Wang et al. Behav Brain Funct (2016) 12:34 DOI 10.1186/s12993-016-0116-xRESEARCHVenlafaxine ameliorates the depression-like behaviors and hippocampal S100B expression in a rat depression modelChang?Hong Wang 1† , Jing?Yang Gu 1† , Xiao?Li Zhang 1 , Jiao Dong 1 , Jun Yang 2,3 , Ying?Li Zhang 1 , Qiu?Fen Ning 1 , Xiao?Wen Shan 1 and Yan Li 4*Abstract Background: Accumulating evidence has indicated that S100B may be involved in the pathophysiology of depres?sion. No published study has examined the ef f ect of the antidepressant drug venlafaxine on S100B in animal models of depression. This study investigated S100B expression in the hippocampus and assessed the ef f ect of venlafaxine on S100B mRNA level and protein expression in rats exposed to chronic unpredictable mild stress (CUMS).Methods: Forty Sprague?Dawley rats were randomly divided into four groups as control, 0, 5 and 10 mg venlafaxine groups. The venlafaxine groups were exposed to CUMS from day 2 to day 43. Venlafaxine 0, 5 and 10 mg/kg were then administered from day 23 to day 43. We performed behavioral assessments with weight change, open?f i eld and sucrose preference, and analyzed S100B protein expression and mRNA level in the hippocampus.Results: The CUMS led to a decrease in body weight, locomotor activity and sucrose consumption, but venlafaxine treatment (10 mg) reversed these CUMS?induced decreases Also, CUMS increased S100B protein expression and mRNA level in the hippocampus, but venlafaxine treatment (10 mg) signif i cantly decreased S100B protein expres?sion and mRNA level, which were signif i cantly lower than the other treatment groups, without signif i cant dif f erence between the 10 mg venlafaxine and the control groups.Conclusions: Our fi ndings showed that venlafaxine treatment (10 mg) may improve the depression?like behaviors and decrease over?expression of S100B protein and mRNA in the hippocampus in a rat model of depression.Keywords: Venlafaxine, Stress, Depression, Hippocampus, S100B protein© The Author(s) 2016. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.BackgroundMajor depressive disorder (MDD) is one of the most common, serious mood disorders with a high recur-rence rate, representing a major socio-economical bur-den [1]. However, the pathogenic mechanisms are still unclear. Understanding the causes and neurobiologi-cal basis of depression remains a challenge. Recently, it has been suggested that mood disorders are character-ized by disease-specif i c glial pathology [2, 3]. Post mor-tem studies showed reductions in glial cell density or glial cell numbers in prefrontal brain regions in patients with mood disorders [4], mainly displaying alterations of astrocytes and oligodendrocytes [5].S100B is a glia-derived neurotrophic marker and an acidic and calcium-binding protein that is primarily pro-duced by astrocytes and oligodendrocytes in the human brain [6]. Astrocytes are the main type of glial cells and are distributed throughout the nervous system. Th ey have a role in the nutrition and protection of neurons and maintain brain and nervous system function. Under normal circumstances, high levels of S100B protein are mainly found in the cerebrospinal fl uid (CSF), but low level of S100B in plasma and brain [7]. After brain injury, the activated microglia can secrete interleukin (IL) such as IL-1β, IL-6, tumor necrosis factor-α, and stimulate Open AccessBehavioral andBrain Functions*Correspondence: liyanzzu2009@126.com † Chang?Hong Wang and Jing?Yang Gu contributed equally to this work 4 Department of Child and Adolescent, Public Health College, Zhengzhou University, 100 Kexue Road, Zhengzhou 450001, Henan, ChinaFull list of author information is available at the end of the article
