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Steroid hormones may act through a rapid mechanism that does not require an intracellular steroid receptor and its effects on gene expression. In this study we have analysed this so-called non-genomic effect of testosterone on social anxiety in rats of both sexes using androgen and oestrogen receptor blockers. Male rats were divided into four groups: SHAM-CTRL (a sham operated group treated with oil as vehicle, n=10), SHAM-TST (a sham operated group treated with testosterone at a dose of 1 mg/kg, n=10), GDX-CTRL (a castrated group treated with oil, n=10) and GDX-TST (a castrated group treated with testosterone at a dose of 1 mg/kg, n=10). Female rats were divided into two groups: OVX-CTRL (an ovariectomized group treated with oil, n=10) and OVX-TST (an ovariectomized group treated with testosterone, n=10). The intracellular androgen receptor was blocked with flutamide and both intracellular oestrogen receptors were blocked with tamoxifen (a selective oestrogen receptor modulator). Rats were tested one hour after oil or testosterone administration in the social interaction test. Although the concentration of testosterone was higher in testosterone groups, no significant difference in social interaction was observed between the groups. In summary, in this first study focusing on the non-genomic effects of testosterone on social interaction no rapid effects of testosterone in adult rats were found. Further studies should analyse potential nongenomic effects of testosterone on other forms of social behaviour.
 Glucocorticoid receptor (GR) is a steroid hormone receptor that has been shown to play important roles in diverse cellular and physiological processes. More and more evidence has revealed that the effects of glucocorticoids are mediated by the glucocorticoid receptor through genomic or nongenomic mechanisms. A growing number of glucocorticoid receptor splice variants have been identified in human tissues, but few are known in rat tissues. In this work, a novel rGR cDNA, called rGRβ, was cloned from Sprague Dawlay (SD) rat liver. Sequence analysis revealed that the rGRβ mRNA was 39 base pairs (bp) shorter than the rGR mRNA reported earlier. The deleted segment is located in exon 1 and encodes 13 repeated glutamine residues. Both the rGR and rGRβ mRNAs were quantitated by Northern blot hybridization using non-homologous glucocorticoid cDNA probes. Results showed that the rGR and rGRβ mRNAs were most abundant in the lung, the least abundant in the heart, and there were more rGR and rGRβ mRNAs in the kidney than in the liver. The identification of rGRβ may contribute to the understanding of the genomic or nongenomic effects of glucocorticoids.
The aim of the study was to establish the effect of the ovarian steroids: 17β-oestradiol (E2) and testosterone (T4) on OT-stimulated PGF2α and PGE2 secretion by bovine endometrial cells. The epithelial endometrial cells from days 14-18 of the oestrous cycle (10⁵/ml) were incubated in DMEM/Ham's F12 with 10% FCS (38°C, atmosphere of air and 5% CO₂) for 72-96 h and the last 24 h in DMEM/Ham's F12 with 0.1% BSA. In Exp.l, the doses of steroids used to study their effect on the secretion of PGF2α and PGE2 from endometrial cells stimulated by OT were determined. In Exp.2, the cells were pre-incubated for 30 min with selected doses of steroids: P4 (10⁻⁵ M), T4 (10⁻⁵ M), and E2 (10⁻⁸ M) and next for 4 d with: arachidonic acid (AA; 10⁻⁵ M), OT (10⁻⁷ M) and OT with each of these steroids. The concentration of PGE2 and PGFM -metabolite of PGF2α was determined by EIA. P4, T4, and E2 did not affect (P>0.05) the basal secretion of PGF2α and PGE2, but all the steroids inhibited (P<0.01) OT- stimulated PGF2α secretion. The stimulating effect of OT on PGE2 secretion was not affected by P4 and T4 (P>0.05). This data suggests that different cellular mechanisms exist for steroids affecting the secretion of both prostaglandins from endometrial cells. Moreover, we suggest that non-genomic effect of P4 on bovine endometrial cells is non-specific since the other steroids can impair the effect of OT on these cells. This effect of the steroids can directly modulate function of endometrial cells.
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