WT mice were also compared to ERKO mice pretreated with 17 beta-estradiol alone and with MPTP. Specific radioligand binding autoradiography and in situ hybridization for DAT, VMAT2 and TH were assayed in the striatum and the substantia nigra (SN). Intact ERKO beta mice had both striatal transporters levels lower than WT and ERKO alpha mice. MPTP caused a dose-dependant loss of both striatal transporters that correlated learn more with striatal DA concentrations. Compared to WT and ERKO beta mice, ERKO alpha mice DAT, VMAT2 and TH were affected at

lower MPTP doses. In the striatum and SN, ERKO alpha mice were more vulnerable and 17 beta-estradiol protected against MPTP toxicity only in WT mice. ERKO alpha mice blood plasma had higher levels of testosterone, dihydrotestosterone and 3 beta-diol compared to the plasma of WT and ERKO beta mice. 17 beta-estradiol treatment increased estradiol plasma levels in all genotypes. Striatal DA concentrations and SN TH mRNA correlated inversely with plasma testosterone and 3 beta-diol levels. Hence, in male mice the lack of ER alpha or ER beta altered their basal plasma steroid levels and both striatal DA transporters as well as their susceptibility

to MPTP toxicity. (C) 2011 Elsevier Ltd. All rights reserved.”
“Recent evidence has suggested Bleomycin molecular weight that microglial activation plays an important role in the pathogenesis of depression. Activated microglia can secrete various pro-inflammatory cytokines and neurotoxic mediators, which may contribute to the development and maintenance of depression. Thus, inhibition of microglial activation may have a therapeutic benefit in the treatment

of depression. In the present study, using BV2 microglial cell line and primary microglial culture, we investigated if fluoxetine, the most widely used antidepressant, can inhibit microglia activation. Our results showed that fluoxetine significantly inhibited lipopolysaccharide (LPS)-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin- 6 (IL-6) and nitric oxide (NO). By RT-PCR, the mRNA level of these pro-inflammatory cytokines and iNOS was also attenuated by fluoxetine. We further investigated the intracellular signaling mechanism regulating the production of pro-inflammatory cytokines and NO from LPS-activated microglia. The results SRT1720 mouse showed that fluoxetine inhibited I kappa B-a degradation, phosphorylation and nuclear translocation of the p65 subunit of NF-kappa B, and phosphorylation of p38 mitogen-activated protein kinase (MAPK) in the LPS-stimulated microglia. Taken together, our results suggest that the therapeutic effects of fluoxetine are partially mediated by modulating microglial activation. (C) 2011 Elsevier Ltd. All rights reserved.”
“Background Excess bodyweight is a major public health concern. However, few worldwide comparative analyses of long-term trends of body-mass index (BMI) have been done, and none have used recent national health examination surveys.