Influence of perinatal androgen on the sexually dimorphic distribution of tyrosine hydroxylase-immunoreactive cells and fibers in the anteroventral periventricular nucleus of the rat
Abstract
Recently we reported that the anteroventral periventricular nucleus (AVPv) of the preoptic region contains a dramatic sexual dimorphism in the distribution of tyrosine hydroxylase-(TH-)immunoreactive cells and fibers in the rat. This sexual dimorphism appears to be due to a greater density of dopaminergic fibers, and a larger number of dopaminergic cell bodies, in the AVPv of the female. In the present study we used an indirect immunohistochemical method to evaluate the distribution of TH-immunoreactive cell bodies and fibers, and of dopamine-beta-hydroxylase-(DBH-)stained fibers, in the AVPv of female rats that were treated with testosterone propionate (TP) perinatally or postnatally, or were left untreated. All of the postnatally TP-treated animals failed to show a phasic pattern of luteinizing hormone (LH) secretion in response to estrogen and progesterone injections. Both the perinatally and postnatally TP-treated females had polyfollicular ovaries that lacked corpora lutea at the time of gonadectomy. Perinatal TP exposure resulted in what appears to be a complete masculinization of both the number of TH-stained cells and the density of TH-stained fibers in the AVPv. The number of TH-stained cells in the postnatally TP-treated females was also completely masculinized, although the density of TH-stained fibers did not appear to be altered significantly. Gonadectomy resulted in a moderate increase in the density of TH-stained fibers in adult males, and did not significantly…
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Because AVP/OT and the dopaminergic pathways they feed into are heavily influenced by sex steroids across the lifespan, their sexually dimorphic ontogeny and function may be particularly vulnerable to endocrine disruption.
“Because AVP/OT and the dopaminergic pathways they feed into are heavily influenced by sex steroids across the lifespan (50–59), it is highly plausible that their sexually dimorphic ontogeny and function may be particularly vulnerable to endocrine disruption.”
From Endocrine Disruption of Vasopressin Systems and Related Behaviors (2017) · cites this paper as [50]
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- Authors
- Simerly, R. B., Swanson, L. W., Handa, R. J., & Gorski, R. A.
- Affiliations
- University of California, Los Angeles (US)
- Salk Institute for Biological Studies (US)
- Venue
- Neuroendocrinology
- Publisher
- S. Karger AG
- Published
- 2008-03-28
- Volume
- 40
- Issue
- 6
- Pages
- 501-510
- ISSN
- 0028-3835 (ISSN-L)
- 1423-0194
- OpenAlex
- W2084737190
- Cited by
- 188
- References
- 0
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 5 · 2014: 6 · 2013: 7 · 2012: 8
- FWCI
- 4.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS-16686.)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-01182, HD-07228, T32HD007228)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- testosterone propionate, sexual dimorphism, anteroventral periventricular nucleus, preoptic area, tyrosine hydroxylase, dopaminergic neurons, dopamine beta-hydroxylase, masculinization, gonadectomy, luteinizing hormone secretion, gonadotropin secretion, ovarian follicle development, critical period, sex reversal
- MeSH terms
- Animals, Animals, Newborn, Castration, Dopamine beta-Hydroxylase, Female, Fetus, Fluorescent Antibody Technique, Histocytochemistry, Male, Nerve Fibers, Preoptic Area, Sex Differentiation, Testosterone, Tyrosine 3-Monooxygenase, Rats
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