The sequential actions of estradiol and progesterone (P) in the arcuate nucleus of the hypothalamus (ARH) are known to facilitate sexual receptivity. Β-endorphin (β-END) neurons express classical progesterone receptors (PGRs), and infusion of P into estradiol benzoate (EB) primed animals induces sexual receptivity within 30 minutes. ARH β-END additionally express Src kinase (Src), which can complex with and signal through PGR-B to facilitate sexual receptivity. Further interactions with PGR and Src include dopamine receptor 1 (D1), as bilateral infusion of dopamine agonist into the ARH rapidly facilitates sexual receptivity within 30 minutes. PGR, Src, and D1 signaling appears to be interdependent. Antagonism of any of these receptors inhibits sexual receptivity, which cannot be induced through subsequent treatment with either P, Src activator, or D1 agonist. I tested the hypothesis that hormonally-dependent PGR, Src, and D1 are expressed and colocalized within β-END neurons in the ARH, and these receptors are within close proximity of each other. To test this, I used double and triple label immunohistochemistry to visualize β-END, PGR, Src, and D1 expression in the ARH in oil, EB, and EB+P treated animals. Duolink proximity ligation assay was used to assess whether two proteins were in close proximity to each other in oil and EB treated animals. PGR and Src are consistently upregulated through treatment with either EB or EB with subsequent P treatment. β-END and D1 expression both appear to be independent of hormone treatment. PGR was found to be within close proximity of both Src and D1. These results support my hypothesis that PGR, Src, and D1 coexpression within ARH β-END neurons and are within close proximity.