Addiction neuroscience最新文献

{"title":"Low frequency deep brain stimulation of nucleus accumbens shell neuronal subpopulations attenuates cocaine seeking selectively in male rats","authors":"Sarah E. Swinford-Jackson ,&nbsp;Matthew T. Rich ,&nbsp;Phillip J. Huffman ,&nbsp;Melissa C. Knouse ,&nbsp;Arthur S. Thomas ,&nbsp;Sharvari Mankame ,&nbsp;Samantha J. Worobey ,&nbsp;R. Christopher Pierce","doi":"10.1016/j.addicn.2023.100133","DOIUrl":"https://doi.org/10.1016/j.addicn.2023.100133","url":null,"abstract":"<div><p>The present study examined the effect of deep brain stimulation (DBS) in the nucleus accumbens shell on cocaine seeking and neuronal plasticity in rats. Electrical DBS of the accumbens shell attenuated cocaine primed reinstatement across a range of frequencies as low as 12 Hz in male rats. Nucleus accumbens medium spiny neurons (MSNs) can be differentiated by expression of dopamine D1 receptors (D1DRs) or D2DRs. Low-frequency optogenetic-DBS in D1DR- or D2DR-containing neurons attenuated cocaine seeking in male but not female rats. In slice electrophysiology experiments, 12 Hz electrical stimulation evoked long term potentiation (LTP) in D1DR-MSNs and D2DR-MSNs from cocaine naive male and female rats. However, in cocaine-experienced rats, electrical and optical DBS only elicited LTP in D2DR-MSNs from male rats. These results suggest that low frequency DBS in the nucleus accumbens shell effectively, but sex-specifically, suppresses cocaine seeking, which may be associated with the reversal of synaptic plasticity deficits in D2DR-MSNs.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"9 ","pages":"Article 100133"},"PeriodicalIF":0.0,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49766031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adolescent alcohol disrupts development of noradrenergic neurons in the nucleus of the tractus solitarius and enhances stress behaviors in adulthood in mice in a sex specific manner","authors":"Liz A. Aguilar ,&nbsp;Caitlin R. Coker ,&nbsp;Zari McCullers ,&nbsp;Alexandra Evans ,&nbsp;Opeyemi Showemimo ,&nbsp;Mariam Melkumyan ,&nbsp;Bailey N. Keller ,&nbsp;Angela E. Snyder ,&nbsp;Sarah S. Bingaman ,&nbsp;Patrick A. Randall ,&nbsp;Andras Hajnal ,&nbsp;Kirsteen N. Browning ,&nbsp;Amy C. Arnold ,&nbsp;Yuval Silberman","doi":"10.1016/j.addicn.2023.100132","DOIUrl":"https://doi.org/10.1016/j.addicn.2023.100132","url":null,"abstract":"<div><p>Alcohol use disorders (AUDs) are common mental health issues worldwide and can lead to other chronic diseases. Stress is a major factor in the development and continuation of AUDs, and adolescent alcohol exposure can lead to enhanced stress-responsivity and increased risk for AUD development in adulthood. The exact mechanisms behind the interaction between adolescence, stress, and alcohol are not fully understood and require further research. In this regard, the nucleus of the tractus solitarius (NTS) provides dense norepinephrine projections to the extended amygdala, providing a key pathway for stress-related alcohol behaviors. While NTS norepinephrine neurons are known to be alcohol sensitive, whether adolescent alcohol disrupts NTS-norepinephrine neuron development and if this is related to altered stress-sensitivity and alcohol preference in adulthood has not previously been examined. Here, we exposed male and female C57Bl/6J mice to the commonly used adolescent intermittent ethanol (AIE) vapor model during postnatal day 28-42 and examined AIE effects on: 1) tyrosine hydroxylase (TH) mRNA expression in the NTS across various ages (postnatal day 21-90), 2) behavioral responses to acute stress in the light/dark box test in adulthood, 3) NTS TH neuron responses to acute stress and ethanol challenges in adulthood, and 4) ethanol conditioned place preference behavior in adulthood. Overall the findings indicate that AIE alters NTS TH mRNA expression and increases anxiety-like behaviors following acute stress exposure in a sex-dependent manner. These mRNA expression and behavioral changes occur in the absence of AIE-induced changes in NTS TH neuron sensitivity to either acute stress or acute alcohol exposure or changes to ethanol conditioned place preference.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"9 ","pages":"Article 100132"},"PeriodicalIF":0.0,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49766028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluoxetine potentiates methylphenidate-induced behavioral responses: Enhanced locomotion or stereotypies and facilitated acquisition of cocaine self-administration","authors":"Lorissa Lamoureux ,&nbsp;Joel A. Beverley ,&nbsp;Michela Marinelli ,&nbsp;Heinz Steiner","doi":"10.1016/j.addicn.2023.100131","DOIUrl":"https://doi.org/10.1016/j.addicn.2023.100131","url":null,"abstract":"<div><p>The medical psychostimulant methylphenidate (MP) is used to treat attention-deficit hyperactivity disorder and recreationally as a “cognitive enhancer”. MP is a dopamine reuptake inhibitor, but does not affect serotonin. Serotonin contributes to addiction-related gene regulation and behavior. Previously, we showed that enhancing serotonin action by adding a selective serotonin reuptake inhibitor, fluoxetine (FLX), to MP potentiates MP-induced gene regulation in striatum and nucleus accumbens, mimicking cocaine effects. Here, we investigated the behavioral consequences of MP+FLX treatment. Young adult male rats received MP (5 mg/kg, i.p.) or MP+FLX (5 mg/kg each) daily for 6-8 days. Behavioral effects were assessed in an open-field test during the repeated treatment. Two weeks later the motor response to a cocaine challenge (25 mg/kg) and the rate of acquisition of cocaine self-administration behavior were determined. Our results demonstrate that FLX potentiates effects of MP on open-field behavior. However, we found differential behavioral responses to MP+FLX treatment, as approximately half of the rats developed high rates of focal stereotypies (termed “MP+FLX/high reactivity” group), whereas the other half did not, and only showed increased locomotion (“MP+FLX/low reactivity” group). Two weeks later, cocaine-induced locomotion and stereotypies were positively correlated with MP+FLX-induced behavior seen at the end of the repeated MP+FLX treatment. Moreover, the MP+FLX/high reactivity group, but not the low reactivity group, showed facilitated acquisition of cocaine self-administration. These results demonstrate that repeated MP+FLX treatment can facilitate subsequent cocaine taking behavior in a subpopulation of rats. These findings suggest that MP+FLX exposure in some individuals may increase the risk for psychostimulant use later in life.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"9 ","pages":"Article 100131"},"PeriodicalIF":0.0,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49766025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spermidine prevents the reinstatement of alcohol conditioned place preference","authors":"Avner Almeida Silva ,&nbsp;Gabrielle de Morais Henriques ,&nbsp;Victor Nascimento-Rocha ,&nbsp;Behaim Correia Dias-Júnior ,&nbsp;Alexia dos Anjos Santos ,&nbsp;Alexandre Justo Oliveira Lima ,&nbsp;Eduardo Ary Villela Marinho ,&nbsp;Maribel Antonello Rubin ,&nbsp;Carlos Fernando Mello","doi":"10.1016/j.addicn.2023.100130","DOIUrl":"https://doi.org/10.1016/j.addicn.2023.100130","url":null,"abstract":"<div><p>This study investigates whether spermidine (SPD), an endogenous polyamine, alters extinction and reinstatement of alcohol-induced conditioned place preference (CPP) in adult female Swiss mice. CPP was induced by injecting alcohol (1.8 g/kg, i.p.) and placing the animals in the drug-associated compartment for 10 min in four alternate days. During extinction, animals received vehicle or SPD (3, 10 or 30 mg/kg), and were placed in the drug-associated compartment for 10 min in 4 alternate days. Alcohol re-exposure was performed in the alcohol-paired compartment. In a second experiment, after conditioning, animals received vehicle, the N-methyl-<span>d</span>-aspartate (NMDA) receptor polyamine binding site antagonist arcaine (ARC, 0.1 mg/kg), SPD (10 mg/kg) or the association of both (ARC+SDP) in the drug-associated compartment. Animals were then sequentially subjected to alcohol re-exposure and a post-reexposure test. Spermidine did not alter CPP extinction, but prevented the reinstatement of CPP induced by alcohol reexposure. Arcaine prevented the effect of spermidine on alcohol-induced CPP reinstatement. The results suggest that SPD may facilitate the reconsolidation of conditioning memory, disrupting CPP. This effect seems to involve the polyamine binding site at the NMDA receptor, because it is prevented by ARC.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"9 ","pages":"Article 100130"},"PeriodicalIF":0.0,"publicationDate":"2023-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49759534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic alcohol exposure differentially alters calcium activity of striatal cell populations during actions.","authors":"Emily T. Baltz ,&nbsp;Rafael Renteria ,&nbsp;Christina M. Gremel","doi":"10.1016/j.addicn.2023.100128","DOIUrl":"10.1016/j.addicn.2023.100128","url":null,"abstract":"<div><p>Alcohol Use Disorder (AUD) can induce long lasting alterations to executive function. This includes altered action control, which can manifest as dysfunctional goal-directed control. Cortical and striatal circuits mediate goal-directed control over behavior, and prior research has found chronic alcohol disrupts these circuits. In particular, prior in vivo and ex vivo work have identified alterations to function and activity of dorsal medial striatum (DMS), which is necessary for goal-directed control. However, unknown is whether these alterations manifest as altered activity of select DMS populations during behavior. Here we examine effects of prior chronic alcohol exposure on calcium activity modulation during action-related behaviors via fiber photometry of genetically-identified DMS populations including the direct and indirect output pathways, and fast-spiking interneurons. We find that prior chronic alcohol exposure leads to increased calcium modulation of the direct pathway during action related behavior. In contrast, prior chronic alcohol exposure led to decreased calcium activity modulation of the indirect pathway and the fast-spiking interneuron population around action-related events. Together, our findings suggest an imbalance in striatal activity during action control. This disruption may contribute to the altered goal-directed control previously reported.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"8 ","pages":"Article 100128"},"PeriodicalIF":0.0,"publicationDate":"2023-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10569208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41241535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “Circuit dysfunctions of associative and sensorimotor basal ganglia loops in alcohol use disorder: insights from animal models” (Addiction Neuroscience 5 (2023) 100056)","authors":"Giacomo Sitzia ,&nbsp;David M. Lovinger","doi":"10.1016/j.addicn.2023.100094","DOIUrl":"10.1016/j.addicn.2023.100094","url":null,"abstract":"","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"7 ","pages":"Article 100094"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45081302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"No evidence of accelerated epigenetic aging among black heroin users: A case vs control analysis","authors":"Jermaine D. Jones ,&nbsp;Suky Martinez ,&nbsp;Ingrid Gonzalez ,&nbsp;Gabriel J. Odom ,&nbsp;Sandra D. Comer","doi":"10.1016/j.addicn.2023.100096","DOIUrl":"10.1016/j.addicn.2023.100096","url":null,"abstract":"<div><p>This study sought to assess the association between illicit opioid use and accelerated epigenetic aging (A.K.A. DNAm Age) among people of African ancestry who use heroin. DNA was obtained from participants with opioid use disorder (OUD) who confirmed heroin as their primary drug of choice. Clinical inventories of drug use included: the Addiction Severity Index (ASI) Drug-Composite Score (range: 0–1), and Drug Abuse Screening Test (DAST-10; range: 0–10). A control group of participants of African ancestry who did not use heroin was recruited and matched to heroin users on sex, age, socioeconomic level, and smoking status. Methylation data were assessed in an epigenetic clock to determined and compare Epigenetic Age to Chronological Age (i.e., age acceleration or deceleration). Data were obtained from 32 controls [mean age 36.3 (±7.5) years] and 64 heroin users [mean age 48.1 (±6.6) years]. The experimental group used heroin for an average of 18.1 (±10.6) years, reported use of 6.4 (±6.1) bags of heroin/day, with a mean DAST-10 score of 7.0 (±2.6) and ASI Score of 0.33 (±0.19). Mean age acceleration for heroin users [+0.56 (± 9.5) years] was significantly (<em>p</em>&lt; 0.05) lower than controls [+5.19 (± 9.1) years]. This study did not find evidence that heroin use causes epigenetic age acceleration.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"7 ","pages":"Article 100096"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10120225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum regarding missing statement in previously published article","authors":"","doi":"10.1016/j.addicn.2023.100088","DOIUrl":"10.1016/j.addicn.2023.100088","url":null,"abstract":"","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"7 ","pages":"Article 100088"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47454720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic medicine to reduce tobacco and related disorders: Translation to precision prevention and treatment","authors":"Li-Shiun Chen ,&nbsp;Timothy B. Baker ,&nbsp;Alex Ramsey ,&nbsp;Christopher I. Amos ,&nbsp;Laura J. Bierut","doi":"10.1016/j.addicn.2023.100083","DOIUrl":"10.1016/j.addicn.2023.100083","url":null,"abstract":"<div><p>Genomic medicine can enhance prevention and treatment. First, we propose that advances in genomics have the potential to enhance assessment of disease risk, improve prognostic predictions, and guide treatment development and application. Clinical implementation of polygenic risk scores (PRSs) has emerged as an area of active research. The pathway from genomic discovery to implementation is an iterative process. Second, we provide examples on how genomic medicine has the potential to solve problems in prevention and treatment using two examples: Lung cancer screening and evidence-based tobacco treatment are both under-utilized and great opportunities for genomic interventions. Third, we discuss the translational process for developing genomic interventions from evidence to implementation by presenting a model to evaluate genomic evidence for clinical implementation, mechanisms of genomic interventions, and patient desire for genomic interventions. Fourth, we present potential challenges in genomic interventions including a great need for evidence in all diverse populations, little evidence on treatment algorithms, challenges in accommodating a dynamic evidence base, and implementation challenges in real world clinical settings. Finally, we conclude that research to identify genomic markers that are associated with smoking cessation success and the efficacy of smoking cessation treatments is needed to empower people of all diverse ancestry. Importantly, genomic data can be used to help identify patients with elevated risk for nicotine addiction, difficulty quitting smoking, favorable response to specific pharmacotherapy, and tobacco-related health problems.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"7 ","pages":"Article 100083"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/35/40/nihms-1899409.PMC10434839.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10138590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of sex hormones in targeting stress-induced tobacco craving, stress-reactivity, and smoking with guanfacine among women who smoke","authors":"MacKenzie R. Peltier ,&nbsp;Sherry A. McKee","doi":"10.1016/j.addicn.2023.100084","DOIUrl":"10.1016/j.addicn.2023.100084","url":null,"abstract":"<div><p>Women who smoke are particularly vulnerable to tobacco craving, smoking behaviors, and relapse in the context of stress when compared to men who smoke. One factor in this sex difference may be sex hormones, including estradiol and progesterone; however, smoking cessation medication trials often do not explore the impact of sex hormones on drug effects. This secondary analysis of a double-blind, placebo-controlled study explored the impact of levels of actual estradiol and progesterone on guanfacine, a noradrenergic α2a agonist, which attenuates stress-induced smoking behaviors in women. Women who smoke (<em>n</em> = 43) completed a stress induction laboratory paradigm followed by an ad-libitum smoking period. Assessment of tobacco craving, and stress-reactivity (via cortisol response) occurred pre- and post-stress induction. Results indicated that guanfacine attenuated stress-induced tobacco craving (<em>F</em> = 10.94, <em>p</em> = 0.02) and cortisol response (<em>F</em> = 14.23, <em>p</em> &lt; 0.001); however, high levels of estradiol overrode guanfacine's effect on craving (<em>F</em> = 4.00, <em>p</em> = 0.05), cortisol response (<em>F</em> = 14.23, <em>p</em> &lt; 0.001), and smoking during the ad-libitum period (<em>F</em> = 12.23, <em>p</em> = 0.001). Additionally, progesterone proved to be protective against tobacco craving and enhanced guanfacine's medication effect on craving (<em>F</em> = 5.57, <em>p</em> = 0.02). The present study found that sex hormones had a significant impact on medication effects in a smoking cessation trial and thus underscore the importance of examining the role of sex hormones in future medication trials.</p></div>","PeriodicalId":72067,"journal":{"name":"Addiction neuroscience","volume":"7 ","pages":"Article 100084"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/65/f3/nihms-1909950.PMC10311966.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10138003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}