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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

After smoking cessation, the brain dismantles the Withdrawal-Related Adaptations but is unable to dismantle the Tolerance-Related Adaptations (TRA). Unless something is done to re-establish homeostasis, craving would continue forever. To restore homeostasis, Abstinence-Related Adaptations (ARA) develop to provide inhibitory input to the Craving Generation System (CGS) counter-balancing the stimulatory input from the TRA. At this point, withdrawal-related craving ends, but craving could still be stimulated by smoking or emotional cues.
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brainsci-02-00523-f007: After smoking cessation, the brain dismantles the Withdrawal-Related Adaptations but is unable to dismantle the Tolerance-Related Adaptations (TRA). Unless something is done to re-establish homeostasis, craving would continue forever. To restore homeostasis, Abstinence-Related Adaptations (ARA) develop to provide inhibitory input to the Craving Generation System (CGS) counter-balancing the stimulatory input from the TRA. At this point, withdrawal-related craving ends, but craving could still be stimulated by smoking or emotional cues.

Mentions: 7. The withdrawal and tolerance-related adaptations are now disrupting homeostasis. In an attempt to restore homeostasis the brain removes the withdrawal-related adaptations but cannot remove the tolerance-related adaptations. To restore homeostasis, abstinence-related adaptations develop to provide inhibitory input to the Craving Generation System counter-balancing the stimulatory input from the persistent tolerance-related adaptations (Figure 7).


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

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

After smoking cessation, the brain dismantles the Withdrawal-Related Adaptations but is unable to dismantle the Tolerance-Related Adaptations (TRA). Unless something is done to re-establish homeostasis, craving would continue forever. To restore homeostasis, Abstinence-Related Adaptations (ARA) develop to provide inhibitory input to the Craving Generation System (CGS) counter-balancing the stimulatory input from the TRA. At this point, withdrawal-related craving ends, but craving could still be stimulated by smoking or emotional cues.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

brainsci-02-00523-f007: After smoking cessation, the brain dismantles the Withdrawal-Related Adaptations but is unable to dismantle the Tolerance-Related Adaptations (TRA). Unless something is done to re-establish homeostasis, craving would continue forever. To restore homeostasis, Abstinence-Related Adaptations (ARA) develop to provide inhibitory input to the Craving Generation System (CGS) counter-balancing the stimulatory input from the TRA. At this point, withdrawal-related craving ends, but craving could still be stimulated by smoking or emotional cues.
Mentions: 7. The withdrawal and tolerance-related adaptations are now disrupting homeostasis. In an attempt to restore homeostasis the brain removes the withdrawal-related adaptations but cannot remove the tolerance-related adaptations. To restore homeostasis, abstinence-related adaptations develop to provide inhibitory input to the Craving Generation System counter-balancing the stimulatory input from the persistent tolerance-related adaptations (Figure 7).

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