Exposure to threshold doses of nicotine in utero: II. Neuroendocrine response to nicotine in adult male offspring
Abstract
Groups of gravid female rats were injected subcutaneously with saline (SAL), a low-dose of nicotine (LN) (0.05 mg/kg, bid) or a high-dose of nicotine (HN) (3.0 mg/kg, bid) from day 4 to day 20 of gestation, or were left undisturbed. In adult 120-day-old male offspring, the ACTH and prolactin responses to acute nicotine challenge were evaluated. The experiment was performed on three separate occasions. Based upon dose-response and time-course studies with nicotine in normal animals, the neuroendocrine responses to nicotine (0.75 and 1.0 mg/kg, sc) were measured 7.5 min after nicotine administration, the peak response-time for both hormones. The ACTH response to acute nicotine administration was blunted significantly in the HN rats, but normal in the LN rats, for all three experiments. In two experiments, the prolactin response to acute nicotine administration was blunted significantly in the HN rats, but enhanced significantly in the LN offspring. The results indicate that prenatal nicotine administration can produce long-term neuroendocrine effects involving nicotinic-receptor coupled circuits, with long-term functional sequelae produced by dosages of nicotine considerably smaller than previously shown to be pharmacologically/toxicologically active.
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Animal studies found that prenatal nicotine exposure disrupts stress hormone regulation in offspring.
“animal studies found evidence that prenatal nicotine exposure disrupts stress hormone regulation in offspring.”
From Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products (2017) · cites this paper as [138]
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Self-citation
- Authors
- Poland, R. E., Lutchmansingh, P., Au, D., Hsieh, C., Afrane, S., Lydecker, S., & McCracken, J. T.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Poland, Russell E.
- Venue
- Developmental Brain Research
- Publisher
- Elsevier BV
- Published
- 1994-12
- Volume
- 83
- Issue
- 2
- Pages
- 278-284
- ISSN
- 0165-3806 (ISSN-L)
- OpenAlex
- W2003530319
- Cited by
- 10
- References
- 36
- Citations by year
- 2020: 1 · 2016: 1 · 2014: 1 · 2013: 1
- FWCI
- 1.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Developmental Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k11mh000722-05)
- National Institute of Mental Health (MH-00722, MH-00534, K02MH000534)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- prenatal nicotine exposure, neuroendocrine response, ACTH, prolactin, nicotinic acetylcholine receptors, dose-response relationship, male offspring
- MeSH terms
- Adrenocorticotropic Hormone, Animals, Brain, Dose-Response Relationship, Drug, Female, Male, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Prolactin, Receptors, Nicotinic, Stress, Physiological, Rats, Sprague-Dawley, Rats
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