Literature DB >> 6305633

Retarded development of castration cells after adrenalectomy or sham adrenalectomy.

G V Childs, D G Ellison, J R Lorenzen, T J Collins, N B Schwartz.   

Abstract

Castration produces hypertrophy of gonadotropes, stimulates a shift in storage patterns to cells that store LH and FSH together, and results in a significant rise in serum LH and FSH within 12 h. Adrenalectomy retards and attenuates this postcastration rise for 24 h (1, 2). In this study, we examined the effect of adrenalectomy on castration cell morphological development. The increased percentages of LH and FSH cells that are seen normally 24 h after castration were not seen if adrenalectomy or sham adrenalectomy was performed simultaneously. In fact, the percentages of LH cells were below control values. The expansion in the average area of LH and FSH cells was also retarded after simultaneous castration and adrenalectomy or sham adrenalectomy. The corticotrope population responded as expected to adrenalectomy and the surgical stress of castration, with an increase in the percentage and area of stained cells as well as partial degranulation. The serial sections showed no ACTH staining in gonadotropes after any of the surgical treatments. The gonadotropic storage patterns were altered, however. In castrated rats exposed to simultaneous adrenalectomy or sham adrenalectomy, the percentage of LH/FSH cells was reduced from 70% of gonadotropes in intact rats to 30%. Over 60% of the serially sectioned gonadotropes stored only one hormone, and these monohormonal cells tended to occur in clusters. Our experiments thus show that the gonadotropin storage pattern can be shifted with experimental manipulation. This may also reflect shifts in the site of hormone storage within a given cell. We suggest that adrenalectomy or sham adrenalectomy retards the postcastration rise in gonadotropins by preventing the immediate expansion of the granulated cell population and causing an apparent loss in the numbers of certain types of gonadotropes.

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Year:  1983        PMID: 6305633     DOI: 10.1210/endo-113-1-166

Source DB:  PubMed          Journal:  Endocrinology        ISSN: 0013-7227            Impact factor:   4.736


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