• N Arias, M Méndez, and J L Arias.
• Laboratorio de Neurociencias, Departamento de Psicología, Universidad de Oviedo, Plaza Feijoo s/n, 33003 Oviedo, Spain; INEUROPA, Instituto de Neurociencias del Principado de Asturias, Spain. Electronic address: ariasnatalia@uniovi.es.
• Neuroscience. 2015 Jan 22;284:1-10.

AbstractThe hippocampus has been established as a site of plasticity during the acquisition of spatial memory. The memory for spatial locations is impaired in patients who develop hepatic encephalopathy (HE). We wondered how the hippocampus can manage different hippocampal-dependent tasks in a type B model of the early evolutive phases of HE induced by triple portal vein ligation. We used a one-trial object-place recognition task that involves making judgements about whether a stimulus was encountered before in that location and a reversal learning task performed in the Morris water maze that involves reward-guided behavior and decision making. Our behavioral results showed impairments in the acquisition of both tasks by the portal hypertension group compared with the sham-operated group. To label brain areas related to these tasks, we marked the expression of the c-Fos protein and revealed high c-Fos immunoreactivity in cornu ammonis 1 (CA1), cornu ammonis 3 (CA3) and entorhinal (Ent) cortex of the PH group compared with the SHAM group in the object-place recognition task and a decrease in c-Fos-positive cells in the reversal task in the CA1, CA3, dentate gyrus (DG), cingulate (CG), prelimbic (PL), and infralimbic (IL) cortices in the PH group compared with the SHAM group. In conclusion, the study corroborated the pivotal role of the hippocampus in spatial memory deficits found in the early stages of type B HE and noted its differential contribution in each of the tasks.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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