Estradiol benzoate potentiates neuroactive steroids' effects on pain sensitivity.

摘要: Abstract Progesterone (P), its metabolites, and other neuroactive steroids alter pain thresholds consistent with their efficacies at modulating γ-aminobutyric acid (GABAA) receptor complexes. We investigated whether estradiol benzoate (EB) potentiates low dosages of steroids' effects on pain. Subcutaneous EB (10 μg) or sesame oil vehicle was administered to ovariectomized Long-Evans rats (n = 40) 48 h before intracerebroventricular (ICV) infusion a steroid (0.0, 0.1, 0.3, 0.5 in cyclodextrin vehicle. Neuroactive (listed from greatest least efficacious GABAA complexes) were THP [5α-pregnan-3α-ol-20-one], THDOC [5α-pregnan-3α, 21-diol-20-one], DHP [5α-pregnan-3,20-dione], P [4-pregnen-3,20-dione], DHEAS [5-androsten-3β-ol-17-one sulfate]. Pain sensitivity assessed using the radiant heat tail-flick method 20 60 min following infusion. Estradiol interacted latencies. In particular, potentiated antinociceptive effect by significantly increasing latencies above those non-EB-treated animals. A similar pattern increased occurred EB-primed animals that received THDOC. less consistently altered threshold P, which is effective GABAergic activity. Conversely, nociceptive neurosteroid DHEAS, an allosteric antagonist complexes, decreasing EB- compared vehicle-primed rats. Thus, priming threshold.