Ovariectomized and adrenalectomized rats kept in a reversed lighting system received either 5 µg (once) or 1 µg estradiol benzoate (EB) daily for 2, 3, or 4 days. These treatments induced sexual receptivity in a proportion of the rats, and α-melanocyte-stimulating hormone (α-MSH; 20 µg/rat s.c.) enhanced this proportion. In rats made receptive by 5 µg EB alone, the dopamine (DA) activity in preoptic area and arcuate nucleus was significantly reduced, but the α-MSH concentrations were not affected 54–56 h after EB treatment. Addition of α-MSH significantly increased the DA activity in ventromedial nucleus (VMN) and zona incerta, but this action is unlikely to account for its stimulation of sexual receptivity, since this effect was not blocked by 0.1 mg/kg haloperidol. Treatment with 100 mg/kg Dopa, which induces a presynaptic DA action, stimulated the receptivity in the EB-primed rats and selectively increased the concentration of α-MSH in the VMN, while 50 mg/kg Dopa plus 50 mg/kg benserazide, which induces a postsynaptic DA activity, inhibited the receptivity and reduced the α-MSH levels in the VMN. It is suggested that estradiol stimulates the female sexual receptivity by reducing the activity of a dopaminergic system in arcuate nucleus and preoptic area. α-MSH does not appear to affect this action, although it enhances the effect of steroids on the sexual behaviour, probably at the level of the VMN. The secretion of α-MSH may be under a dopaminergic inhibitory control, and the peptide may autoregulate its own secretion via this dopaminergic system which is sited in zona incerta and VMN.

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