Pharmacology Biochemistry and Behavior最新文献

{"title":"Passive cigarette smoke exposure induces dose-dependent conditioned place preference in mice.","authors":"An-Fu Hu, Jian Jiang, Xia Li, Qian Xia, Guo-Jun Zhou, Hong-Juan Wang, Chengyun Xu, Ximei Wu","doi":"10.1016/j.pbb.2026.174288","DOIUrl":"https://doi.org/10.1016/j.pbb.2026.174288","url":null,"abstract":"<p><p>Nicotine reward is a key driver of tobacco dependence; however, the mechanisms underlying reward induced by cigarette smoke, particularly under passive exposure conditions, remain incompletely understood. In the present study, we established an adjustable cigarette smoke exposure system to generate controlled smoke concentrations (0.5, 1.0, and 2.0 g/m³) and investigated the behavioral and molecular consequences of repeated smoke exposure in mice. Animals were exposed to cigarette smoke or air for 2 h daily for 14 or 28 days. Serum nicotine levels were quantified by UPLC-MS/MS, reward-related behavior was evaluated using a conditioned place preference (CPP) paradigm, and the expression of reward-associated signaling proteins in the nucleus accumbens (NAc) was assessed by Western blotting. Cigarette smoke exposure produced a dose-dependent increase in serum nicotine concentrations. No significant CPP was observed after 14 days of exposure; however, after 28 days, mice exhibited a significant and dose-dependent increase in preference for the smoke-paired compartment, accompanied by elevated preference index values. At the molecular level, repeated smoke exposure induced dose-dependent increases in p-ERK, p-CaMKII, and c-Fos expression in the NAc. Furthermore, administration of the nicotinic acetylcholine receptor antagonist mecamylamine significantly attenuated both CPP behavior and the activation of these signaling pathways. These findings demonstrate that repeated cigarette smoke exposure induces nicotine-dependent reward behavior through activation of NAc-associated signaling pathways. This model provides a reproducible and physiologically relevant platform for investigating the neurobiological mechanisms of smoke-induced nicotine reward under passive exposure conditions and may facilitate the development of therapeutic strategies for tobacco dependence.</p>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":" ","pages":"174288"},"PeriodicalIF":2.4,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Co-injections of L-NAC methyl ester reduce the loss of antinociception and prevent the occurrence of hyperalgesia elicited by injections of fentanyl in male rats.","authors":"Paulina M Getsy, Santhosh M Baby, Gregory A Coffee, Yee-Hsee Hsieh, James N Bates, Brian Meshkin, Stephen J Lewis","doi":"10.1016/j.pbb.2026.174286","DOIUrl":"https://doi.org/10.1016/j.pbb.2026.174286","url":null,"abstract":"<p><p>The development of hyperalgesia (i.e., enhanced physical pain and/or psychological distress) during chronic fentanyl use plays a vital role in the continued and accelerated use of this potent synthetic opioid. Numerous biochemical changes in the brain, such as changes in redox status, are thought to contribute to the development of hyperalgesia to fentanyl and other opioids. This study addresses whether the clinically used antioxidant N-acetyl-L-cysteine (L-NAC) and its readily cell-penetrant analogue, L-NAC methyl ester (L-NACme) would affect the progressive loss of antinociception and appearance of hyperalgesia in adult male Sprague Dawley rats. We monitored changes in tail-flick latencies following twice daily co-injections over 5 days (8 AM, 8 PM) of fentanyl (125 μg/kg, IV) + vehicle or L-NAC (500 μmol/kg, IV) or L-NACme (500 μmol/kg, IV) in the rats. The first co-injections of fentanyl + vehicle elicited a long-lasting antinociception, whereas a robust hyperalgesia appeared with co-injections 5 and was even more dramatic following co-injections 6-10. The co-injections of fentanyl + L-NAC partially prevented the loss of antinociception and occurrence of hyperalgesia, and co-injections of fentanyl and L-NACme markedly reduced the loss of antinociception and prevented the appearance of hyperalgesia. This study provides evidence that L-NAC and L-NACme beneficially affect the alterations in pain processing that occurs with sub-chronic administration of fentanyl. The higher efficacy of L-NACme is likely to be due to its greater cell penetrability in brain regions and interaction with intracellular signaling cascades, which may include redox-dependent processes, that mediate fentanyl-induced antinociception and hyperalgesia.</p>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":" ","pages":"174286"},"PeriodicalIF":2.4,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protocadherin 10, a member of cadherin superfamily, increases stress-susceptibility in chronic unpredictable stress-treated rats","authors":"Xin-Mu Li ,&nbsp;Ning-Ning Zhang ,&nbsp;Xiao-Ling Zhang ,&nbsp;Nuo Liu ,&nbsp;Cong-Yuan Xia ,&nbsp;Xiong Yang ,&nbsp;Hui-Qin Wang ,&nbsp;Xu Yan ,&nbsp;Shi-Feng Chu ,&nbsp;Nai-Hong Chen ,&nbsp;Zhen-Zhen Wang","doi":"10.1016/j.pbb.2026.174158","DOIUrl":"10.1016/j.pbb.2026.174158","url":null,"abstract":"<div><div>Depression is a debilitating disorder influenced by individual variation in stress susceptibility. The identification of stress-sensitive and stress-resistant phenotypes is critical for understanding its pathogenesis. We previously identified several proteins associated with these phenotypes, yet their functional roles remain unclear. Here, we investigated whether protocadherin 10 (PCDH10), a brain-enriched non-clustered protocadherin, underlies individual differences in stress susceptibility. Rats were subjected to chronic unpredictable stress and classified as stress-sensitive or stress-resistant individuals based on sucrose preference. We found that PCDH10 mRNA and protein levels were significantly downregulated in the medial prefrontal cortex of stress-sensitive rats but upregulated in stress-resistant rats compared to controls. Conversely, opposing expression patterns were observed in the hippocampus. Functional studies demonstrated that PCDH10 overexpression in the hippocampus promoted depression-like behaviors, whereas its knockdown exerted a protective, antidepressant-like effect. Our findings reveal PCDH10 as a key region-specific regulator of stress susceptibility. Targeted inhibition of PCDH10 in the hippocampus represents a promising new therapeutic strategy for depression.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"261 ","pages":"Article 174158"},"PeriodicalIF":2.5,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146070984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in impact of daily and chronic psychological stressors on diurnal cortisol level","authors":"Nikolai Malykhin ,&nbsp;Joseph Serrano ,&nbsp;Kathleen Hegadoren ,&nbsp;Wojciech Pietrasik","doi":"10.1016/j.pbb.2026.174165","DOIUrl":"10.1016/j.pbb.2026.174165","url":null,"abstract":"<div><div>Chronic stress contributes to multiple physical and mental disorders. The main goal of the present study was to investigate the effects of daily and chronic psychological stressors on hypothalamic-pituitary-adrenal (HPA) axis function measured by diurnal cortisol levels and rhythms using a community sample of adults experiencing different levels of stress.</div><div>78 individuals from the general population were recruited for this study. We measured recent daily stressors, chronic stress (Trier Inventory for Chronic Stress (TICS-E) English version) within the last three months, perceived stress level, mental health outcomes, and salivary cortisol (cortisol awakening response (CAR) and diurnal cortisol slope (DCS)).</div><div>We found that increased morning cortisol output and CAR measures were associated with both more recent and chronic stress levels, while larger cortisol decreases in the afternoon, measured by DCS, were linked to chronic stress. The observed relationships among several TICS-E factors and mental health outcomes with both CAR and DCS differed between men and women. The associations between cortisol measures and TICS-E factors related to pressure to perform and social recognition were observed only in males, while associations with social overload and social tension factors were found in both sexes. In female participants higher HPA axis response was linked to increased levels of perceived stress, anxiety, and general distress.</div><div>Our results demonstrated for the first time that the HPA axis response to chronic stressors might be context-specific in men and women and that changes in HPA axis function and related mental health outcomes are sex-specific.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"261 ","pages":"Article 174165"},"PeriodicalIF":2.5,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146166115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High doses of orally administered cannabigerol produce deficits in sustained attention in female rats","authors":"Catherine F. Moore ,&nbsp;Cecilia L. Bergeria ,&nbsp;Cristina Sempio ,&nbsp;Jost Klawitter ,&nbsp;Uwe Christians ,&nbsp;Elise M. Weerts","doi":"10.1016/j.pbb.2026.174154","DOIUrl":"10.1016/j.pbb.2026.174154","url":null,"abstract":"<div><div>Cannabigerol (CBG) is a phytocannabinoid found in cannabis that is increasingly being sold and used as an isolate product or as the dominant cannabinoid in cannabis products for purported cognitive enhancement (attention, focus, and memory). The purpose of this study was to evaluate the effects of orally administered CBG on sustained attention, motivation, and memory. In a series of experiments, separate groups of male and female adult Sprague Dawley rats received oral CBG (30–600 mg/kg, per os [p.o.]) or sesame oil vehicle prior to testing in 1) the rodent psychomotor vigilance test; 2) progressive ratio responding for food; 3) spontaneous alternation test of working memory (selected doses: 300–600 mg/kg, p.o.). Blood plasma was collected 60 min following oral administration for assessments of circulating CBG levels. CBG produced deficits in sustained attention at the highest doses (300–600 mg/kg) in female, but not male, rats. CBG did not affect motivation to respond for a food reward nor working memory, indicating an effect specific to attention in females. Finally, females showed significantly higher circulating CBG in plasma compared with males following oral CBG. In sum, these data suggest a sex-specific effect of CBG on sustained attention in females.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"260 ","pages":"Article 174154"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145963366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The SIRT1-HMGB1 pathway in hippocampal microglia is involved in chronic heroin-induced cognitive impairment","authors":"Chunlu Li ,&nbsp;Yujie Wei ,&nbsp;Dan Yin ,&nbsp;Chuanrui Zhao ,&nbsp;Guangkun Chen ,&nbsp;Qian Wang ,&nbsp;Mingjuan Shi ,&nbsp;Yan Hong ,&nbsp;Yixin Li ,&nbsp;Baijuan Xia","doi":"10.1016/j.pbb.2026.174155","DOIUrl":"10.1016/j.pbb.2026.174155","url":null,"abstract":"<div><div>Recent studies have found that microglia-mediated hippocampal damage may be involved in cognitive impairment induced by chronic heroin treatment. However, its specific molecular mechanism remains unclear. This study explored the possible role of the SIRT1-HMGB1 pathway in this phenomenon. We found that 30 days, but not 15 days, of chronic heroin treatment could impair the learning and memory of mice in the water maze task; compared with 15 days of heroin treatment, 30 days of chronic heroin treatment induced more hippocampal SIRT1 and HMGB1 expression, especially the number of SIRT1-positive and HMGB1-positive microglia, and promoted the polarization of microglia to proinflammatory types. Selective knockdown of SIRT1 expression in hippocampal microglia exacerbated the learning and memory impairment induced by 30 days of heroin treatment; reduced the number of HMGB1-positive microglia, reversed the polarization of microglia to proinflammatory types, and exacerbated the apoptosis of cells in the hippocampus. These results suggest that chronic heroin treatment may be involved in the cognitive impairment process by activating the SIRT1-HMGB1 pathway in microglia.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"260 ","pages":"Article 174155"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146039146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence of heterogeneity in the opioid withdrawal syndrome: Spontaneous and precipitated withdrawal","authors":"Suky Martinez ,&nbsp;Jermaine D. Jones ,&nbsp;Kelly E. Dunn ,&nbsp;Andrew Huhn ,&nbsp;Joshua A. Lile ,&nbsp;Thomas P. Shellenberg ,&nbsp;Laura Brandt","doi":"10.1016/j.pbb.2026.174153","DOIUrl":"10.1016/j.pbb.2026.174153","url":null,"abstract":"<div><h3>Aims</h3><div>This study characterized the heterogeneity of opioid withdrawal by comparing naturally occurring withdrawal during opioid abstinence (spontaneous withdrawal) with abrupt, pharmacologically induced naloxone-precipitated withdrawal in adults with Opioid Use Disorder (OUD).</div></div><div><h3>Methods</h3><div>A secondary analysis was conducted on de-identified data from 86 adults meeting DSM-5 criteria for moderate-to-severe OUD. Participants either presented in spontaneous withdrawal (<em>n</em> = 28) or underwent naloxone challenge to precipitate withdrawal (<em>n</em> = 58). Withdrawal symptoms were rated using the Wang procedure. Principal Component Analysis (PCA) of binary symptom data was performed to identify dominant patterns of symptom co-occurrence. Separate PCAs were then conducted for the withdrawal syndrome types to delineate group-specific symptom clusters.</div></div><div><h3>Results</h3><div>In the combined sample, four principal components together accounted for 55.6% of the variance in withdrawal symptoms, with the highest loadings observed on autonomic (e.g., temperature change, sweating) and somatic (e.g., restlessness, yawning) domains. Subgroup analyses revealed distinct symptom-loading patterns: the spontaneous withdrawal group displayed a more pronounced autonomic profile dominated by temperature dysregulation and muscle aching, whereas the precipitated withdrawal group exhibited greater variability, with notable gastrointestinal (vomiting, stomach pain) and somatic features. Across analyses, inter-individual variability was substantial, underscoring the multidimensional nature of opioid withdrawal.</div></div><div><h3>Conclusion</h3><div>These findings suggest spontaneous and precipitated withdrawal are distinct clinical phenomena: the former emerges gradually, the latter produces diverse, acute symptoms, though both display heterogeneity. Moreover, relying solely on naloxone-challenge paradigms for treatment development may overlook key aspects of “real-world” spontaneous withdrawal, reinforcing the importance of broader experimental models and individualized care.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"260 ","pages":"Article 174153"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145952733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of short-chain fatty acids and neuroinflammation in PTSD pathogenesis: A gut microbial perspective","authors":"Qian-Zhong Song ,&nbsp;Bing-Yao Liu ,&nbsp;Si-Wei Wang ,&nbsp;Hai-Yan Wang ,&nbsp;Hui Cheng ,&nbsp;Jun-Hua Chen ,&nbsp;Qi-Feng Li ,&nbsp;Sen Li ,&nbsp;Xiu-Min Lu ,&nbsp;Yong-Tang Wang","doi":"10.1016/j.pbb.2026.174157","DOIUrl":"10.1016/j.pbb.2026.174157","url":null,"abstract":"<div><div>Exposure to severe psychological trauma is a recognized etiological precursor to post-traumatic stress disorder (PTSD), a potentially debilitating psychiatric condition. Increasing evidence indicates a strong connection between mental disorders and the metabolic system, in which the gut microbiota, as a key component, exerts significant influence on psychiatric health. The gut is often referred to as the “second brain”, the gut engages in bidirectional communication with the central nervous system to maintain physiological homeostasis. Trauma affecting the nervous system and cognitive functions such as learning and memory can disrupt the gut microbial community and even trigger inflammatory responses. Conversely, changes in the gut microbiota can adversely affect neurocognitive function. This review systematically summarizes the bidirectional relationship between PTSD and gut microbiota, the pathways through which microbial dysbiosis influences PTSD symptoms, and the underlying mechanisms involving immune regulation, microbial metabolites, and vagus nerve signaling. It also discusses microbiota-based intervention strategies for PTSD, aiming to provide a theoretical foundation for microbial-targeted therapeutic approaches.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"260 ","pages":"Article 174157"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Behaviour of female mice defeated in an inter-female aggression protocol predicts resilience to cocaine-induced conditioned place preference","authors":"María Ángeles Martínez-Caballero ,&nbsp;Claudia Calpe-López ,&nbsp;María Pilar García-Pardo ,&nbsp;María Carmen Arenas ,&nbsp;Carmen Manzanedo ,&nbsp;María Asunción Aguilar","doi":"10.1016/j.pbb.2026.174156","DOIUrl":"10.1016/j.pbb.2026.174156","url":null,"abstract":"<div><div>Several studies have demonstrated that exposure to different protocols of social defeat induces anxiety- and depression-like symptoms in male and female mice. Moreover, male mice exposed to an intermittent social defeat (ISD) show increased vulnerability to the rewarding effects of cocaine, although several behavioural traits have been found to confer resilience against this effect. However, the effects of ISD on the vulnerability to drugs of abuse in female mice have not been studied. Thus, our aim was to evaluate the short-term behavioural effects of ISD and its long-term influence on the rewarding effects of cocaine in female mice. Intruder female mice were exposed to an ISD protocol and performed the elevated plus maze, hole-board, social interaction, splash, object recognition and tail suspension tests 24 or 48 h after the last episode of defeat. Three weeks later, female mice underwent the conditioned place preference procedure with cocaine. ISD exposure induced a slight anxiogenic effect, decreased novelty-seeking behaviour and enhanced sensitivity to the conditioned rewarding effects of cocaine. However, defeated female mice characterized by an active coping response during episodes of defeat and an avoidance of potential dangers in unknown environments did not develop cocaine preference. Our results show that defeat in an inter-female aggression protocol is a useful way to study the long-term consequences of social stress on cocaine reward and the behavioural traits associated with resilience.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"260 ","pages":"Article 174156"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146039145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eutylone history selectively impacts the rewarding and aversive effects of cocaine, MDMA, and eutylone in female Sprague-Dawley rats","authors":"Negar G. Ardabili,&nbsp;Shira Tan,&nbsp;María Elisa Márquez de Prado Arrarás,&nbsp;Honeyeh Younesie,&nbsp;Anthony L. Riley","doi":"10.1016/j.pbb.2026.174152","DOIUrl":"10.1016/j.pbb.2026.174152","url":null,"abstract":"<div><div>Both the rewarding and aversive effects of a drug contribute to its abuse potential. One factor known to impact the balance of these effects is concurrent and serial polydrug use. A drug class for which such interactions are common is synthetic cathinones. In prior work, history with the synthetic cathinone eutylone had no effect on cocaine- or MDMA-induced taste avoidance in male rats, possibly as a function of the insufficient overlap between the pharmacological activity of eutylone and the other compounds. To investigate the broader scope of this effect, this study assessed how a history of eutylone influenced drug-induced taste avoidance in female rats. Assessments were also made on the rewarding effects of these drugs, given their importance for abuse vulnerability. In the present study, adult female Sprague-Dawley rats were exposed to eutylone or saline prior to concurrent taste avoidance/place preference conditioning in which saccharin and a distinct compartment were repeatedly paired with cocaine, MDMA, or eutylone. All drugs induced taste avoidance. Avoidance induced by eutylone was attenuated by eutylone history, but those induced by MDMA and cocaine were unaffected. Eutylone history had no effect on place preferences induced by MDMA or eutylone (but increased place preferences induced by cocaine). The failure of eutylone to impact the aversive effects of cocaine and MDMA despite sharing neurochemical actions suggests that eutylone's pharmacological activity may produce subjective effects that differ from those of either MDMA or cocaine. The differential effects of eutylone history on drug reward (increasing cocaine reward but having no impact on eutylone or MDMA) remain unknown but suggests that the basis for the aversive and rewarding effects of these drugs are dissociable.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"260 ","pages":"Article 174152"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145945548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}