Effect of psychological stress on [35S]TBPS binding in rat brain.

This study was designed to determine whether psychological stress alters the function of the GABAergic synapse, examined as biochemical changes of [35S]t-butylbicyclophosphorothionate ([35S]TBPS) binding, in unwashed membranes of rat cerebral cortex. Psychological stress increased the number of [35S]TBPS binding sites by 22%. This enhancement was very similar to that after acute foot shock (24%).

[125I][Tyr14]Orphanin binding to rat brain: evidence for labelling the opioid-receptor-like 1 (ORL1).

[125I][Tyr14]Orphanin binds to a number of saturable non-interacting binding sites in rat brain cortical membrane preparations, with a density of 510 fmol/mg protein and affinity 0.9 nM. This high affinity, saturable [125I][Tyr14]orphanin binding was not inhibited by leu-enkephalin and by other ligands for opiate and neurotransmitter receptors both in membrane preparations and brain sections.

Effects of chronic treatment with fluoxetine and citalopram on 5-HT uptake, 5-HT1B autoreceptors, 5-HT3 and 5-HT4 receptors in rats.

The effect in rats of chronic treatment with two specific 5-HT reuptake inhibitors (SSRI) with antidepressant properties, citalopram (10 mg/kg, i.p. twice a day for 14 days, one day washout) and fluoxetine (15 mg/kg, p.

Early detection of the anthracycline-induced cardiotoxicity. A non-invasive haemodynamic study.

Anthracyclines are the most frequent cause of iatrogenic congestive heart failure ranging from acute reversible minor, irreversible reduction in the left ventricular ejection fraction and death despite preventive measures. Sensitive methods are needed to detect earliest preclinical cardiotoxicity along with the development of new protective agents. Thirty breast cancer patients were randomly treated with q 21 120 mg/m2 Epirubicin (EPI) x 3, alone (10 patients), or + ICRF-187 (1000 mg/m2) (10 patients) or + C0Q10 (50 mg/day) (10 patients) and monitored by Thoracic Electrical Bioimpedance (TEB) cardiography before (T0) and at the end of chemotherapy (T1), then at 1, 3, 6 months of follow up (F1, F2, F3).

DHEAS inhibits TNF production in monocytes, astrocytes and microglial cells.

We previously reported that neurosteroids, including dehydroepiandrosterone sulfate (DHEAS), inhibit the production of TNF in vitro and in vivo. In this paper we evaluated the effect of DHEAS on TNF production by cultured rat astrocytes and murine glial cell clones, and compared it with the effect on monocytic THP-1 cells. We found that DHEAS at a concentration of 10(-4)-10(-7) M inhibits TNF production induced by lipopolysaccharide (LPS, 1 microgram/ml) in these cells.