Physiological implications of pituitary trophic activity.
A complete inventory of pituitary trophic responses depends on precise estimates of mitotic activity and apoptotic events, and accurate characterization and quantification of pituitary cell subtypes irrespective of previous and current physiological demand. For a discrete structure that has been so extensively studied, it is disappointing but perhaps not surprising that none of these measures is available and therefore that the relative contributions to changes in the proportions of pituitary cellular subpopulations of trophic activity, differentiation of pluripotent cells and variations in the secretory profiles of apparently committed cells remain almost impossible to determine. To fully appreciate the extent of this dilemma, it should be remembered that conservative estimates of the proportion of corticotrophs in the rat anterior pituitary under basal conditions vary over twofold and that it is still not clear whether the apparent threefold increase in mammotrophs during pregnancy is the result of maturation of uncommitted cells, transdifferentiation of other cells such as somatotrophs, cell division, or a mixture of all three. Equally, while it has been known for some time that adrenalectomy results in a transient increase in anterior pituitary mitotic activity and appropriately timed supraphysiological glucocorticoid replacement with a wave of apoptosis, the precise identity of the cells involved in both of these responses is open to question. Thus, although many of the physiological stimuli associated with apparent changes in the proportions of pituitary cellular subpopulations are known, the precise mechanism of the changes and the consequences of the same remain obscure. This review summarizes the limited literature on pituitary trophic activity and asks what, if anything, analysis of pituitary trophic activity using current technology can tell us.
Levy
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University Research Centre for Neuroendocrinology, University of Bristol, Bristol Royal Infirmary, Marlborough Street, Bristol BS2 8HW, UK. a.levy@bris.ac.uk
D000311:Adrenal Glands / Q000502:physiology; D000375:Aging / Q000502:physiology; D000818:Animals; D002452:Cell Count; D002940:Circadian Rhythm; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D013007:Growth Hormone-Releasing Hormone / Q000494:pharmacology; D006801:Humans; D008297:Male; D008938:Mitosis / Q000187:drug effects / Q000502:physiology*; D010903:Pituitary Gland, Anterior / Q000166:cytology* / Q000502:physiology; D011247:Pregnancy / Q000502:physiology*; D011453:Prostaglandins / Q000494:pharmacology; D051381:Rats; D013961:Thyroid Gland / Q000502:physiology; D014667:Vasopressins / Q000494:pharmacology
D005938:Glucocorticoids; D011453:Prostaglandins; D014667:Vasopressins; D003346:Corticotropin-Releasing Hormone; D013007:Growth Hormone-Releasing Hormone; D004298:Dopamine