Pub Date : 2023-10-01Epub Date: 2023-06-15DOI: 10.1037/bne0000560
Caitlyn J Bartsch, Sophia Aaflaq, Jessica T Jacobs, Molly Smith, Fletcher Summa, Savannah Skinner, Elana Qasem, Rylee Thompson, Zheng Li, Jacob C Nordman
Ketamine is a dissociative anesthetic that has been shown to have antidepressant effects in humans and has been proposed as a potential treatment for mood disorders such as posttraumatic stress disorder and aggression. However, previous studies from our lab and others have demonstrated that ketamine's effects are highly context- and dose-dependent. In a recent study, we found that 10 mg/kg ketamine could exacerbate the effects of early life stress on excessive aggression in mice. To further investigate, the effect of ketamine on moods, such as fear, anxiety, depression, and aggression, we used a mouse model of early life stress, involving chronic social isolation followed by acute traumatic stress in the form of noncontingent, unpredictable foot shock during adolescence. We find this is necessary to induce long-lasting excessive aggression in a novel environment. Seven- to eight-week-old socially isolated mice were given IP injections of 10 mg/kg ketamine 30 min before being subjected to foot shock and then assessed 7 days later for changes in sociability, aggression, mobility, anxiety-like behavior, and depression-like behavior. The results show that ketamine selectively increases long-lasting aggression in mice exposed to foot shock, but does not affect mood-related behaviors or locomotion. These findings suggest that during early life stress, ketamine may exert its effects by specifically targeting aggression brain circuitry that is distinct from brain circuits responsible for nonaggressive social or emotional behaviors. Therefore, while ketamine may be a promising treatment for various mood disorders, caution should be exercised when using ketamine to treat disorders associated with early life stress. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
{"title":"A single dose of ketamine enhances early life stress-induced aggression with no effect on fear memory, anxiety-like behavior, or depression-like behavior in mice.","authors":"Caitlyn J Bartsch, Sophia Aaflaq, Jessica T Jacobs, Molly Smith, Fletcher Summa, Savannah Skinner, Elana Qasem, Rylee Thompson, Zheng Li, Jacob C Nordman","doi":"10.1037/bne0000560","DOIUrl":"10.1037/bne0000560","url":null,"abstract":"<p><p>Ketamine is a dissociative anesthetic that has been shown to have antidepressant effects in humans and has been proposed as a potential treatment for mood disorders such as posttraumatic stress disorder and aggression. However, previous studies from our lab and others have demonstrated that ketamine's effects are highly context- and dose-dependent. In a recent study, we found that 10 mg/kg ketamine could exacerbate the effects of early life stress on excessive aggression in mice. To further investigate, the effect of ketamine on moods, such as fear, anxiety, depression, and aggression, we used a mouse model of early life stress, involving chronic social isolation followed by acute traumatic stress in the form of noncontingent, unpredictable foot shock during adolescence. We find this is necessary to induce long-lasting excessive aggression in a novel environment. Seven- to eight-week-old socially isolated mice were given IP injections of 10 mg/kg ketamine 30 min before being subjected to foot shock and then assessed 7 days later for changes in sociability, aggression, mobility, anxiety-like behavior, and depression-like behavior. The results show that ketamine selectively increases long-lasting aggression in mice exposed to foot shock, but does not affect mood-related behaviors or locomotion. These findings suggest that during early life stress, ketamine may exert its effects by specifically targeting aggression brain circuitry that is distinct from brain circuits responsible for nonaggressive social or emotional behaviors. Therefore, while ketamine may be a promising treatment for various mood disorders, caution should be exercised when using ketamine to treat disorders associated with early life stress. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 5","pages":"281-288"},"PeriodicalIF":1.6,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10694802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10498269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Supplemental Material for Electric Barrier-Induced Voluntary Abstinence Reduces Alcohol Seeking in Male, but Not Female, iP Rats","authors":"","doi":"10.1037/bne0000566.supp","DOIUrl":"https://doi.org/10.1037/bne0000566.supp","url":null,"abstract":"","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2023-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47355204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-01Epub Date: 2023-03-06DOI: 10.1037/bne0000555
Changjiu Zhao, Lauren V Riters
The medial preoptic area (MPOA) is well known for its role in sexual and maternal behaviors. This region also plays an important role in affiliative social behaviors outside reproductive contexts. We recently demonstrated that the MPOA is a central nucleus in which opioids govern highly rewarding social play behavior in adolescent rats. However, the neural circuit mechanisms underlying MPOA-mediated social play remain largely unresolved. We hypothesized that the MPOA unites a complementary neural system through which social play induces reward via a projection to the ventral tegmental area (VTA) and reduces a negative affective state through a projection to the periaqueductal gray (PAG). To test whether the two projection pathways are activated in response to social play behavior, we combined retrograde tract tracing with immediate early gene (IEG) expression and immunofluorescent labeling to identify opioid-sensitive projection pathways from the MPOA to VTA and PAG that are activated after performance of social play. Retrograde tracer, fluoro-gold (FG), was microinjected into the VTA or PAG. IEG expression (i.e., Egr1) was assessed and triple immunofluorescent labeling for mu opioid receptor (MOR), Egr1, and FG in the MPOA was performed after social play. We revealed that play animals displayed an increase in neurons double labeled for Egr1 + FG and triple labeled for MOR + Egr1 + FG in the MPOA projecting to both the VTA and PAG when compared to no-play rats. The increased activation of projection neurons that express MORs from MPOA to VTA or PAG after social play suggests that opioids may act through these projection pathways to govern social play. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
{"title":"The medial preoptic area and its projections to the ventral tegmental area and the periaqueductal gray are activated in response to social play behavior in juvenile rats.","authors":"Changjiu Zhao, Lauren V Riters","doi":"10.1037/bne0000555","DOIUrl":"10.1037/bne0000555","url":null,"abstract":"<p><p>The medial preoptic area (MPOA) is well known for its role in sexual and maternal behaviors. This region also plays an important role in affiliative social behaviors outside reproductive contexts. We recently demonstrated that the MPOA is a central nucleus in which opioids govern highly rewarding social play behavior in adolescent rats. However, the neural circuit mechanisms underlying MPOA-mediated social play remain largely unresolved. We hypothesized that the MPOA unites a complementary neural system through which social play induces reward via a projection to the ventral tegmental area (VTA) and reduces a negative affective state through a projection to the periaqueductal gray (PAG). To test whether the two projection pathways are activated in response to social play behavior, we combined retrograde tract tracing with immediate early gene (IEG) expression and immunofluorescent labeling to identify opioid-sensitive projection pathways from the MPOA to VTA and PAG that are activated after performance of social play. Retrograde tracer, fluoro-gold (FG), was microinjected into the VTA or PAG. IEG expression (i.e., Egr1) was assessed and triple immunofluorescent labeling for mu opioid receptor (MOR), Egr1, and FG in the MPOA was performed after social play. We revealed that play animals displayed an increase in neurons double labeled for Egr1 + FG and triple labeled for MOR + Egr1 + FG in the MPOA projecting to both the VTA and PAG when compared to no-play rats. The increased activation of projection neurons that express MORs from MPOA to VTA or PAG after social play suggests that opioids may act through these projection pathways to govern social play. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 4","pages":"223-235"},"PeriodicalIF":1.6,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10230877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-01Epub Date: 2023-05-04DOI: 10.1037/bne0000558
Craig A Taswell, Miriam Janssen, Elisabeth A Murray, Bruno B Averbeck
The ventral striatum (VS) and amygdala are two structures often implicated as essential structures for learning. The literature addressing the contribution of these areas to learning, however, is not entirely consistent. We propose that these inconsistencies are due to learning environments and the effect they have on motivation. To differentiate aspects of learning from environmental factors that affect motivation, we ran a series of experiments with varying task factors. We compared monkeys (Macaca mulatta) with VS lesions, amygdala lesions, and unoperated controls on reinforcement learning (RL) tasks that involve learning from both gains and losses as well as from deterministic and stochastic schedules of reinforcement. We found that for all three groups, performance varied by experiment. All three groups modulated their behavior in the same directions, to varying degrees, across the three experiments. This behavioral modulation is why we find deficits in some experiments, but not others. The amount of effort animals exhibited differed depending on the learning environment. Our results suggest that the VS is important for the amount of effort animals will give in rich deterministic and relatively leaner stochastic learning enivornments. We also showed that monkeys with amygdala lesions can learn stimulus-based RL in stochastic environments and environments with loss and conditioned reinforcers. These results show that learning environments shape motivation and that the VS is essential for distinct aspects of motivated behavior. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
腹侧纹状体(VS)和杏仁核这两个结构经常被认为是学习的基本结构。然而,有关这些区域对学习的贡献的文献并不完全一致。我们认为,造成这些不一致的原因是学习环境及其对学习动机的影响。为了将影响学习动机的学习因素与环境因素区分开来,我们进行了一系列任务因素各不相同的实验。我们比较了VS病变猴、杏仁核病变猴和未接受手术的对照组猴在强化学习(RL)任务中的表现,这些任务包括从收益和损失中学习,以及从确定性和随机性的强化计划中学习。我们发现,所有三组人的表现都因实验而异。在这三个实验中,所有三个小组都在不同程度上朝着相同的方向调节自己的行为。这种行为调控是我们在某些实验中发现缺陷,而在其他实验中却没有发现的原因。学习环境不同,动物所表现出的努力程度也不同。我们的结果表明,在丰富的确定性学习环境和相对较少的随机学习环境中,VS 对动物的努力程度非常重要。我们的研究还表明,杏仁核病变的猴子可以在随机环境以及有损失强化物和条件强化物的环境中学习基于刺激的RL。这些结果表明,学习环境塑造了动机,而VS对动机行为的不同方面至关重要。(PsycInfo Database Record (c) 2023 APA, 版权所有)。
{"title":"The motivational role of the ventral striatum and amygdala in learning from gains and losses.","authors":"Craig A Taswell, Miriam Janssen, Elisabeth A Murray, Bruno B Averbeck","doi":"10.1037/bne0000558","DOIUrl":"10.1037/bne0000558","url":null,"abstract":"<p><p>The ventral striatum (VS) and amygdala are two structures often implicated as essential structures for learning. The literature addressing the contribution of these areas to learning, however, is not entirely consistent. We propose that these inconsistencies are due to learning environments and the effect they have on motivation. To differentiate aspects of learning from environmental factors that affect motivation, we ran a series of experiments with varying task factors. We compared monkeys (<i>Macaca mulatta</i>) with VS lesions, amygdala lesions, and unoperated controls on reinforcement learning (RL) tasks that involve learning from both gains and losses as well as from deterministic and stochastic schedules of reinforcement. We found that for all three groups, performance varied by experiment. All three groups modulated their behavior in the same directions, to varying degrees, across the three experiments. This behavioral modulation is why we find deficits in some experiments, but not others. The amount of effort animals exhibited differed depending on the learning environment. Our results suggest that the VS is important for the amount of effort animals will give in rich deterministic and relatively leaner stochastic learning enivornments. We also showed that monkeys with amygdala lesions can learn stimulus-based RL in stochastic environments and environments with loss and conditioned reinforcers. These results show that learning environments shape motivation and that the VS is essential for distinct aspects of motivated behavior. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 4","pages":"268-280"},"PeriodicalIF":1.6,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10662269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Recent studies indicated that positive symptoms of schizophrenia, such as hallucination and delusion, can be modeled using Pavlovian conditioning procedures. Various schizophrenia model animals exhibit abnormally strong associative activations of absent stimuli (i.e., conditioned hallucination) and readily form further associations involving the absent cues (i.e., enhanced mediated conditioning). In the present study using mice, we examined whether the acquisition of appetitive trace conditioning, another Pavlovian task in which animals must form associations between two stimuli that never occur together, is facilitated by injections of ketamine, an N-methyl-D-aspartate-receptor antagonist and a known hallucinogen at low doses in humans and nonhuman animals. Ketamine administration before each conditioning session significantly enhanced the acquisition of 4-s trace conditioning but not delay conditioning. The trace conditioning-specific facilitatory effect of ketamine was replicated in subsequent experiments in which slightly modified procedures were used to enhance the overall levels of conditioned responses. Taken together, the current results demonstrated that low-dose ketamine promotes associative learning between stimuli over a temporal gap, which adds to existing literature illustrating aberrant learning involving absent stimuli in schizophrenia model animals. We discuss potential associative mechanisms through which ketamine promoted trace conditioning with reference to Wagner's (1981) Standard Operating Procedures model. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
最近的研究表明,精神分裂症的阳性症状,如幻觉和妄想,可以用巴甫洛夫条件反射程序来建模。各种精神分裂症模型动物对缺失刺激(即条件性幻觉)表现出异常强烈的联想激活,并容易形成涉及缺失线索(即增强的介导条件反射)的进一步关联。在目前的小鼠研究中,我们检验了在人类和非人类动物中,注射氯胺酮(一种n -甲基- d -天冬氨酸受体拮抗剂和一种已知的低剂量致幻剂)是否促进了食欲痕迹条件反射的获得,这是另一种巴甫洛夫任务,动物必须在从未同时发生的两种刺激之间形成联系。每次条件训练前给予氯胺酮可显著提高4-s微量条件训练的习得,但对延迟条件训练无显著影响。在随后的实验中,氯胺酮的痕量条件特异性促进效应被复制,在这些实验中,使用轻微修改的程序来提高条件反应的总体水平。综上所述,目前的研究结果表明,低剂量氯胺酮促进了刺激物之间的关联学习,这增加了现有文献中关于精神分裂症模型动物中涉及缺乏刺激物的异常学习的解释。我们参考Wagner(1981)的标准操作程序模型,讨论氯胺酮促进微量调节的潜在联想机制。(PsycInfo数据库记录(c) 2023 APA,版权所有)。
{"title":"Ketamine facilitates appetitive trace conditioning in mice: Further evidence for abnormal stimulus representation in schizophrenia model animals.","authors":"Riria Suzuki, Yutaka Kosaki","doi":"10.1037/bne0000559","DOIUrl":"https://doi.org/10.1037/bne0000559","url":null,"abstract":"<p><p>Recent studies indicated that positive symptoms of schizophrenia, such as hallucination and delusion, can be modeled using Pavlovian conditioning procedures. Various schizophrenia model animals exhibit abnormally strong associative activations of absent stimuli (i.e., conditioned hallucination) and readily form further associations involving the absent cues (i.e., enhanced mediated conditioning). In the present study using mice, we examined whether the acquisition of appetitive trace conditioning, another Pavlovian task in which animals must form associations between two stimuli that never occur together, is facilitated by injections of ketamine, an <i>N</i>-methyl-D-aspartate-receptor antagonist and a known hallucinogen at low doses in humans and nonhuman animals. Ketamine administration before each conditioning session significantly enhanced the acquisition of 4-s trace conditioning but not delay conditioning. The trace conditioning-specific facilitatory effect of ketamine was replicated in subsequent experiments in which slightly modified procedures were used to enhance the overall levels of conditioned responses. Taken together, the current results demonstrated that low-dose ketamine promotes associative learning between stimuli over a temporal gap, which adds to existing literature illustrating aberrant learning involving absent stimuli in schizophrenia model animals. We discuss potential associative mechanisms through which ketamine promoted trace conditioning with reference to Wagner's (1981) <i>Standard Operating Procedures</i> model. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 4","pages":"236-253"},"PeriodicalIF":1.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9789248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-01Epub Date: 2023-04-27DOI: 10.1037/bne0000557
Daniel B K Gabriel, Anna E Liley, Hunter T Franks, Grace L Minnes, Monika Tutaj, Melinda R Dwinell, Tristan V de Jong, Robert W Williams, Megan K Mulligan, Hao Chen, Nicholas W Simon
Substance use disorder (SUD) is associated with a cluster of cognitive disturbances that engender vulnerability to ongoing drug seeking and relapse. Two of these endophenotypes-risky decision-making and impulsivity-are amplified in individuals with SUD and are augmented by repeated exposure to illicit drugs. Identifying genetic factors underlying variability in these behavioral patterns is critical for early identification, prevention, and treatment of SUD-vulnerable individuals. Here, we compared risky decision-making and different facets of impulsivity between two fully inbred substrains of Lewis rats-LEW/NCrl and LEW/NHsd. We performed whole genome sequencing of both substrains to identify almost all relevant variants. We observed substantial differences in risky decision-making and impulsive behaviors. Relative to LEW/NHsd, the LEW/NCrl substrain accepts higher risk options in a decision-making task and higher rates of premature responses in the differential reinforcement of low rates of responding task. These phenotypic differences were more pronounced in females than males. We defined a total of ∼9,000 polymorphisms between these substrains at 40× whole genome short-read coverage. Roughly half of variants are located within a single 1.5 Mb region of Chromosome 8, but none impact protein-coding regions. In contrast, other variants are widely distributed, and of these, 38 are predicted to cause protein-coding variants. In conclusion, Lewis rat substrains differ significantly in risk-taking and impulsivity and only a small number of easily mapped variants are likely to be causal. Sequencing combined with a reduced complexity cross should enable identification of one or more variants underlying multiple complex addiction-relevant behaviors. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
{"title":"Divergent risky decision-making and impulsivity behaviors in Lewis rat substrains with low genetic difference.","authors":"Daniel B K Gabriel, Anna E Liley, Hunter T Franks, Grace L Minnes, Monika Tutaj, Melinda R Dwinell, Tristan V de Jong, Robert W Williams, Megan K Mulligan, Hao Chen, Nicholas W Simon","doi":"10.1037/bne0000557","DOIUrl":"10.1037/bne0000557","url":null,"abstract":"<p><p>Substance use disorder (SUD) is associated with a cluster of cognitive disturbances that engender vulnerability to ongoing drug seeking and relapse. Two of these endophenotypes-risky decision-making and impulsivity-are amplified in individuals with SUD and are augmented by repeated exposure to illicit drugs. Identifying genetic factors underlying variability in these behavioral patterns is critical for early identification, prevention, and treatment of SUD-vulnerable individuals. Here, we compared risky decision-making and different facets of impulsivity between two fully inbred substrains of Lewis rats-LEW/NCrl and LEW/NHsd. We performed whole genome sequencing of both substrains to identify almost all relevant variants. We observed substantial differences in risky decision-making and impulsive behaviors. Relative to LEW/NHsd, the LEW/NCrl substrain accepts higher risk options in a decision-making task and higher rates of premature responses in the <i>differential reinforcement of low rates of responding</i> task. These phenotypic differences were more pronounced in females than males. We defined a total of ∼9,000 polymorphisms between these substrains at 40× whole genome short-read coverage. Roughly half of variants are located within a single 1.5 Mb region of Chromosome 8, but none impact protein-coding regions. In contrast, other variants are widely distributed, and of these, 38 are predicted to cause protein-coding variants. In conclusion, Lewis rat substrains differ significantly in risk-taking and impulsivity and only a small number of easily mapped variants are likely to be causal. Sequencing combined with a reduced complexity cross should enable identification of one or more variants underlying multiple complex addiction-relevant behaviors. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 4","pages":"254-267"},"PeriodicalIF":1.6,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10524952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10167752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Supplemental Material for Proteome Analysis Indicates Participation of the Dorsal Hippocampal Formation in Fear-Motivated Memory in a Time-Dependent Manner","authors":"","doi":"10.1037/bne0000563.supp","DOIUrl":"https://doi.org/10.1037/bne0000563.supp","url":null,"abstract":"","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"1 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2023-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42414600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01Epub Date: 2023-02-23DOI: 10.1037/bne0000550
Britny A Hildebrandt, Hayley Fisher, Susanne E Ahmari
Binge eating is a persistent behavior associated with a chronic course of illness and poor treatment outcomes. While clinical research is unable to capture the full course of binge eating, preclinical approaches offer the opportunity to examine binge-like eating from onset through chronic durations, allowing identification of factors contributing to binge eating persistence. The present study quantified the trajectories of binge-like eating onset and modeled cycles of abstinence/relapse to develop a translational model for binge eating persistence. Adult male and female C57Bl6/J mice were randomized to a binge-like palatable food access schedule (daily 2-hr, 3×/week) or continuous, nonbinge like palatable food access for 12 days (Experiment 1). Persistence of palatable food consumption in both binge-like palatable food access groups was then examined across three cycles of forced abstinence and reexposure to palatable food (incubation) to model the persistence of binge eating in clinical populations. Mice with daily 2-hr palatable food access escalated their intake more than mice in the 3×/week or continuous groups (Experiment 1). This pattern was more pronounced in females. In addition, this pattern of palatable food intake reemerged across multiple cycles of behavioral incubation (Experiment 2). These findings provide a model of binge-like eating in mice that can be used in future studies examining both environmental factors and neural mechanisms contributing to binge eating persistence. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
{"title":"Examination of onset trajectories and persistence of binge-like eating behavior in mice after intermittent palatable food exposure.","authors":"Britny A Hildebrandt, Hayley Fisher, Susanne E Ahmari","doi":"10.1037/bne0000550","DOIUrl":"10.1037/bne0000550","url":null,"abstract":"<p><p>Binge eating is a persistent behavior associated with a chronic course of illness and poor treatment outcomes. While clinical research is unable to capture the full course of binge eating, preclinical approaches offer the opportunity to examine binge-like eating from onset through chronic durations, allowing identification of factors contributing to binge eating persistence. The present study quantified the trajectories of binge-like eating onset and modeled cycles of abstinence/relapse to develop a translational model for binge eating persistence. Adult male and female C57Bl6/J mice were randomized to a binge-like palatable food access schedule (daily 2-hr, 3×/week) or continuous, nonbinge like palatable food access for 12 days (Experiment 1). Persistence of palatable food consumption in both binge-like palatable food access groups was then examined across three cycles of forced abstinence and reexposure to palatable food (incubation) to model the persistence of binge eating in clinical populations. Mice with daily 2-hr palatable food access escalated their intake more than mice in the 3×/week or continuous groups (Experiment 1). This pattern was more pronounced in females. In addition, this pattern of palatable food intake reemerged across multiple cycles of behavioral incubation (Experiment 2). These findings provide a model of binge-like eating in mice that can be used in future studies examining both environmental factors and neural mechanisms contributing to binge eating persistence. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 3","pages":"170-177"},"PeriodicalIF":1.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10191968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9481828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ping Chen, Dirk E M Geurts, Jessica I Määttä, Ruben van den Bosch, Lieke Hofmans, Danae Papadopetraki, Hanneke den Ouden, Roshan Cools
Interaction between Pavlovian and instrumental control systems is key for adaptive motivated behavior, but also plays an important role in various neuropsychiatric disorders, including depression, addiction, and anxiety. Here, we employed the flouorodopa positron emission tomography ([¹⁸F]-DOPA PET) in healthy participants (N = 100) to assess whether dopamine synthesis capacity (Ki), specifically in the ventral striatum, accounts for individual variation in Pavlovian-to-instrumental transfer (PIT). Surprisingly, this was not the case. Rather, the relationship of ventral striatal Ki with PIT depended on working memory (WM) capacity. Ventral striatal dopamine boosted the effects of Pavlovian cues on instrumental responding to a greater degree in participants with higher WM capacity. Caution is warranted to interpret this post hoc four-way interaction given the modest sample size. Nonetheless, these results chime with prior findings demonstrating that dopaminergic drugs boost Pavlovian biases to a greater degree in participants with greater WM capacity and highlight the importance of interactions between striatal dopamine and WM capacity. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
{"title":"Effect of striatal dopamine on Pavlovian bias. A large [¹⁸F]-DOPA PET study.","authors":"Ping Chen, Dirk E M Geurts, Jessica I Määttä, Ruben van den Bosch, Lieke Hofmans, Danae Papadopetraki, Hanneke den Ouden, Roshan Cools","doi":"10.1037/bne0000547","DOIUrl":"https://doi.org/10.1037/bne0000547","url":null,"abstract":"<p><p>Interaction between Pavlovian and instrumental control systems is key for adaptive motivated behavior, but also plays an important role in various neuropsychiatric disorders, including depression, addiction, and anxiety. Here, we employed the flouorodopa positron emission tomography ([¹⁸F]-DOPA PET) in healthy participants (<i>N</i> = 100) to assess whether dopamine synthesis capacity (K<sub>i</sub>), specifically in the ventral striatum, accounts for individual variation in Pavlovian-to-instrumental transfer (PIT). Surprisingly, this was not the case. Rather, the relationship of ventral striatal Ki with PIT depended on working memory (WM) capacity. Ventral striatal dopamine boosted the effects of Pavlovian cues on instrumental responding to a greater degree in participants with higher WM capacity. Caution is warranted to interpret this post hoc four-way interaction given the modest sample size. Nonetheless, these results chime with prior findings demonstrating that dopaminergic drugs boost Pavlovian biases to a greater degree in participants with greater WM capacity and highlight the importance of interactions between striatal dopamine and WM capacity. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 3","pages":"184-195"},"PeriodicalIF":1.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9472227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aggression is a complex social behavior that evolved in the context of defending a territory, fighting for limited resources, and competing for mates and protection. Although aggression considered as a negative or undesirable emotion is an essential part of many species' repertoire of social behaviors. For humans, the motivations, actions, and limits of aggressive acts are not always clear. However, uncontrolled aggression may have destructive consequences, and it develops inappropriately into violence. At the neural level, several studies demonstrated that aggression is related to cortical abnormalities, including the anterior cingulate cortex (ACC). This review summarizes the state of the literature regarding the involvement of ACC in the neurobiology of aggression and impulsivity. We will first review structural and neuroanatomical studies, including volumetric and functional investigations of aggression. Next, we will discuss the neurochemical and neuropharmacological studies of aggression related to the ACC. We will focus mainly on the gamma-aminobutyric acid/glutamate balance, as well as the serotoninergic system. Finally, we will try to integrate these results and reconcile discrepancies in the field and suggest recommendations for future studies. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
{"title":"The role of the anterior cingulate cortex in aggression and impulsivity.","authors":"Ilias Chaibi, Otmane Bouchatta, Mohamed Bennis, Saadia Ba-M'hamed","doi":"10.1037/bne0000552","DOIUrl":"https://doi.org/10.1037/bne0000552","url":null,"abstract":"<p><p>Aggression is a complex social behavior that evolved in the context of defending a territory, fighting for limited resources, and competing for mates and protection. Although aggression considered as a negative or undesirable emotion is an essential part of many species' repertoire of social behaviors. For humans, the motivations, actions, and limits of aggressive acts are not always clear. However, uncontrolled aggression may have destructive consequences, and it develops inappropriately into violence. At the neural level, several studies demonstrated that aggression is related to cortical abnormalities, including the anterior cingulate cortex (ACC). This review summarizes the state of the literature regarding the involvement of ACC in the neurobiology of aggression and impulsivity. We will first review structural and neuroanatomical studies, including volumetric and functional investigations of aggression. Next, we will discuss the neurochemical and neuropharmacological studies of aggression related to the ACC. We will focus mainly on the gamma-aminobutyric acid/glutamate balance, as well as the serotoninergic system. Finally, we will try to integrate these results and reconcile discrepancies in the field and suggest recommendations for future studies. (PsycInfo Database Record (c) 2023 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":"137 3","pages":"155-169"},"PeriodicalIF":1.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9842778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}