Decreased expression of CD200 and CD200R1 by human decidual tissues in spontaneous early abortion.

Objective: To examine the cellular distribution and the expression of CD200 and its receptor 1 (CD200R1) in human deciduas in first-trimester pregnant women with spontaneous early abortion (SEA) and normal pregnancy, and to explore their role in the etiology of SEA.Subjects and methods: Thirty-five women at 6-10-week gestation with SA and 30 women of similar gestational age with a healthy pregnancy were recruited. Expression of CD200 and CD200R1 in the deciduas was determined using immunohistochemistry, confocal laser scanning microscope, Western blot, and real-time PCR (RT-PCR).Results: The decidual stromal cells, glandular epithelial cells, and vessel endothelial cells during the first trimester of pregnancy express both CD200 and CD200R1 proteins. During this period, the expression of CD200 in glandular epithelial cells and vessel endothelial cells is significantly higher in normal pregnancy than that in women with SEA (0.3079 ± 0.0674 versus 0.2735 ± 0.0515; 0.4077 ± 0.1366 versus 0.3249 ± 0.0993); the expression of CD200R1 in stromal cells, decidual stromal cells, glandular epithelial cells is significantly higher during normal pregnancy than SEA (0.2574 ± 0.0588 versus 0.2292 ± 0.0415; 0.3617 ± 0.1046 versus 0.2804 ± 0.0640). Western blot analysis showed an approximately 44% decrease in CD200R1expression in decidua in the SEA versus the controls. Finally, in decidua, the expression of both CD200 protein and CD200R1 transcript are significantly higher in healthy first-trimester pregnancy than in SEA (CD200: 2.2089 ± 1.2754 versus 0.7241 ± 0.2143; CD200R1: 15.7843 ± 10.7085 versus 7.3381 ± 5.8529).Conclusions: Women with SEA have a lower level of CD200 and CD200R1 expression in deciduas compared with normal pregnant women suggesting that under physiological conditions, CD200 and CD200R1 expression by deciduas is important to prevent fetal loss ensure a successful pregnancy.

Effects of immobilization stress on emotional behaviors in dopamine D3 receptor knockout mice.

A central problem in understanding the dopamine system in anxiety and depression is to specify functions of different members of the dopamine receptor family. Recent studies have reported that the dopamine D2/D3 receptor agonist pramipexole exerts an antidepressant-like effect in the chronic mild stress model and in the behavioral despair model, suggesting dopamine D3 receptor may be an important target for antidepressant actions. The aim of the present study was to examine the role of dopamine D3 receptor on the anxiety-like and depression-like behaviors induced by immobilization stress. We subjected D3 receptor knockout (D3KO) mice to a series of behavioral paradigms after acute (1 h) or chronic (1 h a day for 14 days) immobilization stress. The results showed that immobilization stress significantly altered the anxiety-like behaviors (open field test and elevated plus maze) and depression-like behaviors (tail suspension test) in both D3KO mice and their wild-type littermates. Moreover, further analysis of the data indicated that the D3KO mice, but not their littermates, failed to show a change in immobility time in the tail suspension test after the acute and chronic stress as compared to intact controls, suggesting an increased resistance to the immobilization stress given before behavioral tests. Although our study did not suggest a significant role of D3 receptor in regulating basal anxiety-like and depression-like behaviors, it demonstrated the mice lacking D3 receptor might be more resistant to stressful procedure than their WT littermates.

[Structural plasticity associated with drugs addiction].

An essential feature of drug addiction is that an individual continues to use drug despite the threat of severely adverse physical or psychosocial consequences. Persistent changes in behavior and psychological function that occur as a function of drugs of abuse are thought to be due to the reorganization of synaptic connections (structural plasticity) in relevant brain circuits (especially the brains reward circuits). In this paper we summarized evidence that, indeed, exposure to amphetamine, cocaine, nicotine or morphine produced persistent changes in the structure of dendrites and dendritic spines on cells in relevant brain regions. We also approached the potential molecular mechanisms of these changes. It is suggested that structural plasticity associated with exposure to drugs of abuse reflects a reorganization of patterns of synaptic connectivity in these neural systems, a reorganization that alters their operation, thus contributing to some of the persistent sequela associated with drug use-including addiction.