Corticosterone-mediated microglia activation affects dendritic spine plasticity and motor learning functions in minimal hepatic encephalopathy

摘要: Minimal hepatic encephalopathy (MHE) is characterized as cognitive deficits including memory and learning dysfunctions after liver injuries or diseases. Our understandings of neurological mechanisms MHE-associated syndromes, however, are far from complete. In the current study we generated a mouse MHE model by repetitive administrations thioacetamide (TAA), which induced hyperammonemia plus elevated proinflammatory cytokines in both general circulation motor cortex. mice presented prominent deficits, were associated with excess dendritic spine pruning cortex under 2-photon vivo microscopy. The pharmaceutical blockade glucocorticoid receptor suppression its biosynthesis further rescued synaptic protein loss. Moreover, microglial activation, can be alleviated pathway inhibition. sum, our data demonstrates corticosterone-induced over-pruning impairments MHE, providing new insights for pathogenesis potential targets clinical interventions.