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Repeated stress alters the ability of nicotine to activate the hypothalamic–pituitary–adrenal axis
Author(s) -
Lutfy Kabirullah,
Brown Maria C.,
Nerio Namiko,
Aimiuwu Otaren,
Tran Benjamin,
Anghel Adrian,
Friedman Theodore C.
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.04217.x
Subject(s) - nicotine , corticosterone , endocrinology , medicine , adrenocorticotropic hormone , saline , hypothalamic–pituitary–adrenal axis , hormone , hypothalamus
Acute nicotine administration has been shown to activate the hypothalamic–pituitary–adrenal (HPA) axis and stimulate secretion of adrenocorticotrophic hormone (ACTH), corticosterone/cortisol and β‐endorphin (beta‐END) in both rodents and humans, raising the possibility that activation of the HPA axis by nicotine may mediate some of the effects of nicotine. Since stress can increase the risk of drug use and abuse, we hypothesized that repeated stress would increase the ability of nicotine to stimulate the secretion of HPA hormones. To test our hypothesis, mice were exposed to repeated stress (swimming in 15°C water for 3 min/day for 5 days) and killed 15 min after injection of saline or nicotine (0.1 mg/kg, s.c.). Repeated exposure to stress increased the ability of nicotine to stimulate plasma ACTH ( p < 0.05) and beta‐END ( p < 0.05), but not corticosterone secretion. In contrast, repeated exposure to stress increased the post‐saline injection levels of corticosterone ( p < 0.05), but not ACTH and beta‐END. The present results suggest that chronic stress leads to an enhanced sensitivity of some components of the HPA axis to a subsequent nicotine challenge.