Frederic J. Seidler

DUKE, School of Medicine, Pharmacology & Cancer Biology

Scopus Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in Scopus. This abstract is what is used to create the fingerprint of the publication.

Adolescent nicotine administration changes the responses to nicotine given subsequently in adulthood: Adenylyl cyclase cell signaling in brain regions during nicotine administration and withdrawal, and lasting effects

Theodore A. Slotkin; Ian T. Ryde; Emiko A. MacKillop; Bethany E. Bodwell; Frederic J. Seidler (Profiled Authors: Frederic J. Seidler; Theodore Alan Slotkin)

Brain Research Bulletin. 2008;76(5):522-530.

Neurodevelopmental vulnerability to nicotine extends into adolescence, the stage at which most smokers begin using tobacco. The "sensitization-homeostasis" model postulates that nicotine treatment permanently reprogrammes neural communication, so that underlying functional changes remain present despite the apparent restoration of behavioral normality. We administered nicotine to adolescent rats (postnatal days PN30-47) or adults (postnatal days PN90-107), using regimens that reproduce plasma levels in smokers, and assessed effects on the adenylyl cyclase (AC) signaling cascade, which is involved in nicotine dependence and withdrawal but also mediates numerous other neurotransmitter responses. Evaluations were made in the cerebral cortex, brainstem and cerebellum on PN105, PN110, PN120, PN130 and PN180. Adolescent nicotine exposure elicited persistent suppression of basal AC activity and eventual compromise of responses to β-adrenergic receptor stimulation, with effects emerging in late adulthood; maximal AC activity as monitored with forskolin was elevated and in general, all the effects were more notable in males. Nicotine treatment in adulthood produced an immediate increase in AC activity in males that disappeared upon withdrawal; there were late-emerging deficits similar to, but smaller in magnitude than those seen with adolescent nicotine exposure. Adolescent treatment greatly exacerbated the response to subsequent nicotine administration in adulthood, producing profound AC deficits during withdrawal that persisted through at least 6 months of age. Our results reinforce the concept that adolescence is a critical developmental period in which nicotine disrupts neural cell signaling in a lasting manner, and provide a mechanistic framework for understanding the biological substrates that determine the relationship between adolescent nicotine exposure and life-long susceptibility to nicotine addiction. © 2008 Elsevier Inc. All rights reserved.

PMID: 18534261    

Scientific Context

This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.