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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: 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.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

At any time cues could trigger minor craving by directly stimulating the Craving Generation System (CGS). The smoker might lapse by smoking a single cigarette.
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Related In: Results  -  Collection

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brainsci-02-00523-f008: At any time cues could trigger minor craving by directly stimulating the Craving Generation System (CGS). The smoker might lapse by smoking a single cigarette.

Mentions: 8. The model also explains why smoking a single cigarette so often causes a relapse (Figure 8, Figure 9, Figure 10).


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

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

At any time cues could trigger minor craving by directly stimulating the Craving Generation System (CGS). The smoker might lapse by smoking a single cigarette.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

brainsci-02-00523-f008: At any time cues could trigger minor craving by directly stimulating the Craving Generation System (CGS). The smoker might lapse by smoking a single cigarette.
Mentions: 8. The model also explains why smoking a single cigarette so often causes a relapse (Figure 8, Figure 9, Figure 10).

Bottom Line: 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.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