018

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Adiponectin, the most abundant plasma adipokine, plays an important role in the regulation of glucose and lipid metabolism. Adiponectin also possesses insulin-sensitizing, anti-inflammatory, angiogenic, and vasodilatory properties which may influence central nervous system (CNS) disorders. Although initially not thought to cross the blood-brain barrier, adiponectin enters the brain through peripheral circulation. In the brain, adiponectin signaling through its receptors, AdipoR1 and AdipoR2, directly influences important brain functions such as energy homeostasis, hippocampal neurogenesis, and synaptic plasticity. Overall, based on its central and peripheral actions, recent evidence indicates that adiponectin has neuroprotective, antiatherogenic, and antidepressant effects. However, these findings are not without controversy as human observational studies report differing correlations between plasma adiponectin levels and incidence of CNS disorders. Despite these controversies, adiponectin is gaining attention as a potential therapeutic target for diverse CNS disorders, such as stroke, Alzheimer's disease, anxiety, and depression. Evidence regarding the emerging role for adiponectin in these disorders is discussed in the current review.

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“…Cognitive decline in AD is attributed to synaptic dysfunction in the hippocampus 11 , related to a loss of long-term potentiation (LTP), a molecular mechanism of hippocampal synaptic plasticity 12–14 . Adiponectin treatment was shown to enhance synaptic function 15 and promote presynaptic release 16 , and increases in circulating adiponectin levels alleviate memory dysfunction in models of dementia 5,17 . To evaluate the effects of adiponectin on hippocampal LTP as well as the mobility of cell surface ionotropic glutamate receptors in AD, we utilised a mouse model harbouring five familial AD mutations, the 5XFAD mouse.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin improves long-term potentiation in the 5XFAD mouse brain

Wang

Song

2019

Sci Rep

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Adiponectin is an adipokine that regulates apoptosis, glucose and lipid metabolism, and insulin sensitivity in metabolic diseases. As recent studies have associated changes in adipokines and other metabolites in the central nervous system with a risk for Alzheimer’s disease (AD), we investigated the effects of adiponectin treatment on hippocampal cells in the 5XFAD mouse model of AD and neuronal SH-SY5Y cells under amyloid beta toxicity. Adiponectin treatment reduced levels of cleaved caspase 3 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) apoptosis signalling and decreased glycogen synthase kinase 3 beta (GSK3β) activation. Moreover, adiponectin treatment triggered long-term potentiation in the hippocampi of 5XFAD mice, which was associated with reduced expression of N -methyl- d -aspartate and its receptor as well as surface expression of the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor. These findings suggest that adiponectin inhibits neuronal apoptosis and inflammatory mechanisms and promotes hippocampal long-term potentiation. Thus, adiponectin exhibits beneficial effect on hippocampal synaptic plasticity in Alzheimer’s disease mouse model.

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Adiponectin modulates synaptic plasticity in hippocampal dentate gyrus

Cited by 31 publications

References 27 publications

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

Role of Adiponectin in Central Nervous System Disorders

Adiponectin improves long-term potentiation in the 5XFAD mouse brain

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