Addiction Neuroscience成瘾神经科学
Addiction Neuroscience(英文缩写 ADDICT NEUROSCI),ISSN 2772-3925,eISSN 2772-3925,中文译名:成瘾神经科学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
Addiction Neuroscience 最新收录文献
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1. Exercise as a Neurobiological Intervention: Utilizing NAc Circuitry to Combat Addiction.
PMID:日期:2026-08-12Preclinical evidence demonstrates that various forms of exercise can attenuate conditioned place preference (CPP) and self-administration of psychostimulants and opioids. However, the underlying neurobiological mechanisms behind how exercise attenuates drug CPP and self-administration remains unclear. Of particular interest is the role of dopamine receptor-expressing medium spiny neurons (MSNs) in the nucleus accumbens (NAc), as their activity becomes dysregulated after chronic substance use. Functional differences in D1R and D2R MSNs has been observed alongside neurobiological adaptations related to exercise and drug-seeking behaviors. Here, we review mainly preclinical evidence for exercise attenuating psychostimulant and opioid CPP and self-administration along with observed neurobiological adaptations in NAc circuitry. Additionally, we propose utilizing miniscopes to further parse the role of D1R and D2R MSNs during exercise and drug self-administration .
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2. Stress-coping behavior during predator odor exposure is associated with differences in decision making.
PMID:日期:2026-07-25Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are chronic psychiatric disorders that have overlapping symptomology and risk factors, including altered motivation and impulsive behavior. Exposure to a predator odor stressor (2,3,5-Trimethyl-3-Thiazoline (TMT)) produces PTSD-like symptomology in rats. Individual differences in stress-coping behaviors such as freezing and defensive digging during TMT exposure can predict long-term differences in alcohol-related behaviors and altered neurobiology. Here, we evaluated the relationship between stress-coping behavior during TMT exposure and reward-related decision making. In Experiment 1, delay discounting curves in male and female rats were evaluated before and >2 weeks after TMT exposure using an adjusting-amounts delay discounting task. In Experiment 2, using a concurrent choice self-administration procedure, lever responses and preference for alcohol over sucrose were evaluated before and >2 weeks after TMT exposure in females. Additionally, motivation for competing reinforcers was evaluated using progressive ratios. Digging during TMT exposure was correlated with greater post-TMT impulsive choice (Experiment 1), reduced sucrose lever responses both before and after TMT exposure (Experiment 2), and reduced sucrose lever breakpoint after TMT (Experiment 2). High-digging rats showed greater delay discounting than low-digging rats after TMT exposure, though neither were different from controls. Additionally, compared to controls, TMT-exposed females had greater motivation for both alcohol and sucrose self-administration when available concurrently. Overall, these findings suggest that behavior prior to and during a stressful experience can predict individual differences in decision making, which may help future studies identify the neurobiology underlying risk for aberrant reward-related behaviors after a traumatic event.
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3. Adolescent social isolation promotes oxycodone consumption and augments mu opioid receptor responsiveness in the ventral pallidum.
PMID:日期:2026-07-03Exposure to adversity during adolescence augments vulnerability to opioid use disorders in adulthood, yet the neurobiological mechanisms underlying this risk remain incompletely understood. The ventral pallidum (VP) is a region highly implicated in reward valuation and is sensitive to both stress and opioid modulation. Here, we examined whether adolescent social isolation (aSI) alters consumption of oxycodone and mu-opioid receptor (MOR) mediated inhibition of dopamine release in the VP. Male and female rats were exposed to aSI or group housing during adolescence (aGH) and assessed in adulthood for oxycodone consumption and pallidal dopamine release using fast-scan cyclic voltammetry (FSCV). aSI increased oxycodone intake, with females consuming significantly more oxycodone than males. While aSI did not alter baseline dopamine release, MOR activation with DAMGO or oxycodone produced greater inhibition of dopamine release in aSI females, but not males, indicating a sex-specific enhancement of MOR functional responsivity following aSI. Pallidal enkephalin abundance was not affected by aSI, suggesting that aSI induces receptor-level regulation rather than changes in the endogenous ligand. Together, these findings indicate that aSI produces enduring, sex-specific alterations in MOR modulation of dopamine in the VP. These effects may underlie maladaptive behaviors observed in adulthood, and aid in the understanding of how stress in adolescence serves as a risk factor for opioid use disorder.
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4. Nicotine self-administration suppresses both pro- and anti-inflammatory accumbens cytokines but does not induce apoptosis in female rats.
PMID:日期:2026-06-12Nicotine can alter neuroimmune signaling within the brain reward pathway, and specifically, within the nucleus accumbens (NAc). Despite clinically meaningful sex differences in nicotine use as well as known sex differences in immune system function, no studies have evaluated NAc neuroimmune consequences following nicotine use in females. Thus, the present study evaluated cytokine expression and neuronal apoptosis in the ventral striatum (which encompasses the NAc) in ovary-intact female Long-Evans rats following nicotine or saline self-administration. Circulating cytokine levels were also evaluated in serum. Overall, pro-inflammatory cytokine levels were suppressed within the ventral striatum, with tumor necrosis factor-alpha (TNFα) being the most significantly suppressed. Interestingly, there was an increase in the chemokine fractalkine (FKN), a neuronal "help me" signal during distress. These results raise the possibility that chronic volitional nicotine use results in cleavage of FKN in response to neuronal distress, and glial cells may be unresponsive to these signals. In contrast, circulating serum cytokine levels remained mostly unchanged except for an increase in TNFα, suggesting that the immunosuppression observed following nicotine self-administration was largely localized to the brain. No measurable NAc apoptotic debris was identified, in line with our findings that interleukin-1β (IL-1β) was suppressed and raising the possibility that nicotine use suppresses NAc inflammasome activation. Thus, chronic nicotine use in female rats may disrupt ventral striatal neuroimmune homeostasis. Together, targeting nicotine-induced disruptions in neuroimmune homeostasis may represent novel therapeutic opportunities to mitigate the harmful effects of nicotine in females.
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5. Moderate prenatal alcohol exposure differentially alters acute ethanol sensitivity of GABAergic transmission in CRFR1- and CRFR1+ CeM Neurons.
PMID:日期:2026-06-10Prenatal exposure to alcohol (PAE) increases the risk for misusing alcohol and/or developing an alcohol use disorder (AUD) by adulthood. The corticotropin releasing factor (CRF) system is a major target of pre- and post-natal ethanol (EtOH) exposure. CRF and its receptor (CRFR1), in part, mediate EtOH potentiated GABA release in the medial nucleus of the central amygdala (CeM) of adult male rodents. Interestingly, our lab has shown a disruption in the function and expression of CeM CRFR1 and acute EtOH's effects on GABA transmission in PAE adolescent animals, but it is unknown whether these alterations to the CRF system persist into adulthood or alter the actions of acute EtOH on GABAergic transmission in the CeM. Using CRF-Cre-Tomato rats, this study examined how PAE alters acute EtOH modulation of GABAergic neurotransmission onto CRFR1+ and CRFR1- CeM neurons in adult offspring (P80-105). Pregnant dams were exposed to vaporized ethanol or room air (control) on gestational day 12 (G12) for 6 hours and whole-cell electrophysiology was performed in the CeM to assess the actions of acute EtOH (44, 66, & 88 mM) on GABAergic transmission onto CRFR1+ and CRFR1- neurons. We found unique effects of PAE that were cell type- and concentration-dependent in males and females, suggesting PAE dysregulates acute EtOH's modulation of GABA transmission within the CeM in a sex-specific manner. This study contributes to the expanding body of research exploring the effects of PAE and how a single exposure can impact neurophysiological mechanisms in brain regions associated with AUD.
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6. The central amygdala corticotropin releasing factor system regulates anxiety-like behavior in an age- and sex- dependent manner in rats.
PMID:日期:2026-02-11The corticotropin releasing factor (CRF) system is a key regulator of anxiety-like behavior and a major contributor to addiction. The canonical anxiogenic role of CRF has been largely based on CRF manipulations in adult male rodents, particularly within the central amygdala (CeA), despite evidence that underlying neurobiological mechanisms of anxiety are sex- and age-dependent. Our lab has shown that the physiological response to CRF receptor 1 (CRFR1) activation within the medial CeA, a brain region associated with anxiety and addiction, varies with both age and sex. Therefore, in the current study, we investigated the effects of CRFR1 activation in the CeA on anxiety-like behavior in naïve juvenile (~postnatal day [P] 25), adolescent (~P45), or adult (~P80) male and female Sprague Dawley rats. Rats were given bilateral cannula in the CeA and then tested in the light-dark box test following an infusion of either the CRFR1 agonist Stressin-1 (1 μM) or vehicle. In contrast to the previously established anxiogenic effects of CRF agonists, we found that intra-CeA Stressin-1 decreased anxiety-like behavior in females regardless of age and juvenile males, with no significant effects evident in adolescent or adult males. Notably, RNAscope hybridization revealed no differences in CRFR1 or CRF mRNA across age or sex. Taken together, these findings further highlight the importance of age and sex on CRF system regulation of anxiety-like behavior, providing a background for the development of more targeted treatments of anxiety disorders and addiction.
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7. Effects of prenatal methadone and buprenorphine exposure on motivated responding for sucrose and gene expression in adult male and female rats.
PMID:日期:2026-01-27The opioid crisis has resulted in escalating rates of opioid use disorder in women of reproductive age and increased prevalence of fetal drug exposure. While medication for opioid use disorder (MOUD) - e.g., buprenorphine or methadone - improves maternal health outcomes, infants exposed to MOUD show a variety of physical and behavioral consequences. There are, however, few clinical or preclinical studies investigating long-term effects of MOUD exposure. The current work investigates the long-term effects of prenatal MOUD exposure on effort-based responding to a palatable food reward and gene expression in regions of the brain related to reward and feeding, including the nucleus accumbens and hypothalamus. Female Sprague Dawley rats were implanted with osmotic minipumps filled with methadone (10 mg/kg/day) or buprenorphine (1 mg/kg/day) or saline control (2.5 μL/hour for 28 days) and mated four days later. In adulthood, male and female offspring began sucrose pellet self-administration to assess the motivational strength of a food reward in MOUD-exposed animals compared to saline controls, followed by analysis of gene expression via RNAscope hybridization. We observed long-term changes in reward motivation, where adults gestationally exposed to methadone - but not buprenorphine - demonstrated increased motivated responding for sucrose. We observed modest sex-dependent effects of MOUD on gene expression in the nucleus accumbens and arcuate nucleus of the hypothalamus following sucrose self-administration. These data suggest differential effects of methadone and buprenorphine on the brain and behavior, providing insight into the potential neuromolecular underpinnings of MOUD-induced changes in neural modulation of reward-motivated behavior.
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8. Influence of sex, anxiety, and risk-taking behavior on opioid and alcohol polysubstance consumption patterns.
PMID:日期:2026-01-24Polysubstance use is prevalent in the population but remains understudied in preclinical models. Alcohol and opioid polysubstance use is associated with negative outcomes, worse treatment prognosis, and higher overdose risk; but underlying mechanisms are still being uncovered. Examining factors that motivate use of one substance over another in different contexts in preclinical models will better our understanding of polysubstance use and improve translational value. Here we assessed baseline anxiety-like and locomotive behavior and then measured voluntary consumption of multiple doses of alcohol and fentanyl in group housed male and female mice using our novel Socially Integrated Polysubstance (SIP) system. Fifty-six male ( = 32) and female ( = 24) adult mice were housed in groups of 4 for one week with continuous access to food, water, two doses of ethanol (5 % and 10 %) and two doses of fentanyl (5 ug/ml and 20 ug/ml). Our analyses revealed sex differences across multiple domains - female mice consumed more liquid, had higher activity, a higher preference for fentanyl over the other available substances, and their fentanyl preference increased over the seven days. Furthermore, both male and female mice displayed polysubstance consumption patterns (drinking multiple substances within an hour), with female mice displaying more prolonged polysubstance use across days in the SIP cages. We then used machine-learning techniques to reveal underlying relationships between baseline behavioral phenotypes and subsequent polysubstance consumption patterns, where anxiety- and risk-taking-like behavioral phenotypes mapped onto discrete patterns of polysubstance use, preference, and escalation. By simulating more translationally relevant substance use and improving our understanding of the motivations for different patterns of consumption, this study contributes to the developing preclinical literature on polysubstance use with the goal of facilitating better treatment outcomes and novel therapeutic strategies.
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9. Hippocampal Volume and Brain Tau Pathology in Opioid Use Disorder: Associations with Non-Fatal Opioid Overdose.
PMID:日期:2026-01-22Opioid use disorder (OUD) is associated with high rates of overdose (OD)-related morbidity and mortality. OD can cause hypoxic-ischemic injury to oxygen-sensitive brain regions such as the hippocampus. Post-mortem studies show Alzheimer's disease-like hyperphosphorylated tau pathology in the brains of individuals with OUD. Neurocognitive impairments in individuals with OUD may reflect incipient dementia and contribute to poor clinical outcomes. Alternatively, OUD and OD could be independent risk factors for Alzheimer's disease. To date, no study has evaluated the effects of non-fatal ODs or chronic OUD on hippocampal volume and tau deposition in the human brain . To fill this gap, we examined hippocampal volumes in OUD individuals (n=60) and healthy controls (HC, n=30) using T1-weighted magnetic resonance imaging (MRI). We found lower bilateral hippocampal volumes in OUD patients than HCs (p<0.001), but no differences between OUD individuals with a history of OD and those without (NOD) (p=0.92). We measured brain tau deposition using Positron Emission Tomography (PET) with [F]PI-2620 in n=4 HC, n=4 OUD-NOD, and n=4 OUD-OD individuals, and found no difference in brain tau between groups. Functional MRI assessment of episodic memory showed no differences in memory performance or hippocampal activity between groups, although OUD-OD individuals had poorer performance than HC with a medium effect size (d=0.56). In summary, we confirm prior findings of smaller hippocampal volumes in participants with OUD than in HC. However, with a limited sample size, our findings do not show evidence of brain tau deposition in OUD participants with or without OD histories.
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10. Transgenerational memory deficits in cocaine-sired male rat offspring and grand-offspring.
PMID:日期:2026-01-12Environmental insults, including exposure to drugs of abuse, can influence offspring physiology and behavior through intergenerational epigenetic modifications. The present data indicated that paternal rat cocaine self-administration had no effect on stress responses, impulse control or cocaine seeking in male offspring. We also replicated previous findings showing that paternal cocaine intake impaired memory function, measured by the object location memory task, only in male offspring. We extended this work by breeding cocaine-exposed males with naïve females 90 days after the last cocaine self-administration session; that is, after one complete cycle of spermatogenesis. Impaired object recognition was observed in cocaine-sired male offspring with delayed mating, suggesting persistent cocaine-induced changes in sperm. We next wanted to discern if this hippocampal-dependent memory deficit would extend to the grand-offspring (i.e. the F2 generation). Our results indicated that male, but not female, cocaine grand-sired offspring displayed object location memory deficits, although the hippocampal mechanisms underlying this effect appear to differ between F1 and F2 generations. Taken together, our findings indicate that paternal cocaine exposure results in transgenerational hippocampal-dependent memory deficits.