ArticleEndocrinology2012
Uncovering novel reproductive defects in neurokinin B receptor null mice: closing the gap between mice and men.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 124 citations in OpenAlex.
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- Functional Integration of Different-Sex Gonad Transplants Into the Adult Mouse Hypothalamic Pituitary Gonadal Axis.Advanced biology · 2026Article
- The Biological Properties of theFoods (Basel, Switzerland) · 2025Article
- Kisspeptin and neurokinin B: roles in reproductive health.Physiological reviews · 2025Review
- New methods to investigate the GnRH pulse generator.Journal of molecular endocrinology · 2024Review
- Male animal sterilization: history, current practices, and potential methods for replacing castration.Frontiers in veterinary science · 2024Review
- Genetic variants underlying spermatogenic arrests in men with non-obstructive azoospermia.Cell cycle (Georgetown, Tex.) · 2023Article
- Hypothalamic Kisspeptin Neurons: Integral Elements of the GnRH System.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Polycystic ovary syndrome: pathophysiology and therapeutic opportunities.BMJ medicine · 2023Review
- Neuroendocrine control of gonadotropin-releasing hormone: Pulsatile and surge modes of secretion.Journal of neuroendocrinology · 2022Review
- Tachykinins, new players in the control of reproduction and food intake: A comparative review in mammals and teleosts.Frontiers in endocrinology · 2022Review
- Kisspeptin, Neurokinin B, and Dynorphin Expression during Pubertal Development in Female Sheep.Biology · 2021Article
- The Differential Roles for Neurodevelopmental and Neuroendocrine Genes in Shaping GnRH Neuron Physiology and Deficiency.International journal of molecular sciences · 2021Review
- Characterization of the Action of Tachykinin Signaling on Pulsatile LH Secretion in Male Mice.Endocrinology · 2021Article
- Loss-of-function variants in SEMA3F and PLXNA3 encoding semaphorin-3F and its receptor plexin-A3 respectively cause idiopathic hypogonadotropic hypogonadism.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Congenital ablation ofAmerican journal of physiology. Endocrinology and metabolism · 2021Article
- A Bioinformatics Model of Human Diseases on the Basis of Differentially Expressed Genes (of Domestic Versus Wild Animals) That Are Orthologs of Human Genes Associated with Reproductive-Potential Changes.International journal of molecular sciences · 2021Article
- Tachykinin Signaling Is Required for Induction of the Preovulatory Luteinizing Hormone Surge and Normal Luteinizing Hormone Pulses.Neuroendocrinology · 2021Article
- Tachykinin signaling in the control of puberty onset.Current opinion in endocrine and metabolic research · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Patients bearing mutations in TAC3 and TACR3 (which encode neurokinin B and its receptor, respectively) have sexual infantilism and infertility due to GnRH deficiency. In contrast, Tacr3(-/-) mice have previously been reported to be fertile. Because of this apparent phenotypic discordance between mice and men bearing disabling mutations in Tacr3/TACR3, Tacr3 null mice were phenotyped with close attention to pubertal development, estrous cyclicity, and fertility. Tacr3(-/-) mice demonstrated normal timing of preputial separation and day of first estrus, markers of sexual maturation. However, at postnatal d 60, Tacr3(-/-) males had significantly smaller testes and lower FSH levels than their wild-type littermates. Tacr3(-/-) females had lower uterine weights and abnormal estrous cyclicity. Approximately half of Tacr3(-/-) females had no detectable corpora lutea on ovarian histology at postnatal d 60. Despite this apparent ovulatory defect, all Tacr3(-/-) females achieved fertility when mated. However, Tacr3(-/-) females were subfertile, having both reduced numbers of litters and pups per litter. The subfertility of these animals was not due to a primary ovarian defect, because they demonstrated a robust response to exogenous gonadotropins. Thus, although capable of fertility, Tacr3-deficient mice have central reproductive defects. The remarkable ability of acyclic female Tacr3 null mice to achieve fertility is reminiscent of the reversal of hypogonadotropic hypogonadism seen in a high proportion of human patients bearing mutations in TACR3. Tacr3 mice are a useful model to examine the mechanisms by which neurokinin B signaling modulates GnRH release.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.