Stress-Induced Reinstatement of Nicotine Preference Requires Dynorphin/Kappa Opioid Activity in the Basolateral Amygdala.
Stephanie K NygardNicholas J HourguettesGabriel G SobczakWilliam A CarlezonMichael R BruchasPublished in: The Journal of neuroscience : the official journal of the Society for Neuroscience (2017)
Considering the major impact of nicotine use on human health, understanding the mechanisms by which stress triggers reinstatement of drug-seeking behaviors is particularly pertinent to nicotine. The dynorphin (DYN)/kappa-opioid receptor (KOR) system has been implicated in stress-induced reinstatement of drug seeking for other commonly abused drugs. However, the specific role, brain region, and mechanisms that this system plays in reinstatement of nicotine seeking has not been characterized. Here, we report region-specific engagement of the DYN/KOR system and subsequent activation of inhibitory (Gi-linked) intracellular signaling pathways within the basolateral amygdala during stress-induced reinstatement of nicotine preference. We show that the DYN/KOR system is necessary to produce this behavioral state. This work may provide novel insight for the development of therapeutic approaches to prevent stress-related nicotine relapse.
Keyphrases
- stress induced
- smoking cessation
- human health
- mental health
- nuclear factor
- risk assessment
- chronic pain
- pain management
- functional connectivity
- prefrontal cortex
- resting state
- signaling pathway
- drug induced
- emergency department
- social media
- white matter
- adverse drug
- epithelial mesenchymal transition
- multiple sclerosis
- free survival
- blood brain barrier
- induced apoptosis