Estrogen receptor-alpha (ERα) dimerizes with unliganded progesterone receptor (PR) in target tissues to trigger genomic and non-genomic effects. In ovariectomized rats the antiprogestin RU486 or antisense nucleotides against PR antagonize estradiol-induced sexual receptivity. We determined the relevance of unliganded PR for the expression of estrogen-dependent scent-marking (chinning) and sexual receptivity by injecting RU486 to: a) ovariectomized (ovx) rabbits given estradiol benzoate (EB; 5 μg/day); b) intact rabbits. Chinning and lordosis were quantified in ovx animals before (5 days; baseline) and during hormonal treatments: EB + RU486 (20 mg/day; n = 18) or EB + vehicle (n = 18). On treatment day 4 LQ (lordosis quotient) increased in both groups, relative to baseline (mean ± se): LQ = 1 ± 5 (baseline) vs 25 ± 21 (EB + RU486) and 2 ± 6 (baseline) vs 37 ± 29 (EB + vehicle). On day 9 LQ values were: 22 ± 23 (EB + RU486) and 54 ± 39 (EB + vehicle). Chinning increased only in the EB + vehicle group (day 9 = 55 ± 46 vs baseline = 17 ± 20 marks/10 min). In intact rabbits one RU486 injection: reduced the LQ from 72 ± 7to 36 ± 8 five hrs later, increased the latency to receive first ejaculation from 45 to 98 s, and decreased the number of ejaculations received in the test from 3 to 2 but did not modify mounting latency or chinning. Results support a participation of unliganded PR for the induction (ovx) and maintenance (intact) of rabbit estrous behavior by estrogens.