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Zusammenfassung:
Urocortin 2 (UCN2) is a neuropeptide of the CRH family, involved in homeostatic mechanisms, the stress response, and control of anxiety. To
elucidate the effects of UCN2 on steroidogenesis, we developed a mouse
model that allows a Cre recombinase-determined conditional
overexpression of UCN2 (UCN2-COE). In these mice SF1-Cre-driven
overexpression of UCN2 was restricted to the adrenal glands, gonads, and
parts of the hypothalamus. UCN2-COE animals of both sexes revealed
significantly higher plasma UCN2 levels and significantly higher UCN2
expression levels in the adrenals and ovaries. In contrast, the baseline
expression of UCN2 was already high in the testes of control mice with
no further increase achievable in UCN2-COE animals. Adrenal
steroidogenesis of UCN2-COE animals was investigated under baseline
conditions, upon an ACTH stimulation test, and following a restraint
stress test. A tendency toward lower expression of steroidogenic enzymes
was detectable in UCN2-COE animals of both sexes with slight differences
between males and females. A similar reduction in the expression levels
of the final steps of ovarian steroidogenesis, accompanied by reduced
plasma estradiol levels, was observed in female UCN2-COE animals. Thus,
adrenal UCN2 overexpression resulted in down-regulation of adrenal
steroidogenesis, suggesting a reduction in the stress response in the
mouse (stress coping behavior). Similarly, UCN2 overexpression in the
ovaries caused a decrease in steroidogenesis and reduction of follicles
that had undergone ovulation. Nevertheless, this finding was not
associated with reduced fertility.
