TY - JOUR

T1 - Role of tumor necrosis factor gene in acute lipopolysacharide effect on behavior, brain expression of interleukins and brain serotonin system in mice

AU - Bazovkina, D.

AU - Pershina, A.

AU - Fursenko, D.

AU - Khotskin, N.

AU - Kulikova, E.

AU - Bazhenova, E.

AU - Kulikov, A.

PY - 2019

Y1 - 2019

N2 - Tumor necrosis factor (TNF) is cytokine, an important pro-inflammatory mediator in response to the immune system activation by lipopolysaccharide (LPS). In rodents, acute LPS exposure caused decreased locomotor activity, enhanced cataleptic immobility [1], increased neuroinflammatory factors expression (TNF, interleukins IL-1beta and IL-6) [2] and changes in brain serotonin metabolism [3]. The aim was to evaluate the involvement of gene encoding TNF in the effect of acute LPS administration on behavior, brain expression of interleukins and state of brain serotonin system using adult TNF knockout mice (TNF KO) generated on a genetically pure C57BL/6 background and mice of C57BL/6 (WT) strain. The impact of acute LPS treatment (50 and 200 µg/kg, i.p., control groups received saline) was estimated on 1) behavior in the open-field test and cataleptic immobility duration; 2) brain expression of genes encoding 5-HT1A, 5-HT2A receptors, tryptophan hydroxylase-2, 5-HT transporter and IL-1beta, IL-6; 3) brain concentration of 5-HT and its main catabolite 5-HIAA using high performance liquid chromatography (HPLC). Catalepsy was induced by the pinch at the scruff of a neck, then animal was placed on parallel bars, catalepsy was evaluated by immobility duration. The data were analyzed by two-way ANOVA followed by Fisher's LSD post-hoc comparison. LPS administration decreased the horizontal (distance run) and vertical (number of rearings) locomotor activities in the open-field test only in WT mice (p

AB - Tumor necrosis factor (TNF) is cytokine, an important pro-inflammatory mediator in response to the immune system activation by lipopolysaccharide (LPS). In rodents, acute LPS exposure caused decreased locomotor activity, enhanced cataleptic immobility [1], increased neuroinflammatory factors expression (TNF, interleukins IL-1beta and IL-6) [2] and changes in brain serotonin metabolism [3]. The aim was to evaluate the involvement of gene encoding TNF in the effect of acute LPS administration on behavior, brain expression of interleukins and state of brain serotonin system using adult TNF knockout mice (TNF KO) generated on a genetically pure C57BL/6 background and mice of C57BL/6 (WT) strain. The impact of acute LPS treatment (50 and 200 µg/kg, i.p., control groups received saline) was estimated on 1) behavior in the open-field test and cataleptic immobility duration; 2) brain expression of genes encoding 5-HT1A, 5-HT2A receptors, tryptophan hydroxylase-2, 5-HT transporter and IL-1beta, IL-6; 3) brain concentration of 5-HT and its main catabolite 5-HIAA using high performance liquid chromatography (HPLC). Catalepsy was induced by the pinch at the scruff of a neck, then animal was placed on parallel bars, catalepsy was evaluated by immobility duration. The data were analyzed by two-way ANOVA followed by Fisher's LSD post-hoc comparison. LPS administration decreased the horizontal (distance run) and vertical (number of rearings) locomotor activities in the open-field test only in WT mice (p

UR - https://www.mendeley.com/catalogue/22741353-fda6-341b-bb1a-36cfe8c7faf1/

U2 - 10.1016/j.euroneuro.2018.11.694

DO - 10.1016/j.euroneuro.2018.11.694

M3 - Meeting Abstract

VL - 29

SP - S464-S464

JO - European Neuropsychopharmacology

JF - European Neuropsychopharmacology

SN - 0924-977X

T2 - 31st Congress of the European-College-of-Neuropsychopharmacology (ECNP)

Y2 - 6 October 2018 through 9 October 2018

ER -