Transitory Activation of the Central and Ovarian Norepinephrine Systems During Cold Stress-Induced Polycystic Ovary in Rats
Author
dc.contributor.author
Bernuci, M. P.
Author
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Leite, C. M.
es_CL
Author
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Barros, P.
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Author
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Kalil, B.
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Author
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Leoni, G. B.
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Author
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Bianco Borges, B. Del
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Author
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Franci, C. R.
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Author
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Szawka, R. E.
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Author
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Lara Peñaloza, Hernán
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Author
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Anselmo Franci, J. A.
es_CL
Admission date
dc.date.accessioned
2014-01-30T18:32:32Z
Available date
dc.date.available
2014-01-30T18:32:32Z
Publication date
dc.date.issued
2013
Cita de ítem
dc.identifier.citation
Journal of Neuroendocrinology 2013, 25, 23–33
en_US
Identifier
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doi: 10.1111/j.1365-2826.2012.02373.x
Identifier
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https://repositorio.uchile.cl/handle/2250/121811
General note
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Artículo de publicación ISI
en_US
Abstract
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Cold stress-induced ovarian sympathetic activation is associated with the development of ovarian
cysts in rats. Although we have hypothesised that polycystic ovary (PCO) features induced
by cold stress, as prevented by lesion of the noradrenergic nucleus locus coeruleus (LC), were a
result of the increased activity of the ovarian norepinephrine (NE) system, this was not evident
after 8 weeks of stress. In the present study, we investigated the temporal changes in LC and
ovarian NE activities and steroid secretion in rats exposed to single (SS) or repeated (RS) cold
stress. SS and 4 week (4W)-RS but not 8 week (8W)-RS increased c-Fos expression in the LC
and ovarian NE release. Plasma oestradiol, testosterone and progesterone levels tended to
increase in 4W-RS and were elevated in 8W-RS rats, which displayed PCO morphology. b-adrenergic
receptor agonist increased steroid hormone release from the ovary of unstressed (US) but
not from 8W-RS rats. To determine whether increased activity of noradrenergic system during
the initial 4 weeks of RS would be sufficient to promote PCO, rats were exposed to 4 weeks of
cold stress and kept in ambient temperature for the next 4 weeks (4W-RS/4W-US). Accordingly,
PCO morphology, increased steroid secretion and decreased ovulation rate were found in 4WRS/
4W-US rats, strengthening the hypothesis that the initial increase in NE release triggers the
development of PCO. The correlated activity of LC neurones and ovarian noradrenergic terminals
and the induction of PCO in 4W-RS/4W-US rats provide functional evidence for a major role of
NE in disrupting follicular development and causing the long-lasting endocrine abnormalities
found in stress-induced PCO.