We report the effects that sectioning the superior ovarian nerve of infantile female rats has on their follicular development at different ages before puberty. Compared with the control group, sham-operated animals showed a significant decrease in the number of measured follicles in right and left ovaries, although no difference in the follicular atresia ratio was observed. Animals with a sectioned left superior ovarian nerve (SON), killed 12 days after surgery had a significant increase in the number of follicles in the ovaries. Most of the follicles were atretic. Sectioning the right SON induced contrasting effects in the ovaries of animals killed 4 and 16 days after surgery. Rats with a denervated (right) ovary showed a decrease in the number of follicles and a greater number of atretic follicles compared with the control group, whereas the innervated (left) ovary showed an increase in measured follicles compared with the control group. Bilateral sectioning had no apparent effect on the total number of follicles measured, although an increased number of atretic follicles in both ovaries was observed. Animals with a unilateral section of the SON, killed 8 and 12 days after surgery, showed a decrease in serum concentrations of estradiol. In turn, animals killed 16 days after surgery showed a significant increase in estradiol and a decrease in the progesterone serum concentration. These results suggest that sympathetic innervation of the ovary via the SON has a stimulatory role in the regulation and differentiation of follicular growth.
C Moran, L Morales, U Quiroz and R Dominguez
E J Agnew, A Garcia-Burgos, R V Richardson, H Manos, A J W Thomson, K Sooy, G Just, N Z M Homer, C M Moran, P J Brunton, G A Gray and K E Chapman
Endogenous glucocorticoid action is important in the structural and functional maturation of the fetal heart. In fetal mice, although glucocorticoid concentrations are extremely low before E14.5, glucocorticoid receptor (GR) is expressed in the heart from E10.5. To investigate whether activation of cardiac GR prior to E14.5 induces precocious fetal heart maturation, we administered dexamethasone in the drinking water of pregnant dams from E12.5 to E15.5. To test the direct effects of glucocorticoids upon the cardiovascular system we used SMGRKO mice, with Sm22-Cre-mediated disruption of GR in cardiomyocytes and vascular smooth muscle. Contrary to expectations, echocardiography showed no advancement of functional maturation of the fetal heart. Moreover, litter size was decreased 2 days following cessation of antenatal glucocorticoid exposure, irrespective of fetal genotype. The myocardial performance index and E/A wave ratio, markers of fetal heart maturation, were not significantly affected by dexamethasone treatment in either genotype. Dexamethasone treatment transiently decreased the myocardial deceleration index (MDI; a marker of diastolic function), in control fetuses at E15.5, with recovery by E17.5, 2 days after cessation of treatment. MDI was lower in SMGRKO than in control fetuses and was unaffected by dexamethasone. The transient decrease in MDI was associated with repression of cardiac GR in control fetuses following dexamethasone treatment. Measurement of glucocorticoid levels in fetal tissue and hypothalamic corticotropin-releasing hormone (Crh) mRNA levels suggest complex and differential effects of dexamethasone treatment upon the hypothalamic–pituitary–adrenal axis between genotypes. These data suggest potentially detrimental and direct effects of antenatal glucocorticoid treatment upon fetal heart function.