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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