Endocytosis of AMPA receptors: Role in neurological conditions

Bencsik, Norbert; Morales, Carlos O. Oueslati; Haußer, Angelika; Schlett, Katalin

doi:10.1016/bs.pmbts.2022.09.007

Cited by 5 publications

(4 citation statements)

References 190 publications

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“…This reduction is in line with the synaptic plasticity declines in BPA-exposed mouse pups. At the last step of LTP, tra cking of overexpression of GluR1 contribute to the rapid accumulation of AMPA receptors on the postsynaptic sites [53]. The expression declines of GluR1 in the mPFC provide a molecular mechanism for mPFC-dependent synaptic plasticity and function impairment following perinatal BPA exposure.…”

Section: Discussionmentioning

confidence: 99%

Blunted synaptic plasticity in the vHPC-mPFC pathway involving the working memory deficits of mice with perinatal bisphenol-A exposure

Hu,

Li,

Zhang

et al. 2024

Preprint

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Working memory guides human decisions and actions by temporarily holding and manipulating information, yet it has been well-documented as impaired in children with bisphenol A (BPA) exposure. However, neither its underlying neural circuit mechanism nor synaptic basis has been rigorously examined. In the present study, mouse pups were exposed to BPA from dams with BPA exposure (0.735 mg/kg/day) during the gestation and lactation periods to simulate children exposure situation. We found that there was a significant decline in working memory during T maze and objective recognition testing. The in vivo electrophysiological results showed that there was a noticeable decline in theta (θ)/gamma (γ) oscillation power in the medial prefrontal cortex (mPFC) and θ-γ oscillation coupling in the ventral hippocampus (vHPC)-mPFC circuit during retrieval of spatial cues (choice phase) in the novelty-driven T maze task. This fail retrieval of spatial cues and network activity appears to be mediated by down-regulated synaptic plasticity within the vHPC-mPFC circuit. Further patch-clamp recording results revealed a pronounced decrease in the amplitude, rather than the frequency, of excitatory postsynaptic currents (EPSCs) in the mPFC of BPA-exposed mice. Importantly, the spine density of pyramidal neurons and the expression of excitatory receptors (GluA1) in the mPFC were significantly decreased after BPA exposure, providing the postsynaptic basis for BPA-induced synaptic plasticity impairment. Our findings in this study provide rigorous physiological and structural mechanism at circuit and synaptic level underlying working memory deficits resulting from BPA exposure during the critical developmental stage.

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Section: Discussionmentioning

confidence: 99%

Blunted synaptic plasticity in the vHPC-mPFC pathway involving the working memory deficits of mice with perinatal bisphenol-A exposure

Hu,

Li,

Zhang

et al. 2024

Preprint

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“…Synaptic dysfunction is another major pathological process that might be responsible for memory impairment in the progression of AD [ 60 , 61 ]. AMPA receptors, typically located on the postsynaptic membrane of neurons, mediate fast excitatory synaptic transmission [ 62 ]. When activated by neurotransmitters, AMPA receptors are internalized into the postsynaptic neuron, a process known as AMPA receptor endocytosis [ 62 , 63 ].…”

Section: Biological Mechanisms Underlying the Benefits Of Transcrania...mentioning

confidence: 99%

“…AMPA receptors, typically located on the postsynaptic membrane of neurons, mediate fast excitatory synaptic transmission [ 62 ]. When activated by neurotransmitters, AMPA receptors are internalized into the postsynaptic neuron, a process known as AMPA receptor endocytosis [ 62 , 63 ]. The dynamic interplay between AMPA receptor endocytosis and exocytosis, leading to the insertion of receptors into the membrane, allows synapses to adapt to changes in neuronal activity.…”

Section: Biological Mechanisms Underlying the Benefits Of Transcrania...mentioning

confidence: 99%

Photobiomodulation in experimental models of Alzheimer’s disease: state-of-the-art and translational perspectives

Huang,

Hamblin,

Zhang

2024

Alz Res Therapy

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Alzheimer’s disease (AD) poses a significant public health problem, affecting millions of people across the world. Despite decades of research into therapeutic strategies for AD, effective prevention or treatment for this devastating disorder remains elusive. In this review, we discuss the potential of photobiomodulation (PBM) for preventing and alleviating AD-associated pathologies, with a focus on the biological mechanisms underlying this therapy. Future research directions and guidance for clinical practice for this non-invasive and non-pharmacological therapy are also highlighted. The available evidence indicates that different treatment paradigms, including transcranial and systemic PBM, along with the recently proposed remote PBM, all could be promising for AD. PBM exerts diverse biological effects, such as enhancing mitochondrial function, mitigating the neuroinflammation caused by activated glial cells, increasing cerebral perfusion, improving glymphatic drainage, regulating the gut microbiome, boosting myokine production, and modulating the immune system. We suggest that PBM may serve as a powerful therapeutic intervention for AD.

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“…This complex mechanism implicates a competition between exocytosis and endocytosis of AMPA receptors (alpha-amino-3-hydroxy-5methyl-isoxasolepropionic acid receptors, the ionotropic transmembrane receptors for glutamate) that mediate synaptic transmission in the central nervous system (CNS) at the level of presynaptic membrane. Bencsik et al (2023) showed that AMPA receptor trafficking plays a major role in the functioning of neurons and neural networks. Briefly, data have been accumulating suggesting that synthetic sex hormones negatively affect the neurodevelopment of the exposed fetus.…”

Section: Introductionmentioning

confidence: 99%

Effects of prenatal exposure to synthetic sex hormones on neurodevelopment: a biological mechanism.

Soyer-Gobillard,

Gaspari,

Paris

et al. 2023

Front. Mol. Neurosci.

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Since the middle of the 20th century, synthetic sex hormones (estrogens and progestins) have been administered to millions of pregnant or not women worldwide, mainly to avoid miscarriage or for comfort, although their mode of action and their effects on the mother and fetus were ignored. Despite the alerts and the description of somatic and psychiatric disorders in children exposed in utero, synthetic estrogens were prohibited for pregnant women only in the 1970s and 1980s, but some progestins are still authorized. In this review, we summarize the psychiatric disorders described in children exposed in utero to such hormones, focusing particularly on schizophrenia, bipolar disorders, severe depression, eating disorders, suicide and suicide attempts. Moreover, only in 2017 the mechanism of action of these xenohormones has started to be deciphered. Some studies showed that in the fetus exposed in utero, they alter the DNA methylation profile (mainly hypermethylation), and consequently the expression of genes implicated in neurodevelopment and in regulating the sexual organ morphogenesis and also of the promoter of estrogen receptors, located in the amygdala. These deleterious effects may be transmitted also to the next generations, thus affecting the children directly exposed and also the following generations.

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Endocytosis of AMPA receptors: Role in neurological conditions

Cited by 5 publications

References 190 publications

Blunted synaptic plasticity in the vHPC-mPFC pathway involving the working memory deficits of mice with perinatal bisphenol-A exposure

Blunted synaptic plasticity in the vHPC-mPFC pathway involving the working memory deficits of mice with perinatal bisphenol-A exposure

Photobiomodulation in experimental models of Alzheimer’s disease: state-of-the-art and translational perspectives

Effects of prenatal exposure to synthetic sex hormones on neurodevelopment: a biological mechanism.

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