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V. Gayrard, B. Malpaux, and J. C. Thiéry


Giving a subcutaneous oestradiol implant during anoestrus to ovariectomized ewes inhibits pulsatile LH secretion. This effect results from an increased negative feedback of oestradiol and depends on the synthesis of biogenic amines, mainly from the mediobasal hypothalamus. In the present study, we examined the effect of oestradiol on the extracellular levels of amines and their metabolites. Eight ewes were sampled by microdialysis from the lateral retrochiasmatic area, including the dopaminergic A15 nucleus, during inhibition of LH secretion by long days. Two dialysis sessions were carried out on each ewe; one after a 10-day oestradiol treatment and the other one after 10 days without oestradiol treatment. Half of the ewes were first oestradiol-treated then untreated, the other half received the treatment in the reverse order.

Oestradiol caused a decline in pulsatile LH secretion without affecting the secretion of prolactin. This steroid also led to a significant increase in the levels of amine metabolites: 3,4-dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindolacetic acid in the extracellular medium. These results demonstrate the effect of oestradiol on aminergic activity as related to changes in hormonal secretions during long days (16 h of light per 24 h). Thus our data support the hypothesis that amines inhibit gonadotrophic secretion during anoestrus in the ewe and suggest that there is an activation of the aminergic neurones from the retrochiasmatic area in this regulatory mechanism.

Journal of Endocrinology (1992) 135, 421–430

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F Bertrand, J Thiery, S Picard, and B Malpaux

In ewes, photoperiod modulates LH release and dopaminergic terminals in the median eminence (ME) have a critical role in the establishment of long-day inhibition of LH secretion. This study was undertaken to determine the type of dopaminergic receptors, D1-like or D2-like, that mediate the action of dopamine on LH secretion at the ME level in this situation. This was assessed, in ovariectomized and estradiol-treated ewes, with the use of reverse microdialysis in the ME in three experiments: first, when LH secretion was stimulated by short days, by determining the response to three doses (0.01, 0.1 or 1 mg/ml) of a D1-like (SKF38393) and a D2-like (quinpirole) agonist; secondly, during early long-day inhibition of LH secretion, by determining the ability of SKF38393 and quinpirole (1 mg/ml) to mimic the inhibitory effects of dopamine, after a blockade of its synthesis with alpha-methyl-para-tyrosine (alphaMPT; 2 mg/ml); and thirdly, during early long-day inhibition of LH secretion, by determining the response to three doses (0.009, 0.09 or 0.9 mg/ml) of a D1-like (SCH23390) and a D2-like (sulpiride) antagonist. In none of the conditions was effect of the D1-like analogs on LH secretion found, compared with the control treatments. In contrast, the D2-like analogs caused changes in LH secretion. First, with short days, quinpirole in the highest dose significantly reduced mean LH concentration (P<0.05) and LH pulse frequency (P<0.01). Secondly, with long days, addition of quinpirole to alphaMPT caused a significant decrease in LH secretion relative to alphaMPT alone (P<0.05). Thirdly, with long days, sulpiride at the highest dose significantly increased mean LH concentration (during the first 3 h of treatment, P<0.05) and LH pulse frequency (P<0.05). Prolactin secretion was also determined in these experiments, and D2-like agonist and antagonist caused an inhibition and a stimulation of prolactin secretion, respectively. These results demonstrate that, in the ME, inhibitory action of dopamine on LH secretion, critical for the initiation of long-day-induced inhibition, is mediated by D2-like, not D1-like, dopaminergic receptors.

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J Gallegos-Sanchez, S Picard, B Delaleu, B Malpaux, and J C Thiéry


In the ewe, the inhibition of pulsatile LH secretion by oestradiol during long days depends on dopaminergic activity and could involve amino acid transmitters. In the first experiment of the present study we observed the changes in LH secretion in ovariectomised ewes under long days immediately after subcutaneous implantation of oestradiol (peripheral treatment). In the second experiment, in order to identify the site of action of oestradiol, we observed the LH changes following intracerebral infusion of oestradiol through a microdialysis membrane (central treatment) within the preoptic area, the mediobasal hypothalamus (MBH) or the retrochiasmatic area (RCh) and measured amino acids and catecholaminergic transmitters and metabolites within the dialysates. With peripheral treatment, the amplitude, the nadir and the area under the LH pulse curve decreased within 4 to 8 h of the insertion of a subcutaneous oestradiol implant. After 18 h, the amplitude and the area under the pulses increased, as well as the intervals between pulses (from 49·9 ± 1·4 min to 75·6 ± 5·9 min). With central oestradiol treatment, LH changes were similar whatever the site of oestradiol infusion, suggesting either multiple sites of action or diffusion between structures. Twenty hours after the beginning of intracerebral oestradiol treatment, the amplitude and the area under the pulses increased, as did the interval between LH pulses (from 49·5 ± 4·1 min to 73·2 ± 14·2 min). Comparison of peripheral with central oestradiol treatment suggested that the long-lasting decrease in the nadir, as well as the transitory decrease in the amplitude and area, before 18 h in experiment 1 are reflections of hypophysial effects. In contrast, the increases in amplitude and area under the LH pulse curve seen 18–20 h after oestradiol in the two experiments could be due to the higher amplitude of LHRH pulses, as a result of an early stimulatory effect of oestradiol. After central oestradiol infusion, there was a decline in the concentration in the dialysate of two metabolites of dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid in the RCh, suggesting an early inhibition of monoamine oxidase by the steroid. During the inhibition of LH pulsatility the concentration of γ-aminobutyric acid in the dialysate from the RCh and the MBH increased, suggesting the participation of this transmitter in the changes induced by oestradiol under long days.

Journal of Endocrinology (1996) 151, 19–28

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A Gomez Brunet, A Gomez Brunet, B Malpaux, A Daveau, C Taragnat, and P Chemineau

Genetic variability in plasma melatonin concentrations in ewes results from variations in pineal weight. This study investigated whether it is due to a difference in the number of pinealocytes, or in their size. Two groups of lambs were assigned before birth to being extremes (18 High and 21 Low) by calculating their genetic value on the basis of the melatonin concentrations of their parents. Lambs were bled from 1 week of age until 14 weeks of age. Pineal gland, brain and pituitary weights, length and width of the brain, and length of the hypothalamus were recorded. A significant effect (ANOVA) of genetic group (P<0.05) and age (P<0.05) was detected on mean nocturnal plasma melatonin concentrations, as soon as the first week after birth (mean +/- s.e.m.; High: 51.7 +/- 10.7 vs Low: 31.9 +/- 3.2 pg/ml). There was no difference between the two genetic groups in any of the brain parameters measured, but the pineal glands of the High group were heavier and contained significantly more pinealocytes (High: 27.8 +/- 2.4 vs Low: 21.0 +/- 2.4 x 10(6); P<0.05) than those in the Low group. The mean size of pinealocytes did not differ between the two genetic groups. Thus, the genetic variability in nocturnal plasma melatonin concentrations in sheep is expressed by 1 week of age and higher levels of secretion are the consequence of larger pineal glands containing a greater number of pinealocytes.

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B. Malpaux, J. E. Robinson, N. L. Wayne, and F. J. Karsch


Three experiments were conducted to evaluate the role that the increasing day lengths of late winter and spring play in timing the breeding season of the Suffolk ewe. In the first experiment, ewes were denied their normal complement of increasing day length by maintaining them on the photoperiod experienced at the winter solstice. This prevented the breeding season from occurring the subsequent autumn. In the second experiment, ewes were exposed to increases in day length at different time-intervals after the winter solstice: the normal time, later than normal or earlier than normal. Once the summer solstice photoperiod was reached, it was maintained until the end of the study. When increasing photoperiod was provided early, the breeding season was advanced; when it was provided late, reproduction was delayed. In the third experiment, ewes were exposed to a continuously increasing photoperiod matching the maximal rate of rise in natural conditions; this treatment was begun on the spring equinox and continued until mid-autumn. The steadily increasing photoperiod did not alter the time of reproductive onset in the autumn.

These findings support the following conclusions for timing of the breeding season of the Suffolk ewe. (1) The lengthening photoperiod between the winter and summer solstices is required for the occurrence of the breeding season in the autumn. (2) The time of initial exposure to this lengthening photoperiod provides an important cue for determining when the reproductive period occurs. (3) The time of onset of the breeding season does not depend upon the decreasing photoperiod after the summer solstice, nor does it require the photoperiod to stop increasing as the summer solstice approaches. These findings have been incorporated into a conceptual model for temporal regulation of the annual reproductive cycle of the ewe. An important component of this model is a critical role for increasing photoperiod to initiate a process in the late winter–spring which ultimately leads to an obligatory reproductive onset in the autumn.

Journal of Endocrinology (1989) 122, 269–278