In:
Developmental Neuroscience, S. Karger AG, Vol. 31, No. 1-2 ( 2009), p. 58-70
Abstract:
Developmental nicotine exposure produces lasting changes in serotonin (5-HT) function. We gave nicotine to adolescent rats (postnatal days, PD, 30–47), simulating plasma levels in smokers, and then examined the subsequent effects of nicotine given again in young adulthood (PD 90–107), focusing on 5-HT 〈 sub 〉 1A 〈 /sub 〉 and 5-HT 〈 sub 〉 2 〈 /sub 〉 receptors and the 5-HT transporter during nicotine treatment (PD 105) and withdrawal (PD 110, 120, 130), and long-term changes (PD 180). Adolescent nicotine exposure by itself evoked long-term elevations in cerebrocortical binding parameters in males that emerged in young adulthood. Nicotine given in adulthood produced transient elevations in 5-HT receptor expression in both males and females during withdrawal, and persistent upregulation in the male cerebral cortex. In contrast, females showed decrements in cerebrocortical 5-HT receptors by PD 180. Adolescent nicotine exposure altered the responses to nicotine given in adulthood, sensitizing the initial effects and changing both the withdrawal response and long-term actions. Our results thus provide mechanistic evidence that nicotine exposure, during the period in which nearly all smokers begin to use tobacco, reprograms the future response of 5-HT systems to nicotine.
Type of Medium:
Online Resource
ISSN:
0378-5866
,
1421-9859
Language:
English
Publisher:
S. Karger AG
Publication Date:
2009
detail.hit.zdb_id:
1482201-5
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