The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
Regulation of Arcuate Neurons Coexpressing Kisspeptin, Neurokinin B, and Dynorphin by Modulators of Neurokinin 3 and κ-Opioid Receptors in Adult Male Mice
Open accessAbstract
Pulsatile GnRH release is essential to fertility and is modulated by gonadal steroids, most likely via steroid-sensitive afferents. Arcuate neurons coexpressing kisspeptin, neurokinin B (NKB), and dynorphin (KNDy neurons) are steroid-sensitive and have been postulated to both generate GnRH pulses and mediate steroid feedback on pulse frequency. KNDy neurons are proposed to interact with one another via NKB and dynorphin to activate and inhibit the KNDy network, respectively, and thus alter kisspeptin output to GnRH neurons. To test the roles of NKB and dynorphin on KNDy neurons and the steroid sensitivity of these actions, targeted extracellular recordings were made of Tac2(NKB)-GFP-identified neurons from castrate and intact male mice. Single-cell PCR confirmed most of these cells had a KNDy phenotype. The neurokinin 3 receptor (NK3R) agonist senktide increased action potential firing activity of KNDy neurons. Dynorphin reduced spontaneous KNDy neuron activity, but antagonism of κ-opioid receptors (KOR) failed to induce firing activity in quiescent KNDy neurons. Senktide-induced activation was greater in KNDy neurons from castrate mice, whereas dynorphin-induced suppression was greater in KNDy neurons from intact mice. Interactions of dynorphin with senktide-induced activity were more complex; dynorphin treatment after senktide had no consistent inhibitory effect, whereas pretreatment with dynorphin decreased senktide-induced activity only in KNDy neurons from intact but not castrate mice. These data suggest dynorphin-mediated inhibition of senktide-induced activity requires gonadal steroid feedback. Together, these observations support the hypotheses that activation of NK3R and KOR, respectively, excites and inhibits KNDy neurons and that gonadal steroids modulate these effects.
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“Complete coexpression of kisspeptin, NKB and dynorphin is not always found (Hrabovszky et al., 2012; Navarro et al., 2011), but this issue is complicated by limitations in the sensitivity of detection (Ruka et al., 2013) and differential expression depending on developmental stage (Gill et al., 2012) or physiological state of the animal (Foradori et al., 2005; Navarro et al., 2011; Rance and Bruce”
From Modulation of body temperature and LH secretion by hypothalamic KNDy (kisspeptin, neurokinin B and dynorphin) neurons: A novel hypothesis on the mechanism of hot flushes (2013) · cites this paper as Ruka et al., 2013
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Cites
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Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54
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Rance, N. E., Dacks, P. A., Mittelman-Smith, M. A., Romanovsky, A. A., & Krajewski-Hall, S. J. (2013) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2013.07.003 · Cited by 380
The Gonadotropin-Releasing Hormone Pulse Generator
Herbison, A. E. (2018) · Endocrinology · doi:10.1210/en.2018-00653 · Cited by 261
Qiu, J., Nestor, C. C., Zhang, C., Padilla, S. L., Palmiter, R. D., Kelly, M. J., & Rønnekleiv, O. K. (2016) · eLife · doi:10.7554/elife.16246 · Cited by 199
“…shown that dynorphin and k-opioid receptor agonist U69,593 inhibit the activity of spontaneously firing Kiss1ARH neurons, although it has not been established whether this was a postsynaptic or presynaptic action on excitatory input to Kiss1ARH neurons (de Croft et al., 2013; Ruka et al., 2013).”
BackgroundMoore, A. M., Coolen, L. M., Porter, D. T., Goodman, R. L., & Lehman, M. N. (2018) · Endocrinology · doi:10.1210/en.2018-00389 · Cited by 190
Neuroendocrine control of gonadotropin‐releasing hormone: Pulsatile and surge modes of secretion
Goodman, R. L., Herbison, A. E., Lehman, M. N., & Navarro, V. M. (2022) · Journal of Neuroendocrinology · doi:10.1111/jne.13094 · Cited by 157
Metadata
- Authors
- Ruka, K. A., Burger, L. L., & Moenter, S. M.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Moenter, Suzanne M.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2013-08-01
- Volume
- 154
- Issue
- 8
- Pages
- 2761-2771
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC3713217
- OpenAlex
- W2001560124
- Cited by
- 150
- References
- 72
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 12 · 2023: 12 · 2022: 13 · 2021: 15 · 2020: 8 · 2019: 12 · 2018: 13 · 2017: 7 · 2016: 8 · 2015: 9 · 2014: 21 · 2013: 5
- FWCI
- 17.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01 HD34860, R01HD034860)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- kisspeptin, neurokinin B, dynorphin, KNDy neurons, arcuate nucleus, neurokinin-3 receptor, kappa opioid receptor, senktide, gonadal steroid feedback, pulsatile GnRH release, neuronal firing, castration
- MeSH terms
- Animals, Arcuate Nucleus of Hypothalamus, Dynorphins, Gonadotropin-Releasing Hormone, Male, Membrane Potentials, Mice, Transgenic, Neurons, Orchiectomy, Peptide Fragments, Pyrrolidines, Substance P, Time Factors, Neurokinin B, Receptors, Opioid, kappa, Receptors, Neurokinin-3, Benzeneacetamides, Green Fluorescent Proteins, Mice, Kisspeptins
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