A population of non-luteinising hormone/non-adrenocorticotrophic hormone-positive cells in the male rat anterior pituitary responds mitotically to both gonadectomy and adrenalectomy.
The male rat anterior pituitary responds highly reproducibly to specific hormonal stimuli in terms of the extent and timing of mitotic and apoptotic (trophic) activity. The principal objective of the present study was to define the contribution of hormonally identifiable cells to the trophic responses to bilateral gonadectomy and bilateral adrenalectomy. The patterns of pituitary mitotic responses to adrenalectomy and gonadectomy are similar in amplitude and duration. When adrenalectomy and gonadectomy are combined, the amplitude of the pituitary mitotic response is unchanged. That is, the trophic stimuli are not additive. Dexamethasone-induced apoptosis in nascent cells is amplified not only by recent adrenalectomy, but also, and to an almost identical extent, by gonadectomy. Combining adrenalectomy and gonadectomy does not further enhance the size of the apoptotically-responsive cell population. Dual bromodeoxyuridine and adrenocorticotrophic hormone (ACTH) or luteinising hormone (LH) immunolabelling showed that more than 95% of all dividing cells are not and do not become positive for either of these hormones during the period of peak mitotic response. Following adrenalectomy, most newly-formed ACTH cells are derived from differentiation of pre-existing hormonally undifferentiated cells. Despite an overall increase in mitotic activity, there is no measurable increase in the number of LH immunopositive cells after gonadectomy. The nonadditive pituitary mitotic and apoptotic responses to adrenalectomy and gonadectomy strongly suggest that the same progenitor cell population responds mitotically to both. This weakens the prevailing view that hormonally identifiable cells with specific trophic profiles contribute significantly to pituitary cell subpopulation revision.
Nolan
L A
LA
Henry Wellcome Laboratories for Integrative, Neuroscience & Endocrinology, University of Bristol, Bristol, UK. lesley.a.nolan@bris.ac.uk
Levy
A
A
D000311:Adrenal Glands / Q000502:physiology*; D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D002369:Castration; D049109:Cell Proliferation / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology; D007150:Immunohistochemistry; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D008938:Mitosis / Q000502:physiology*; D008940:Mitotic Index; D010903:Pituitary Gland, Anterior / Q000166:cytology* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013234:Stem Cells / Q000187:drug effects / Q000502:physiology; D013268:Stimulation, Chemical; D013737:Testis / Q000502:physiology*
D005938:Glucocorticoids; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D007986:Luteinizing Hormone