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Study · Measured the body's own peptide · 2004

3 results

Prenatal cocaine exposure potentiates paroxetine-induced desensitization of 5-HT2A receptor function in adult male rat offspring.

Chen Z, Waimey K, Van de Kar LD, Carrasco GA, Landry M, Battaglia G

Neuropharmacology1 Jun 2004Cited by 6 (Europe PMC)

PMID15081791 (opens in a new tab)DOI10.1016/j.neuropharm.2004.01.013 (opens in a new tab)PepBankPUB-15081791
Publisher pagePubMedAsk about this study
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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 study3

No result from this study comes from a test of the peptide.

Natural levels measured3

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In adult male rats, prenatal cocaine exposure did not alter 5-HT2A receptor-mediated neuroendocrine responses, including the oxytocin response.

    In plain wordsIn rats, exposure to cocaine before birth did not change the response of the body's own oxytocin to a serotonin receptor stimulus.

    Peptide
    Oxytocin
    Outcome
    No significant changeDOI-stimulated oxytocin response after prenatal cocaine exposure
    Study

    ratn: not reported in source

    Adult male rat offspring after prenatal saline or cocaine exposure
    Comparator
    Prenatal saline offspring
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    Prenatal cocaine exposure did not alter 5-HT(2A) receptor-mediated neuroendocrine responses or 5-HT(2A) receptor densities.
    2 context sentences
    Summary · context
    Following exposure to saline or (-)cocaine (15 mg/kg, s.c., b.i.d.), during gestational days 13-20, adult male offspring were treated with either saline or paroxetine (10 mg/kg/day, i.p. 14 days).
    Summary · context
    Eighteen hours post-treatment, changes in the stimulation of oxytocin, adrenocorticotropic hormone (ACTH) and corticosterone by (-)4-iodo-2,5-dimethoxyphenylisopropylamine (DOI, 0.5 or 2.0 mg/kg, s.c.) and in 5-HT(2A) receptor densities were determined.

    This result measures the body's own Oxytocin. Nobody was given the peptide. It is not evidence about taking it.

  2. 02AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In adult male rats from both prenatal groups, paroxetine desensitized the 5-HT2A receptor-mediated oxytocin response.

    In plain wordsIn rats, the antidepressant paroxetine lowered the response of the body's own oxytocin to a serotonin receptor stimulus.

    Peptide
    Oxytocin
    Outcome
    Decrease5-HT2A receptor-mediated oxytocin response after paroxetine
    Study

    ratn: not reported in source

    Adult male rat offspring after prenatal saline or cocaine exposure
    Comparator
    Saline-treated offspring
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    In contrast, paroxetine treatment reduced cortical 5-HT(2A) receptors (18-25%) and desensitized 5-HT(2A) receptor-mediated oxytocin responses in both offspring groups.
    2 context sentences
    Summary · context
    Following exposure to saline or (-)cocaine (15 mg/kg, s.c., b.i.d.), during gestational days 13-20, adult male offspring were treated with either saline or paroxetine (10 mg/kg/day, i.p. 14 days).
    Summary · context
    Eighteen hours post-treatment, changes in the stimulation of oxytocin, adrenocorticotropic hormone (ACTH) and corticosterone by (-)4-iodo-2,5-dimethoxyphenylisopropylamine (DOI, 0.5 or 2.0 mg/kg, s.c.) and in 5-HT(2A) receptor densities were determined.

    This result measures the body's own Oxytocin. Nobody was given the peptide. It is not evidence about taking it.

  3. 03AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In adult male rats exposed to cocaine before birth, paroxetine produced a greater attenuation of the oxytocin response to DOI.

    In plain wordsIn rats exposed to cocaine before birth, paroxetine lowered the body's own oxytocin response to a serotonin stimulus more strongly.

    Peptide
    Oxytocin
    Outcome
    DecreaseOxytocin response to DOI after paroxetine in cocaine-exposed offspring
    Study

    ratn: not reported in source

    Adult male rat offspring after prenatal saline or cocaine exposure
    Comparator
    Paroxetine in prenatal saline offspring
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    and a greater attenuation of the oxytocin responses to (-)DOI.
    2 context sentences
    Summary · context
    Following exposure to saline or (-)cocaine (15 mg/kg, s.c., b.i.d.), during gestational days 13-20, adult male offspring were treated with either saline or paroxetine (10 mg/kg/day, i.p. 14 days).
    Summary · context
    Eighteen hours post-treatment, changes in the stimulation of oxytocin, adrenocorticotropic hormone (ACTH) and corticosterone by (-)4-iodo-2,5-dimethoxyphenylisopropylamine (DOI, 0.5 or 2.0 mg/kg, s.c.) and in 5-HT(2A) receptor densities were determined.

    This result measures the body's own Oxytocin. Nobody was given the peptide. It is not evidence about taking it.

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

    11 Oct 2026, 20:03 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:51 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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