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G. Bono, R. Gaiani and E. Seren

Summary. The effect of PGF-2α on LH release in immature ewes was studied. One intramuscular injection of PGF-2α induced LH release 36–72 h after treatment in 3/4 ewes. The LH variations were not associated with changes in the plasma concentration of progesterone and oestrogens. These results suggest that the LH release in immature ewes is due to PGF-2α acting at central structures.

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M. Mattioli, F. Conte, Giovanna Galeati and E. Seren

Summary. Six lactating sows were injected through an indwelling vena cava cannula with naloxone (2·5 mg/kg body weight) on Day 15 post partum. Blood samples were collected through the cannulas at 10-min intervals for 8 h before and 10 h after naloxone administration. Plasma prolactin and LH concentrations were measured by radioimmunoassay. Naloxone caused a marked suppression of plasma prolactin concentrations lasting 4–6 h. LH concentrations were also affected by naloxone: LH rose to reach maximum values 20–50 min after naloxone treatment. Pretreatment values were recorded 200–300 min after the treatment. These results indicate that endogenous opioids are involved in causing the endocrine patterns occurring during lactation, i.e. high prolactin and low LH concentrations.

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E. Seren, C. Tamanini, R. Gaiani and G. Bono

Summary. Plasma concentrations of progesterone and 17α-hydroxyprogesterone were high in the 2nd and 3rd months of gestation, but 20α-dihydroprogesterone increased from a level of 2 ng/ml, during the first 3 months, to 10–15 ng/ml during months 5–10, to reach 80–120 ng/ml during the last 30 days before foaling.

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M. Mattioli, G. Galeati, B. Barboni and E. Seren

Intracellular concentrations of cyclic AMP (cAMP) were measured in pig oocytes maturing in vivo or in vitro. Maturation in vivo was induced with 500 iu hCG administered to gilts treated with pregnant mares' serum gonadotrophin (PMSG). Although PMSG did not affect cAMP concentrations (basal values, 1.69 ± 0.28 fmol per oocyte), hCG induced a transient rise (8.86 ± 1.15 fmol per oocyte 12 h after hCG injection). Similarly, the cAMP concentration rose in oocytes maturing in vitro if the oocytes (surrounded or not by cumulus cells) were co-cultured with the follicle wall in the presence of LH. The same increase in cAMP was obtained when denuded oocytes were co-cultured with mural granulosa cells. Theca cells exhibited only a moderate activity, while cumulus cells were totally ineffective. Granulosa cells exposed to LH lost their stimulating influence after 24 h of culture. In the presence of FSH, cAMP production by the oocyte was unaffected by any type of follicle cell. The role of cAMP in the control of oocyte maturation was investigated using dibutyryl cAMP. The presence of dibutyryl cAMP prevented the resumption of meiosis in a dose-dependent manner, but when it was present during the first 12 h of culture only, meiotic progression was accelerated (0 versus 47% of oocytes had germinal vesicles in groups treated with dibutyryl cAMP and control groups, respectively, after 24 h of culture). The results demonstrate that: (i) cAMP concentrations increase transiently in oocytes before the resumption of meiosis; (ii) increased concentrations of cAMP depend on the stimulation of oocyte adenylyl cyclase, possibly by a soluble factor produced by follicle cells exposed to LH; (iii) the increase in cAMP is probably confined to the first 10–20 h of maturation owing to the progressive reduction of the stimulating influence of LH-treated somatic cells; and (iv) a high concentration of cAMP throughout maturation maintains meiotic arrest and a transient increase may facilitate meiosis.

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G Galeati, M Spinaci, N Govoni, A Zannoni, P Fantinati, E Seren and C Tamanini

The aim of this study was to investigate the effect of fasting on both vascular endothelial growth factor (VEGF) production and VEGF mRNA expression in growing ovarian follicles (>5 mm in diameter) from gilts at 48 h after equine chorionic gonadotrophin (eCG) treatment. The concentrations of VEGF and albumin were measured in the follicular fluid of single follicles, and VEGF mRNA was determined in the follicle wall. Fasting resulted in a significant increase in VEGF concentrations in follicular fluid (20.64+/-0.72 versus 10.79+/-0.86 ng ml(-1), P<0.001), but it did not affect the total amount of VEGF mRNA in the follicle wall compared with that of fed animals. However, VEGF mRNA in the theca and granulosa compartments increased and decreased, respectively, compared with that of fed animals. The concentrations of albumin measured in follicular fluid as an index of vessel permeability were higher in fasted than in animals fed normally, most likely as a result of the increased VEGF production. Follicular steroidogenesis was impaired in fasted animals. Progesterone was the most abundant steroid in the follicular fluid and oestradiol was present in lower concentrations, thus indicating an alteration in the steroidogenic enzymatic cascade. In conclusion, fasting induces an increase in both VEGF production and vessel permeability. Such a reaction is unable under severe food deprivation to preserve follicle function, but may represent a mechanism that regulates blood vessel extension and distribution in relation to tissue requirements and availability of systemic nutrient.