Lipopolysaccharide-Induced Striatal Nitrosative Stress and Impaired Social Recognition Memory Are Not Magnified by Paraquat Coexposure

• Published in: Neurochemical research Vol. 43; no. 3; pp. 745 - 759
• Main Authors: Gonçalves, CinaraLudvig, dos Santos, Danúbia Bonfanti, Portilho, Sthéfani Spricigo, Lopes, Mark William, Ghizoni, Heloisa, de Souza, Viviane, Mack, Josiel Mileno, Naime, Aline Aita, Dafre, Alcir Luiz, de Souza Brocardo, Patrícia, Prediger, Rui Daniel, Farina, Marcelo
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-03-2018; Springer Nature B.V
• Subjects: Animal models; Animals; Behavior, Animal - drug effects; Biochemistry; Biomedical and Life Sciences; Biomedicine; Blood-brain barrier; Brain; Cell Biology; Corpus Striatum - drug effects; Corpus Striatum - metabolism; Electron transport chain; Exposure; Fluorescein; Homeostasis; Hydroxylase; Lipopolysaccharides; Lipopolysaccharides - pharmacology; Male; Membrane permeability; Memory - drug effects; Mice; Mitochondria; NADH-ubiquinone oxidoreductase; Neostriatum; Neostriatum - drug effects; Neostriatum - metabolism; Neurochemistry; Neurology; Neurosciences; Neurotoxicity; Neurotoxicity Syndromes - drug therapy; Nitrosative Stress - drug effects; Nitrotyrosine; Original Paper; Paraquat; Paraquat - toxicity; Permeability; Recognition; Rodents; Social interactions; Sodium; Substantia nigra; Substantia Nigra - drug effects; Substantia Nigra - metabolism; Tyrosine; Tyrosine 3-monooxygenase; Lipopolysaccharide; Striatum; Paraquat; Neurotoxicity; blood–brain barrier; Social recognition memory
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-018-2477-z

Systemic inflammation triggered by lipopolysaccharide (LPS) administration disrupts blood–brain barrier (BBB) homeostasis in animal models. This event leads to increased susceptibility of several encephalic structures to potential neurotoxicants present in the bloodstream. In this study, we investigated the effects of alternate intraperitoneal injections of LPS on BBB permeability, social recognition memory and biochemical parameters in the striatum 24 h and 60 days after treatments. In addition, we investigated whether the exposure to a moderate neurotoxic dose of the herbicide paraquat could potentiate LPS-induced neurotoxicity. LPS administration caused a transient disruption of BBB integrity, evidenced by increased levels of exogenously administered sodium fluorescein in the striatum. Also, LPS exposure caused delayed impairment in social recognition memory (evaluated at day 38 after treatments) and increase in the striatal levels of 3-nitrotyrosine. These events were observed in the absence of significant changes in motor coordination and in the levels of tyrosine hydroxylase (TH) in the striatum and
substantia nigra
. PQ exposure, which caused a long-lasting decrease of striatal mitochondrial complex I activity, did not modify LPS-induced behavioral and striatal biochemical changes. The results indicate that systemic administration of LPS causes delayed social recognition memory deficit and striatal nitrosative stress in adult mice and that the coexposure to a moderately toxic dose of PQ did not magnify these events. In addition, PQ-induced inhibition of striatal mitochondrial complex I was also not magnified by LPS exposure, indicating the absence of synergic neurotoxic effects of LPS and PQ in this experimental model.