| First Author | van Heesch F | Year | 2013 |
| Journal | Behav Brain Res | Volume | 253 |
| Pages | 191-5 | PubMed ID | 23896053 |
| Mgi Jnum | J:202103 | Mgi Id | MGI:5517495 |
| Doi | 10.1016/j.bbr.2013.07.038 | Citation | van Heesch F, et al. (2013) Systemic tumor necrosis factor-alpha decreases brain stimulation reward and increases metabolites of serotonin and dopamine in the nucleus accumbens of mice. Behav Brain Res 253:191-5 |
| abstractText | Many patients with chronic inflammatory disorders have an abnormal high prevalence of major depression accompanied by elevated levels of tumor necrosis factor-alpha (TNF-alpha). We hypothesize that systemic TNF-alpha increases brain monoamine metabolism, which might induce anhedonia (i.e. a core symptom of major depression). The effect of an intraperitoneal TNF-alpha injection on extracellular monoamine and metabolite concentrations was investigated by in vivo microdialysis in the nucleus accumbens (NAc) of C57BL/6 mice. In another group, the effects of TNF-alpha on body weight and intracranial self-stimulation (ICSS) thresholds were measured. TNF-alpha reduced body weight and increased ICSS thresholds, suggesting a state of anhedonia. TNF-alpha did not affect serotonin levels, but increased its metabolite 5-HIAA in the NAc. Remarkably, TNF-alpha also increased the dopamine metabolite HVA, without affecting dopamine levels itself. These data concur with earlier findings that pro-inflammatory cytokines enhance serotonin transporter activity, and possibly also dopamine transporter activity in the brain. However, more research is needed to understand the precise molecular mechanisms by which TNF-alpha increases transporter activity and anhedonia. |
