Direct and Indirect Effects of Sex Steroids on Gonadotrope Cell Plasticity in the Teleost Fish Pituitary

Abstract

The pituitary gland controls many important physiological processes in vertebrates, including growth, homeostasis, and reproduction. As in mammals, the teleost pituitary exhibits a high degree of plasticity. This plasticity permits changes in hormone production and secretion necessary to meet the fluctuating demands over the life of an animal. Pituitary plasticity is achieved at both cellular and population levels. At the cellular level, hormone synthesis and release can be regulated via changes in cell composition to modulate both sensitivity and response to different signals. At the cell population level, the number of cells producing a given hormone can change due to proliferation, differentiation of progenitor cells, or transdifferentiation of specific cell types. Gonadotropes, which play an important role in the control of reproduction, have been intensively investigated during the last decades and found to display plasticity. To ensure appropriate endocrine function, gonadotropes rely on external and internal signals integrated at the brain level or by the gonadotropes themselves. One important group of internal signals is the sex steroids, produced mainly by the gonadal steroidogenic cells. Sex steroids have been shown to exert complex effects on the teleost pituitary, with differential effects depending on the species investigated, physiological status or sex of the animal, and dose or method of administration. This review summarizes current knowledge of the effects of sex steroids (androgens and estrogens) on gonadotrope cell plasticity in teleost anterior pituitary, discriminating direct from indirect effects.

Keywords: adenohypophysis; androgen; brain; estrogen; gonads; pituitary; plasticity; steroids.

Figure 1

Schematic representation of the plasticity of the pituitary cells leading to a change in hormone production quantity. At the cellular level (A), the activity of the endocrine cell (hormone synthesis and release) can be modulated through the regulation of the number of different receptors thus changing sensitivity of the pituitary cells to inputs and/or by changing the hormone production rates. At the population level (B), the number of specific cell types can be modified changing the proportion of the different endocrine cell types in the pituitary.

Figure 2

Schematic representation of the mechanisms allowing a change in the number of a specific endocrine cell type in the pituitary: proliferation (mitosis) of endocrine cells themselves (A), proliferation of progenitor cells followed by their differentiation (B), transdifferentiation (phenotypic conversion) of other differentiated cells (C), and cell apoptosis (D). Grey cells represent undifferentiated progenitor cells and colored cells represent differentiated cells.

Figure 3

Schema of the neuroendocrine control of reproduction in teleosts, presenting the brain-pituitary-gonad (BPG) axis and the role of sex steroids in the retro-controls at the different levels.