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Acetaldehyde, a major constituent of tobacco smoke, enhances behavioral, endocrine, and neuronal responses to nicotine in adolescent and adult rats.
Neuropsychopharmacology. 2007 Sep; 32(9):2025-35.N

Abstract

We have previously shown that acetaldehyde, a constituent of tobacco smoke, increases nicotine self-administration in adolescent, but not adult, rats. The aim of this study was to determine whether acetaldehyde influences other behavioral, endocrine, or neuronal responses to nicotine at either age. Juvenile (postnatal day (P) 27) and adult (P90) male Sprague-Dawley rats were treated with saline, acetaldehyde (16 microg/kg/injection x 2, i.v.), nicotine (30 microg/kg/injection x 2, i.v.) or a combination of acetaldehyde and nicotine. Locomotion and center time were evaluated for 30 min in a novel open field, before measurement of plasma corticosterone levels and brain c-fos mRNA. Nicotine increased locomotor activity in juveniles but decreased it in adults; in contrast, center time was increased at both ages. Acetaldehyde potentiated nicotine's locomotor effects, but not center time. Nicotine induced c-fos expression in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA), nucleus accumbens, and the superior colliculus (SC) at both ages, whereas it activated the hypothalamic paraventricular nucleus (PVN) and consequent corticosterone secretion only in adults. Acetaldehyde potentiated nicotine-induced c-fos in CeA and SC, and activation of PVN c-fos expression/plasma corticosterone release; however, this drug interaction was only observed in behaviorally tested animals, not those that were minimally stressed. Thus, acetaldehyde may modulate the interaction of nicotine and stress. Although pharmacokinetic studies showed that acetaldehyde did not change nicotine levels in either brain or serum, nicotine penetration into the brain was slower in juveniles as compared to adults.

Authors+Show Affiliations

Department of Anatomy and Neurobiology, School of Medicine, University of California, Irvine, CA, USA. caoju@mail.nih.govNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17287824

Citation

Cao, Junran, et al. "Acetaldehyde, a Major Constituent of Tobacco Smoke, Enhances Behavioral, Endocrine, and Neuronal Responses to Nicotine in Adolescent and Adult Rats." Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, vol. 32, no. 9, 2007, pp. 2025-35.
Cao J, Belluzzi JD, Loughlin SE, et al. Acetaldehyde, a major constituent of tobacco smoke, enhances behavioral, endocrine, and neuronal responses to nicotine in adolescent and adult rats. Neuropsychopharmacology. 2007;32(9):2025-35.
Cao, J., Belluzzi, J. D., Loughlin, S. E., Keyler, D. E., Pentel, P. R., & Leslie, F. M. (2007). Acetaldehyde, a major constituent of tobacco smoke, enhances behavioral, endocrine, and neuronal responses to nicotine in adolescent and adult rats. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 32(9), 2025-35.
Cao J, et al. Acetaldehyde, a Major Constituent of Tobacco Smoke, Enhances Behavioral, Endocrine, and Neuronal Responses to Nicotine in Adolescent and Adult Rats. Neuropsychopharmacology. 2007;32(9):2025-35. PubMed PMID: 17287824.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acetaldehyde, a major constituent of tobacco smoke, enhances behavioral, endocrine, and neuronal responses to nicotine in adolescent and adult rats. AU - Cao,Junran, AU - Belluzzi,James D, AU - Loughlin,Sandra E, AU - Keyler,Daniel E, AU - Pentel,Paul R, AU - Leslie,Frances M, Y1 - 2007/02/07/ PY - 2007/2/9/pubmed PY - 2007/12/6/medline PY - 2007/2/9/entrez SP - 2025 EP - 35 JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JO - Neuropsychopharmacology VL - 32 IS - 9 N2 - We have previously shown that acetaldehyde, a constituent of tobacco smoke, increases nicotine self-administration in adolescent, but not adult, rats. The aim of this study was to determine whether acetaldehyde influences other behavioral, endocrine, or neuronal responses to nicotine at either age. Juvenile (postnatal day (P) 27) and adult (P90) male Sprague-Dawley rats were treated with saline, acetaldehyde (16 microg/kg/injection x 2, i.v.), nicotine (30 microg/kg/injection x 2, i.v.) or a combination of acetaldehyde and nicotine. Locomotion and center time were evaluated for 30 min in a novel open field, before measurement of plasma corticosterone levels and brain c-fos mRNA. Nicotine increased locomotor activity in juveniles but decreased it in adults; in contrast, center time was increased at both ages. Acetaldehyde potentiated nicotine's locomotor effects, but not center time. Nicotine induced c-fos expression in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA), nucleus accumbens, and the superior colliculus (SC) at both ages, whereas it activated the hypothalamic paraventricular nucleus (PVN) and consequent corticosterone secretion only in adults. Acetaldehyde potentiated nicotine-induced c-fos in CeA and SC, and activation of PVN c-fos expression/plasma corticosterone release; however, this drug interaction was only observed in behaviorally tested animals, not those that were minimally stressed. Thus, acetaldehyde may modulate the interaction of nicotine and stress. Although pharmacokinetic studies showed that acetaldehyde did not change nicotine levels in either brain or serum, nicotine penetration into the brain was slower in juveniles as compared to adults. SN - 0893-133X UR - https://www.unboundmedicine.com/medline/citation/17287824/Acetaldehyde_a_major_constituent_of_tobacco_smoke_enhances_behavioral_endocrine_and_neuronal_responses_to_nicotine_in_adolescent_and_adult_rats_ L2 - https://antibodies.cancer.gov/detail/CPTC-FOS-4 DB - PRIME DP - Unbound Medicine ER -