Depletion of the AMPAR reserve pool impairs synaptic plasticity in a model of hepatic encephalopathy
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Chronic exposure to ammonia reduces neuronal AMPAR expression

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Neurons maintain basal glutamatergic transmission at the expense of the extrasynaptic receptor population

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Synaptic plasticity is impaired by the consumption of the extrasynaptic AMPAR reserve under conditions of high ammonia

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