Gliosis induction on locus coeruleus in a living liver donor experimental model: A brief review
نویسندگان
1 International Collaboration (ID Proyect 1840). India
2 Centro de Investigación Biomédica del Noreste, IMSS. Monterrey, Nuevo León, Mexico
3 Investigadores por México CONAHCyT-Instituto de Neuroetología. Universidad Veracruzana, Xalapa, Veracruz, Mexico
4 Centro de Investigaciones Biomédicas, Universidad Veracruzana, Xalapa, Veracruz, Mexico
5 Instituto de Neuroetología, Universidad Veracruzana, Xalapa, Veracruz, Mexico
6 Laboratorio de Neuropatología Experimental. Instituto Nacional de Neurología y Neurocirugía, CDMX, Mexico
doi
10.22038/ijbms.2023.70847.15389چکیده
Living Donor Liver Transplantation (LDLT) is a promising approach to treating end-stage liver diseases, however, some post-operatory complications such as pneumonia, bacteremia, urinary tract infections, and hepatic dysfunction have been reported. In murine models using partial hepatectomy (PHx), a model that emulates LDLT, it has been determined that the synthesis of hepatic cell proliferation factors that are associated with noradrenaline synthesis are produced in locus coeruleus (LC). In addition, studies have shown that PHx decreases GABA and 5-HT2A receptors, promotes loss of dendritic spines, and favors microgliosis in rat hippocampus. The GABA and serotonin-altered circuits suggest that catecholaminergic neurons such as dopamine and noradrenaline neurons, which are highly susceptible to cellular stress, can also be damaged. To understand post-transplant affections and to perform well-controlled studies it is necessary to know the potential causes that explain as a liver surgical procedure can produce brain damage. In this paper, we review several cellular processes that could induce gliosis in LC after rat PHx.
