Video Experimental Relacionado

Updated: Feb 19, 2026

Electrophoretic Delivery of γ-aminobutyric Acid GABA into Epileptic Focus Prevents Seizures in Mice

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Published on: May 16, 2019

Activación de neuronas GABAérgicas de la SNr impulsa la disfunción del eje hígado-cerebro-ojo en la encefalopatía

Kenan Li^1,2, Zhenhua Wang^3,4, Shaoheng Li^2,5

¹National Demonstrational Center for Preclinical Experimental Medicine, The Fourth Military Medical University, Xi'an, China.

|February 18, 2026

Abstract:

Hepatic encephalopathy (HE) is frequently accompanied by visual dysfunction, yet the mechanisms underlying the liver-brain-eye axis remain unclear. We established mouse models of acute hepatic encephalopathy (AHE) using thioacetamide and chronic hepatic encephalopathy (CHE) using bile duct ligation, confirming hyperammonemia and visual impairment by electroretinogram (ERG) and visual evoked potentials (VEPs). Retinal analyses revealed preserved structure in AHE, whereas CHE induced significant thinning of the ganglion cell layer (GCL), inner nuclear layer (INL), and outer plexiform layer (OPL). Viral anterograde tracing identified aberrant activation of medial substantia nigra pars reticulata glutamate decarboxylase 2-positive (mSNr^GAD2) projections to the superior colliculus (SC) under AHE conditions. Chemogenetic inhibition of this pathway restored retinal function, normalized visual signal transmission, and reduced retinal γ-aminobutyric acid (GABA) release. These findings identify SNr-SC signaling as a key neural mechanism driving liver-brain-eye axis dysfunction in HE.

Palabras clave:

Neurociencia molecular Fisiología molecular Neuroanatomía

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