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Study · Animal study (in vivo) · mouse and rat · 2019

9 results

Kisspeptin Stimulation of Prolactin Secretion Requires Kiss1 Receptor but Not in Tuberoinfundibular Dopaminergic Neurons.

Aquino NSS, Kokay IC, Perez CT, Ladyman SR, Henriques PC, Silva JF, Broberger C, Grattan DR, Szawka RE

Endocrinology1 Mar 2019Cited by 17 (Europe PMC)

PMID30668693 (opens in a new tab)DOI10.1210/en.2018-00932 (opens in a new tab)PepBankPUB-30668693
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study9

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type female mice, intracerebroventricular Kp-10 increased prolactin release.

    In plain wordsIn female mice, kisspeptin‑10 injected into the brain raised prolactin release.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseProlactin release
    Study

    mousen: not reported in source

    Wild-type female mice
    Outcome group
    Pituitary hormones · Endocrine and hormones
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    Intracerebroventricular kisspeptin-10 (Kp-10) increased prolactin release in wild-type but not in Kiss1r-/-R female mice.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In Kiss1r-/-R female mice, intracerebroventricular Kp-10 did not increase prolactin release.

    In plain wordsIn mice lacking the kisspeptin receptor in most cells, kisspeptin‑10 did not raise prolactin release.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeProlactin release
    Study

    mousen: not reported in source

    Kiss1r-deficient female mice with Kiss1r only in GnRH neurons (Kiss1r-/-R)
    Outcome group
    Pituitary hormones · Endocrine and hormones
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    Intracerebroventricular kisspeptin-10 (Kp-10) increased prolactin release in wild-type but not in Kiss1r-/-R female mice.
    1 context sentence
    Summary · context
    Initially, we evaluated prolactin response in a Kiss1r-deficient mouse line, in which Kiss1r had been knocked into GnRH neurons (Kiss1r-/-R).
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In ovariectomized, estradiol-treated rats, Kp-10 increased prolactin release.

    In plain wordsIn female rats, kisspeptin‑10 raised prolactin release.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseProlactin release after Kp-10
    Study

    ratn: not reported in source

    Ovariectomized, estradiol-treated rats
    Outcome group
    Pituitary hormones · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10-induced increase in prolactin release but failed to prevent the concomitant reduction in the activity of tuberoinfundibular dopaminergic (TIDA) neurons, as determined by the 3,4-dihydroxyphenylacetic…
  4. 04AnimalAnimal study (in vivo)Mechanism

    In ovariectomized, estradiol-treated rats, Kp-10 reduced the activity of tuberoinfundibular dopaminergic neurons, measured as the DOPAC/dopamine ratio.

    In plain wordsIn female rats, kisspeptin‑10 lowered the activity of dopamine-producing brain cells that control prolactin.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseTIDA neuron activity (DOPAC/dopamine ratio in median eminence)
    Study

    ratn: not reported in source

    Ovariectomized, estradiol-treated rats
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10-induced increase in prolactin release but failed to prevent the concomitant reduction in the activity of tuberoinfundibular dopaminergic (TIDA) neurons, as determined by the 3,4-dihydroxyphenylacetic…
  5. 05LabEx vivo tissueMechanism

    In juvenile male rats, whole-cell patch clamp recordings showed no direct effect of Kp-10 on the electrical activity of TIDA neurons.

    In plain wordsIn lab recordings from rat brain cells, kisspeptin‑10 had no direct effect on the electrical activity of dopamine-producing cells.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeElectrical activity of TIDA neurons
    Study

    ratn: not reported in source

    Whole-cell patch clamp recordings of TIDA neurons
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using whole-cell patch clamp recordings in juvenile male rats, we found no direct effect of Kp-10 on the electrical activity of TIDA neurons.

Studies that did not test the peptide alone4

In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Kisspeptin-10.

  1. 06AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Efficacy outcome

    In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10-induced increase in prolactin release.

    In plain wordsIn female rats, a kisspeptin receptor blocker stopped the prolactin rise caused by kisspeptin‑10.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseProlactin release after Kp-10 with kisspeptin-234
    Study

    ratn: not reported in source

    Ovariectomized, estradiol-treated rats
    Outcome group
    Pituitary hormones · Endocrine and hormones

    Source sentences

    Summary
    In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10-induced increase in prolactin release but failed to prevent the concomitant reduction in the activity of tuberoinfundibular dopaminergic (TIDA) neurons, as determined by the 3,4-dihydroxyphenylacetic…

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

  2. 07AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Mechanism

    In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 did not prevent the Kp-10-associated reduction in TIDA neuron activity.

    In plain wordsIn female rats, a kisspeptin receptor blocker did not stop the drop in activity of dopamine-producing brain cells.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeTIDA neuron activity after Kp-10 with kisspeptin-234
    Study

    ratn: not reported in source

    Ovariectomized, estradiol-treated rats
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10-induced increase in prolactin release but failed to prevent the concomitant reduction in the activity of tuberoinfundibular dopaminergic (TIDA) neurons, as determined by the 3,4-dihydroxyphenylacetic…

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

  3. 08AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Mechanism

    In female rats, Kiss1r was expressed in the periventricular and arcuate nuclei but not in tyrosine hydroxylase-expressing neurons.

    In plain wordsIn female rats, the kisspeptin receptor was found in two brain regions but not in dopamine-producing cells.

    Peptide
    Kisspeptin-10
    Outcome
    Not applicableKiss1r expression in hypothalamic neurons
    Study

    ratn: not reported in source

    Hypothalamus of female rats
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    In addition, dual-label in situ hybridization in the hypothalamus of female rats showed that Kiss1r is expressed in the periventricular nucleus of the hypothalamus (Pe) and arcuate nucleus of the hypothalamus (ARC) but not in tyrosine hydroxylase (Th)-expressing neurons.

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

  4. 09AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Mechanism

    Npffr1, a receptor to which kisspeptin also binds, was expressed in most periventricular dopaminergic neurons but in only a low proportion of arcuate TIDA neurons.

    In plain wordsAnother receptor that kisspeptin can bind was found in most dopamine cells of one brain region but few of another.

    Peptide
    Kisspeptin-10
    Outcome
    Not applicableNpffr1 expression in dopaminergic neurons
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    Kisspeptin also has affinity for the neuropeptide FF receptor 1 (Npffr1), which was expressed in the majority of Pe dopaminergic neurons but only in a low proportion of TIDA neurons in the ARC.

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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