Hyperprolactinaemia abolishes sensitivity of stria terminalis neurones to testosterone.
Hyperprolactinaemia was induced in castrated, testosterone-treated male rats using ectopic pituitary grafts under the kidney capsules. After 6 weeks the absolute refractory period of stria terminalis neurones in these animals did not differ significantly from long-term castrated rats (mean = 1.72 vs 1.69 ms) in spite of the presence of normal testosterone concentrations. Gonadally intact animals, and sham-operated castrated animals treated with testosterone, showed by comparison the characteristic significantly shorter absolute refractory period normally associated with testosterone stimulation (mean = 1.15 and 1.08 ms respectively). These results provide the first demonstration that hyperprolactinaemia can abolish central sensitivity to testosterone.
D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002369:Castration; D004594:Electrophysiology; D007031:Hypothalamus / Q000502:physiology; D008297:Male; D009431:Neural Conduction / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010902:Pituitary Gland / Q000637:transplantation; D011388:Prolactin / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains; D012032:Refractory Period, Electrophysiological / Q000187:drug effects*; D013739:Testosterone / Q000097:blood / Q000494:pharmacology*
D013739:Testosterone; D011388:Prolactin