title: Testicular recrudescence in the male black bear (Ursus americanus): changes in testicular luteinizing hormone-, follicle-stimulating hormone-, and prolactin-receptor ribonucleic acid abundance and dependency on prolactin.
abstract: Testicular recrudescence in male black bears (Ursus americanus) is initiated in January and completed in May. The goals of this study in the black bear were to determine 1) if testicular abundance of LH-receptor (LHr), FSH-receptor (FSHr), and prolactin-receptor (PRLr) mRNA changes during recrudescence; 2) if these changes in mRNA abundance are associated with changes in serum LH, PRL, and testosterone (T) concentrations; and 3) if the spring increase in serum PRL concentrations is required for testicular recrudescence. Serum was obtained monthly from nine male bears for 2 yr, except in July and August. To suppress endogenous PRL, four bears were treated with Parlodel LAR, 50 mg per 70 kg body weight, monthly from January through May, whereas five bears served as controls. Testicular biopsies were obtained in January, March, and May and analyzed for LHr, FSHr, and PRLr mRNA abundance using reverse transcriptase-competitive polymerase chain reaction. The LHr and PRLr mRNA abundance was low in January, increased in March, and remained high in May, whereas the FSHr mRNA abundance remained constant. Serum concentrations of PRL and T increased in March, coincident with the increase in testicular LHr and PRLr mRNA abundance. Suppression of serum PRL concentrations during testicular recrudescence 1) prevented the increase in testicular LHr and PRLr mRNA abundance observed among control bears in March, 2) lowered serum T concentrations in March and April, and 3) resulted in reduced testis size in May. We conclude that testicular LHr and PRLr mRNA are seasonally regulated, and that PRL has a role in testicular recrudescence in the black bear.
authors.affiliation: Department of Animal Sciences, University of Illinois, Urbana, Illinois 61801, USA.
authors.forename: L A
authors.initials: LA
authors.lastname: Howell-Skalla
authors.forename: D
authors.initials: D
authors.lastname: Bunick
authors.forename: R A
authors.initials: RA
authors.lastname: Nelson
authors.forename: J M
authors.initials: JM
authors.lastname: Bahr
mesh_terms: D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D011388:Prolactin / Q000037:antagonists & inhibitors / Q000097:blood / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D011962:Receptors, FSH / Q000235:genetics*; D011974:Receptors, LH / Q000235:genetics*; D011981:Receptors, Prolactin / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012621:Seasons; D013737:Testis / Q000502:physiology*; D013739:Testosterone / Q000097:blood; D001503:Ursidae / Q000502:physiology*
chemical_list: D006727:Hormone Antagonists; D012333:RNA, Messenger; D011962:Receptors, FSH; D011974:Receptors, LH; D011981:Receptors, Prolactin; D001971:Bromocriptine; D013739:Testosterone; D011388:Prolactin; D007986:Luteinizing Hormone