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Neuroadaptation in nicotine addiction: update on the sensitization-homeostasis model.

DiFranza JR, Huang W, King J - Brain Sci (2012)

Bottom Line: One such theory, the sensitization-homeostasis (SH) model, postulates that nicotine suppresses craving circuits, and this triggers the development of homeostatic adaptations that autonomously support craving.Over the past decade, many controversial aspects of the SH model have become well established by the literature, while some details have been disproven.We conclude by outlining directions for future research based on the updated model, and commenting on how new experimental studies can gain from the framework put forth in the SH model.

View Article: PubMed Central - PubMed

Affiliation: Department of Family Medicine and Community Health, University of Massachusetts Medical School, 55 Lake Avenue, Worcester, MA 01655, USA. difranzj@ummhc.org.

ABSTRACT
The role of neuronal plasticity in supporting the addictive state has generated much research and some conceptual theories. One such theory, the sensitization-homeostasis (SH) model, postulates that nicotine suppresses craving circuits, and this triggers the development of homeostatic adaptations that autonomously support craving. Based on clinical studies, the SH model predicts the existence of three distinct forms of neuroplasticity that are responsible for withdrawal, tolerance and the resolution of withdrawal. Over the past decade, many controversial aspects of the SH model have become well established by the literature, while some details have been disproven. Here we update the model based on new studies showing that nicotine dependence develops through a set sequence of symptoms in all smokers, and that the latency to withdrawal, the time it takes for withdrawal symptoms to appear during abstinence, is initially very long but shortens by several orders of magnitude over time. We conclude by outlining directions for future research based on the updated model, and commenting on how new experimental studies can gain from the framework put forth in the SH model.

No MeSH data available.


Related in: MedlinePlus

Repeated exposures to nicotine promote additional neuroadaptation. The Withdrawal-Related Adaptations (WRA) are bolstered by Tolerance-Related Adaptations (TRA). The TRA also stimulate the Craving Generation System (CGS). TRA have the effect of shortening the latency to the onset of withdrawal-related craving. As TRAs develop smokers notice that the latency to the onset of withdrawal-related craving may shorten from weeks to days, to hours, and in some cases, to minutes. The WRAs and TRAs do not directly block the effect of nicotine as the nicotine from one cigarette is sufficient to alleviate withdrawal-related craving whether a person has been smoking for a few weeks or many decades.
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brainsci-02-00523-f005: Repeated exposures to nicotine promote additional neuroadaptation. The Withdrawal-Related Adaptations (WRA) are bolstered by Tolerance-Related Adaptations (TRA). The TRA also stimulate the Craving Generation System (CGS). TRA have the effect of shortening the latency to the onset of withdrawal-related craving. As TRAs develop smokers notice that the latency to the onset of withdrawal-related craving may shorten from weeks to days, to hours, and in some cases, to minutes. The WRAs and TRAs do not directly block the effect of nicotine as the nicotine from one cigarette is sufficient to alleviate withdrawal-related craving whether a person has been smoking for a few weeks or many decades.

Mentions: 5. Repeated exposures to nicotine promote additional neuroadaptation. The withdrawal-related adaptations are joined by tolerance-related adaptations that also stimulate the Craving Generation System (Figure 5). The tolerance-related adaptations have the effect of shortening the latency to the onset of withdrawal-related craving.


Neuroadaptation in nicotine addiction: update on the sensitization-homeostasis model.

DiFranza JR, Huang W, King J - Brain Sci (2012)

Repeated exposures to nicotine promote additional neuroadaptation. The Withdrawal-Related Adaptations (WRA) are bolstered by Tolerance-Related Adaptations (TRA). The TRA also stimulate the Craving Generation System (CGS). TRA have the effect of shortening the latency to the onset of withdrawal-related craving. As TRAs develop smokers notice that the latency to the onset of withdrawal-related craving may shorten from weeks to days, to hours, and in some cases, to minutes. The WRAs and TRAs do not directly block the effect of nicotine as the nicotine from one cigarette is sufficient to alleviate withdrawal-related craving whether a person has been smoking for a few weeks or many decades.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061804&req=5

brainsci-02-00523-f005: Repeated exposures to nicotine promote additional neuroadaptation. The Withdrawal-Related Adaptations (WRA) are bolstered by Tolerance-Related Adaptations (TRA). The TRA also stimulate the Craving Generation System (CGS). TRA have the effect of shortening the latency to the onset of withdrawal-related craving. As TRAs develop smokers notice that the latency to the onset of withdrawal-related craving may shorten from weeks to days, to hours, and in some cases, to minutes. The WRAs and TRAs do not directly block the effect of nicotine as the nicotine from one cigarette is sufficient to alleviate withdrawal-related craving whether a person has been smoking for a few weeks or many decades.
Mentions: 5. Repeated exposures to nicotine promote additional neuroadaptation. The withdrawal-related adaptations are joined by tolerance-related adaptations that also stimulate the Craving Generation System (Figure 5). The tolerance-related adaptations have the effect of shortening the latency to the onset of withdrawal-related craving.

Bottom Line: One such theory, the sensitization-homeostasis (SH) model, postulates that nicotine suppresses craving circuits, and this triggers the development of homeostatic adaptations that autonomously support craving.Over the past decade, many controversial aspects of the SH model have become well established by the literature, while some details have been disproven.We conclude by outlining directions for future research based on the updated model, and commenting on how new experimental studies can gain from the framework put forth in the SH model.

View Article: PubMed Central - PubMed

Affiliation: Department of Family Medicine and Community Health, University of Massachusetts Medical School, 55 Lake Avenue, Worcester, MA 01655, USA. difranzj@ummhc.org.

ABSTRACT
The role of neuronal plasticity in supporting the addictive state has generated much research and some conceptual theories. One such theory, the sensitization-homeostasis (SH) model, postulates that nicotine suppresses craving circuits, and this triggers the development of homeostatic adaptations that autonomously support craving. Based on clinical studies, the SH model predicts the existence of three distinct forms of neuroplasticity that are responsible for withdrawal, tolerance and the resolution of withdrawal. Over the past decade, many controversial aspects of the SH model have become well established by the literature, while some details have been disproven. Here we update the model based on new studies showing that nicotine dependence develops through a set sequence of symptoms in all smokers, and that the latency to withdrawal, the time it takes for withdrawal symptoms to appear during abstinence, is initially very long but shortens by several orders of magnitude over time. We conclude by outlining directions for future research based on the updated model, and commenting on how new experimental studies can gain from the framework put forth in the SH model.

No MeSH data available.


Related in: MedlinePlus