{"title":"压力和社会失败对尼古丁成瘾从奖赏到戒断神经生物学强化机制的影响。","authors":"Kokila Shankar, Sélène Zahedi, Olivier George","doi":"10.1007/s00213-025-06852-5","DOIUrl":null,"url":null,"abstract":"<p><p>Nicotine and cigarette/tobacco use continue to be a prevalent public health issue worldwide. The transition to nicotine addiction occurs through an allostatic cycle involving the stages of binging/intoxication, withdrawal/negative affective states, and preoccupation/anticipation. This review focuses on the psychological, neurobiological, and molecular mechanisms contributing to the negative affective state during withdrawal from nicotine with an emphasis on stress and how social defeat stress can affect these mechanisms. Psychologically, negative affect during withdrawal is thought to contribute to the transition from positive reinforcement of drug-taking to negative reinforcement of nicotine use. Nicotine binding to nicotinic acetylcholine receptors elicits a variety of neuronal signaling throughout the brain, over time producing within- and between-systems neuroadaptations across brain regions that govern reward, anxiety, pain, and stress responses. Continued nicotine use additionally dysregulates myriad molecular signaling pathways that directly affect nicotine intake/aversion and withdrawal-like symptoms. Throughout all of these mechanisms, non-pharmacological stress also plays an important role in mediating much of the negative affect associated with addiction. Social defeat stress increases a variety of neuropeptide signaling that consequently exacerbates drug taking and negative affective states. Understanding the mechanisms through which these stages manifest can better our understanding of addiction disease biology and provide novel avenues for therapeutic targets.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3000,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The influence of stress and social defeat on neurobiological reinforcement mechanisms across reward to withdrawal in nicotine addiction.\",\"authors\":\"Kokila Shankar, Sélène Zahedi, Olivier George\",\"doi\":\"10.1007/s00213-025-06852-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Nicotine and cigarette/tobacco use continue to be a prevalent public health issue worldwide. The transition to nicotine addiction occurs through an allostatic cycle involving the stages of binging/intoxication, withdrawal/negative affective states, and preoccupation/anticipation. This review focuses on the psychological, neurobiological, and molecular mechanisms contributing to the negative affective state during withdrawal from nicotine with an emphasis on stress and how social defeat stress can affect these mechanisms. Psychologically, negative affect during withdrawal is thought to contribute to the transition from positive reinforcement of drug-taking to negative reinforcement of nicotine use. Nicotine binding to nicotinic acetylcholine receptors elicits a variety of neuronal signaling throughout the brain, over time producing within- and between-systems neuroadaptations across brain regions that govern reward, anxiety, pain, and stress responses. Continued nicotine use additionally dysregulates myriad molecular signaling pathways that directly affect nicotine intake/aversion and withdrawal-like symptoms. Throughout all of these mechanisms, non-pharmacological stress also plays an important role in mediating much of the negative affect associated with addiction. Social defeat stress increases a variety of neuropeptide signaling that consequently exacerbates drug taking and negative affective states. Understanding the mechanisms through which these stages manifest can better our understanding of addiction disease biology and provide novel avenues for therapeutic targets.</p>\",\"PeriodicalId\":20783,\"journal\":{\"name\":\"Psychopharmacology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2025-07-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Psychopharmacology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s00213-025-06852-5\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Psychopharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00213-025-06852-5","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
The influence of stress and social defeat on neurobiological reinforcement mechanisms across reward to withdrawal in nicotine addiction.
Nicotine and cigarette/tobacco use continue to be a prevalent public health issue worldwide. The transition to nicotine addiction occurs through an allostatic cycle involving the stages of binging/intoxication, withdrawal/negative affective states, and preoccupation/anticipation. This review focuses on the psychological, neurobiological, and molecular mechanisms contributing to the negative affective state during withdrawal from nicotine with an emphasis on stress and how social defeat stress can affect these mechanisms. Psychologically, negative affect during withdrawal is thought to contribute to the transition from positive reinforcement of drug-taking to negative reinforcement of nicotine use. Nicotine binding to nicotinic acetylcholine receptors elicits a variety of neuronal signaling throughout the brain, over time producing within- and between-systems neuroadaptations across brain regions that govern reward, anxiety, pain, and stress responses. Continued nicotine use additionally dysregulates myriad molecular signaling pathways that directly affect nicotine intake/aversion and withdrawal-like symptoms. Throughout all of these mechanisms, non-pharmacological stress also plays an important role in mediating much of the negative affect associated with addiction. Social defeat stress increases a variety of neuropeptide signaling that consequently exacerbates drug taking and negative affective states. Understanding the mechanisms through which these stages manifest can better our understanding of addiction disease biology and provide novel avenues for therapeutic targets.
期刊介绍:
Official Journal of the European Behavioural Pharmacology Society (EBPS)
Psychopharmacology is an international journal that covers the broad topic of elucidating mechanisms by which drugs affect behavior. The scope of the journal encompasses the following fields:
Human Psychopharmacology: Experimental
This section includes manuscripts describing the effects of drugs on mood, behavior, cognition and physiology in humans. The journal encourages submissions that involve brain imaging, genetics, neuroendocrinology, and developmental topics. Usually manuscripts in this section describe studies conducted under controlled conditions, but occasionally descriptive or observational studies are also considered.
Human Psychopharmacology: Clinical and Translational
This section comprises studies addressing the broad intersection of drugs and psychiatric illness. This includes not only clinical trials and studies of drug usage and metabolism, drug surveillance, and pharmacoepidemiology, but also work utilizing the entire range of clinically relevant methodologies, including neuroimaging, pharmacogenetics, cognitive science, biomarkers, and others. Work directed toward the translation of preclinical to clinical knowledge is especially encouraged. The key feature of submissions to this section is that they involve a focus on clinical aspects.
Preclinical psychopharmacology: Behavioral and Neural
This section considers reports on the effects of compounds with defined chemical structures on any aspect of behavior, in particular when correlated with neurochemical effects, in species other than humans. Manuscripts containing neuroscientific techniques in combination with behavior are welcome. We encourage reports of studies that provide insight into the mechanisms of drug action, at the behavioral and molecular levels.
Preclinical Psychopharmacology: Translational
This section considers manuscripts that enhance the confidence in a central mechanism that could be of therapeutic value for psychiatric or neurological patients, using disease-relevant preclinical models and tests, or that report on preclinical manipulations and challenges that have the potential to be translated to the clinic. Studies aiming at the refinement of preclinical models based upon clinical findings (back-translation) will also be considered. The journal particularly encourages submissions that integrate measures of target tissue exposure, activity on the molecular target and/or modulation of the targeted biochemical pathways.
Preclinical Psychopharmacology: Molecular, Genetic and Epigenetic
This section focuses on the molecular and cellular actions of neuropharmacological agents / drugs, and the identification / validation of drug targets affecting the CNS in health and disease. We particularly encourage studies that provide insight into the mechanisms of drug action at the molecular level. Manuscripts containing evidence for genetic or epigenetic effects on neurochemistry or behavior are welcome.