title: Effect of liver ischemia-reperfusion injury on the activity of neurons in the rat brain.
abstract: Liver ischemia-reperfusion injury (LIRI) influences different body cells. Little is known about the effect of LIRI on the activity of neurons. Response of neurons to: (1) single ligation of hepatic artery (LIRIa) for 30 min and (2) combined ligation of portal triade (common hepatic artery, portal vein, common bile duct, LIRIb) for 15 min was investigated in Wistar rats. Ninety minutes, 5 h, and 24 h after liver reperfusion, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), interleukin 1alpha (IL-1alpha), and tumor necrosis factor alpha (TNFalpha) serum levels were analyzed and Fos-immunolabeled cells counted in subfornical organ (SFO), suprachiasmatic (SCH), paraventricular (PVN), supraoptic (SON), arcuate (ARC), and ventromedial (VMN) hypothalamic nuclei, locus coeruleus (LC), nucleus of the solitary tract (NTS), and A1/C1 catecholaminergic cell groups. LIRIb increased ALT serum level after 90 min and 24 h while AST activity only after 24 h in all experimental groups. IL-1alpha serum level was increased only after 90 min of LIRIb while TNFalpha level did not change. Ninety minutes after surgeries more Fos-immunostained cells occurred in both LIRIs than sham-operated animals in all structures studied. More distinct Fos expression occurred after LIRIb than LIRIa in SON, PVN, VMN, and NTS. Five hours after both LIRIs, Fos increased in the parabrachial nucleus (PBN) and NTS. Twenty-four hours after both LIRIs Fos incidence decreased in all groups. Although the present data indicate that increased neuronal activity after both LIRIs is mainly a consequence of the liver damage itself partial impact of non-specific factors can not be excluded. However, the anatomical distribution of Fos occurrence detected after LIRIs gives great opportunity to perform a targeted phenotypic identification of the activated neurons by LIRIs in the subsequent experiments.
authors.affiliation: Laboratory of Functional Neuromorphology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, 833 06 Bratislava, Slovak Republic.
authors.forename: Zdeno
authors.initials: Z
authors.lastname: Pirnik
authors.forename: Jana
authors.initials: J
authors.lastname: Bundzikova
authors.forename: Tomas
authors.initials: T
authors.lastname: Francisty
authors.forename: Elena
authors.initials: E
authors.lastname: Cibulova
authors.forename: Lubica
authors.initials: L
authors.lastname: Lackovicova
authors.forename: Boris
authors.initials: B
authors.lastname: Mravec
authors.forename: Alexander
authors.initials: A
authors.lastname: Kiss
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001921:Brain / Q000378:metabolism*; D007150:Immunohistochemistry; D053582:Interleukin-1alpha / Q000097:blood; D007511:Ischemia / Q000097:blood / Q000378:metabolism*; D008099:Liver / Q000098:blood supply; D008297:Male; D009474:Neurons / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D015427:Reperfusion Injury / Q000097:blood / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D053582:Interleukin-1alpha; D016760:Proto-Oncogene Proteins c-fos; D014409:Tumor Necrosis Factor-alpha; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase