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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

The primary addiction-related action of nicotine is to stimulate the Craving Inhibition System (CIS) which is experienced as a sense of satisfaction by the smoker. Stimulation of the CIS results in inhibition of the Craving Generation System (CGS) as indicated by the solid inhibitory arrow. This effect can block the ability of smoking cues to generate craving.
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brainsci-02-00523-f002: The primary addiction-related action of nicotine is to stimulate the Craving Inhibition System (CIS) which is experienced as a sense of satisfaction by the smoker. Stimulation of the CIS results in inhibition of the Craving Generation System (CGS) as indicated by the solid inhibitory arrow. This effect can block the ability of smoking cues to generate craving.

Mentions: 2. Nicotine’s direct action is to activate the Craving Inhibition System, resulting in feelings of satisfaction and relaxation. When activated, the Craving Inhibition System suppresses activity in the Craving Generation System, thereby inhibiting craving. The nicotine-induced activation of the Craving Inhibition System and subsequent suppression of the Craving Generation System exceed that which would occur with satiety to non-drug appetites (Figure 2).


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

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

The primary addiction-related action of nicotine is to stimulate the Craving Inhibition System (CIS) which is experienced as a sense of satisfaction by the smoker. Stimulation of the CIS results in inhibition of the Craving Generation System (CGS) as indicated by the solid inhibitory arrow. This effect can block the ability of smoking cues to generate craving.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

brainsci-02-00523-f002: The primary addiction-related action of nicotine is to stimulate the Craving Inhibition System (CIS) which is experienced as a sense of satisfaction by the smoker. Stimulation of the CIS results in inhibition of the Craving Generation System (CGS) as indicated by the solid inhibitory arrow. This effect can block the ability of smoking cues to generate craving.
Mentions: 2. Nicotine’s direct action is to activate the Craving Inhibition System, resulting in feelings of satisfaction and relaxation. When activated, the Craving Inhibition System suppresses activity in the Craving Generation System, thereby inhibiting craving. The nicotine-induced activation of the Craving Inhibition System and subsequent suppression of the Craving Generation System exceed that which would occur with satiety to non-drug appetites (Figure 2).

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