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Evenamide: A Potential Pharmacotherapeutic Alternative for Treatment-Resistant Schizophrenia. 偶氮酰胺:治疗耐药性精神分裂症的潜在药物疗法替代品。
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2024-02-01 DOI: 10.1093/ijnp/pyae005
Raghunath Singh, Margaret K Hahn, Yashika Bansal, Sri Mahavir Agarwal, Gary Remington
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引用次数: 0
Relapse Rates With Paliperidone Palmitate in Adult Patients With Schizophrenia: Results for the 6-Month Formulation From an Open-label Extension Study Compared to Real-World Data for the 1-Month and 3-Month Formulations. 帕潘立酮棕榈酸酯治疗成人精神分裂症患者的复发率:为期 6 个月的开放标签延长期研究结果与为期 1 个月和 3 个月制剂的实际数据对比。
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2024-02-01 DOI: 10.1093/ijnp/pyad067
Ibrahim Turkoz, Mehmet Daskiran, Uzma Siddiqui, R Karl Knight, Karen L Johnston, Christoph U Correll

Background: The 3 paliperidone palmitate (PP) long-acting injectable antipsychotic formulations, PP 1-month (PP1M), PP 3-month (PP3M), and PP 6-month (PP6M), have shown to reduce the risk of relapse in schizophrenia. The current phase-4 study constructed external comparator arms (ECAs) using real-world data for PP3M and PP1M and compared relapse prevention rates with PP6M from an open-label extension (OLE) study in adult patients with schizophrenia.

Methods: PP6M data were derived from a single-arm, 24-month, OLE study (NCT04072575), which included patients with schizophrenia who completed a 12-month randomized, double-blind, noninferiority, phase-3 study (NCT03345342) without relapse. Patients in the PP3M and PP1M ECAs were identified from the IBM® MarketScan® Multistate Medicaid Database based on similar eligibility criteria as the PP6M cohort.

Results: A total of 178 patients were included in each cohort following propensity score matching. Most patients were men (>70%; mean age: 39-41 years). Time to relapse (primary analysis based on Kaplan-Meier estimates) was significantly delayed in the PP6M cohort (P < .001, log-rank test). The relapse rate was lower in the PP6M cohort (3.9%) vs PP3M (20.2%) and PP1M (29.8%) cohorts. Risk of relapse decreased significantly (P < .001) by 82% for PP6M vs PP3M (HR = 0.18 [95% CI = 0.08 to 0.40]), 89% for PP6M vs PP1M (HR = 0.11 [0.05 to 0.25]), and 35% for PP3M vs PP1M (HR = 0.65 [0.42 to 0.99]; P = .043). Sensitivity analysis confirmed findings from the primary analysis. Although the ECAs were matched to mimic the characteristics of the PP6M cohort, heterogeneity between the groups could exist due to factors including prior study participation, unmeasured confounders, variations in data capture and quality, and completeness of clinical information.

Conclusions: In a clinical trial setting, PP6M significantly delayed time to relapse and demonstrated lower relapse rates compared with PP3M and PP1M treatments in real-world settings among adult patients with schizophrenia.

Trial registration: ClinicalTrials.gov Identifier: NCT04072575; EudraCT number: 2018-004532-30.

背景:帕利哌酮棕榈酸酯(PP)的三种长效注射抗精神病药物配方,即PP 1个月(PP1M)、PP 3个月(PP3M)和PP 6个月(PP6M),已被证明可降低精神分裂症的复发风险。目前的第四阶段研究利用PP3M和PP1M的真实世界数据构建了外部比较臂(ECA),并将精神分裂症成人患者的复发预防率与开放标签扩展(OLE)研究中的PP6M进行了比较:PP6M的数据来自一项为期24个月的单臂OLE研究(NCT04072575),该研究纳入了完成了为期12个月的随机、双盲(DB)、非劣效、3期研究(NCT03345342)且未复发的精神分裂症患者。PP3M 和 PP1M ECA 中的患者是从 IBM® MarketScan® 多州医疗补助数据库中根据与 PP6M 队列相似的资格标准确定的:经过倾向得分匹配后,每个队列共纳入了 178 名患者。大多数患者为男性(>70%);平均年龄为 39-41 岁。PP6M队列的复发时间(基于Kaplan-Meier估计值的主要分析)明显推迟(PC结论:在临床试验中,PP6M队列的复发时间比PP6M队列明显推迟:在临床试验中,与PP3M和PP1M治疗相比,PP6M可显著延迟精神分裂症成年患者的复发时间,并降低复发率。
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引用次数: 0
Ketamine or ECT? What Have We Learned From the KetECT and ELEKT-D Trials? 氯胺酮还是电痉挛疗法?我们从 KetECT 和 ELEKT-D 试验中学到了什么?
IF 4.5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-01-01 DOI: 10.1093/ijnp/pyad065
Joakim Ekstrand, Akihiro Takamiya, Axel Nordenskjold, George Kirov, Pascal Sienaert, Charles H Kellner, Pouya Movahed Rad

1. Two recent clinical trials, KetECT and ELEKT-D, compared the effectiveness of ketamine and electroconvulsive therapy (ECT) for major depressive disorder. Notably, these trials reported marked differences in ECT's clinical outcomes of, with remission rates of 63% for KetECT and a strikingly lower rate of 22% for ELEKT-D, while the remission rates for ketamine were 46% and 38%, respectively. Considering that the primary objective of both trials was to compare the standard treatment (ECT) with an experimental intervention (ketamine), it is crucial to highlight the pronounced disparities in ECT's clinical outcomes. This article offers a comprehensive comparison of these trials while also exploring how patient characteristics, treatment protocols, and study designs may contribute to such pronounced outcome discrepancies. These differences highlight the heterogeneous nature of depression and underscore the need for personalized treatments. These studies also provide valuable insights into identifying the most suitable candidates for ketamine and ECT.

最近进行的两项临床试验(KetECT 和 ELEKT-D)比较了氯胺酮和电休克疗法(ECT)对重度抑郁症的疗效。值得注意的是,这些试验报告显示,电休克疗法的临床疗效存在明显差异,KetECT的缓解率为63%,而ELEKT-D的缓解率则低得惊人,仅为22%,而氯胺酮的缓解率分别为46%和38%。考虑到这两项试验的主要目的是比较标准疗法(电痉挛疗法)和实验性干预(氯胺酮),因此强调电痉挛疗法临床疗效的明显差异至关重要。本文对这些试验进行了全面的比较,同时还探讨了患者特征、治疗方案和研究设计是如何导致如此明显的结果差异的。这些差异凸显了抑郁症的异质性,强调了个性化治疗的必要性。这些研究还为确定氯胺酮和电痉挛疗法的最合适人选提供了宝贵的见解。
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引用次数: 0
Corrigendum to: Characterization of 2 Novel Phosphodiesterase 2 Inhibitors Hcyb1 and PF-05180999 on Depression- and Anxiety-Like Behavior. 更正:两种新型磷酸二酯酶2抑制剂Hcyb1和PF-05180999对抑郁和焦虑行为的表征。
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2024-01-01 DOI: 10.1093/ijnp/pyad068
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引用次数: 0
Reviewer List 审稿人名单
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2024-01-01 DOI: 10.1177/11786221241234437
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引用次数: 0
Chronic Stress-Induced Elevation of Melanin-Concentrating Hormone in the Locus Coeruleus Inhibits Norepinephrine Production and Associated With Depression-Like Behaviors in Rats. 慢性应激诱导的黑色素浓缩荷尔蒙在大鼠神经节位置的升高会抑制去甲肾上腺素的分泌,并与抑郁样行为相关。
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2024-01-01 DOI: 10.1093/ijnp/pyad069
Nurhumar Kurban, Yu Qin, Hui-Ling Zhao, Xiao Hu, Xi Chen, Yi-Yi Zhao, Yu-Shuo Peng, Hong-Bo Wang, Su-Ying Cui, Yong-He Zhang

Background: Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide that projects throughout the central nervous system, including the noradrenergic locus coeruleus (LC). Our previous study suggested that MCH/MCH receptor 1 (MCHR1) in the LC may be involved in the regulation of depression. The present study investigated whether the role of MCH/MCHR1 in the LC in depression-like behaviors is associated with the regulation of norepinephrine.

Method: Chronic unpredictable stress (CUS) and an acute intra-LC microinjection of MCH induced depression-like behaviors in rats. The MCHR1 antagonist SNAP-94847 was also microinjected in the LC in rats that were suffering CUS or treated with MCH. The sucrose preference, forced swim, and locomotor tests were used for behavioral evaluation. Immunofluorescence staining, enzyme-linked immunosorbent assay, western blot, and high-performance liquid chromatography with electrochemical detection were used to explore the mechanism of MCH/MCHR1 in the regulation of depression-like behaviors.

Results: CUS induced an abnormal elevation of MCH levels and downregulated MCHR1 in the LC, which was highly correlated with the formation of depression-like behaviors. SNAP-94847 exerted antidepressant effects in CUS-exposed rats by normalizing tyrosine hydroxylase, dopamine β hydroxylase, and norepinephrine in the LC. An acute microinjection of MCH induced depression-like behaviors through its action on MCHR1. MCHR1 antagonism in the LC significantly reversed the MCH-induced downregulation of norepinephrine production by normalizing MCHR1-medicated cAMP-PKA signaling.

Conclusions: Our study confirmed that the MCH/MCHR1 system in the LC may be involved in depression-like behaviors by downregulating norepinephrine production. These results improve our understanding of the pathogenesis of depression that is related to the MCH/MCHR1 system in the LC.

背景:黑色素浓缩激素(MCH)是一种下丘脑神经肽,可投射到整个中枢神经系统,包括去甲肾上腺素能区(LC)。我们之前的研究表明,LC 中的 MCH/MCH 受体 1(MCHR1)可能参与了抑郁症的调控。本研究探讨了MCH/MCHR1在抑郁样行为中的作用是否与去甲肾上腺素的调节有关:方法:慢性不可预测应激(CUS)和急性LC内显微注射MCH诱导大鼠抑郁样行为。此外,还在大鼠LC内注射了MCHR1拮抗剂SNAP-94847。行为评估采用了蔗糖偏好、强迫游泳和运动试验。采用免疫荧光染色、ELISA、Western blot和HPLC-ECD等方法探讨MCH/MCHR1在抑郁样行为中的调控机制:结果:CUS诱导LC中MCH水平异常升高并下调MCHR1,这与抑郁样行为的形成高度相关。SNAP-94847通过使LC中的酪氨酸羟化酶、多巴胺β羟化酶和去甲肾上腺素正常化,对暴露于CUS的大鼠产生抗抑郁作用。通过对 MCHR1 的作用,MCH 的急性显微注射可诱导抑郁样行为。在LC中拮抗MCHR1可使MCHR1介导的cAMP-PKA信号转导正常化,从而显著逆转MCH诱导的去甲肾上腺素分泌下调:我们的研究证实,LC 中的 MCH/MCHR1 系统可能通过下调去甲肾上腺素的分泌参与了抑郁样行为。这些结果加深了我们对与 LC 中 MCH/MCHR1 系统有关的抑郁症发病机制的理解。
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引用次数: 0
The Ability to Voluntarily Regulate Theta Band Activity Affects How Pharmacological Manipulation of the Catecholaminergic System Impacts Cognitive Control. 自愿调节θ波段活动的能力会影响对儿茶酚胺能系统的药物治疗对认知控制的影响。
IF 4.5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-01-01 DOI: 10.1093/ijnp/pyae003
Astrid Prochnow, Moritz Mückschel, Elena Eggert, Jessica Senftleben, Christian Frings, Alexander Münchau, Veit Roessner, Annet Bluschke, Christian Beste

Background: The catecholaminergic system influences response inhibition, but the magnitude of the impact of catecholaminergic manipulation is heterogeneous. Theoretical considerations suggest that the voluntary modulability of theta band activity can explain this variance. The study aimed to investigate to what extent interindividual differences in catecholaminergic effects on response inhibition depend on voluntary theta band activity modulation.

Methods: A total of 67 healthy adults were tested in a randomized, double-blind, cross-over study design. At each appointment, they received a single dose of methylphenidate or placebo and performed a Go/Nogo task with stimuli of varying complexity. Before the first appointment, the individual's ability to modulate theta band activity was measured. Recorded EEG data were analyzed using temporal decomposition and multivariate pattern analysis.

Results: Methylphenidate effects and voluntary modulability of theta band activity showed an interactive effect on the false alarm rates of the different Nogo conditions. The multivariate pattern analysis revealed that methylphenidate effects interacted with voluntary modulability of theta band activity at a stimulus processing level, whereas during response selection methylphenidate effects interacted with the complexity of the Nogo condition.

Conclusions: The findings reveal that the individual's theta band modulability affects the responsiveness of an individual's catecholaminergic system to pharmacological modulation. Thus, the impact of pharmacological manipulation of the catecholaminergic system on cognitive control most likely depends on the existing ability to self-modulate relevant brain oscillatory patterns underlying the cognitive processes being targeted by pharmacological modulations.

背景:儿茶酚胺能系统会影响反应抑制,但儿茶酚胺能操作的影响程度却不尽相同。理论上认为,θ波段活动的自愿可调控性可以解释这种差异。本研究旨在探讨儿茶酚胺能对反应抑制作用的个体间差异在多大程度上取决于θ波段活动的自愿调节:方法:67 名健康成年人接受了随机、双盲、交叉研究设计的测试。在每次预约时,他们都会接受单剂量的哌醋甲酯或安慰剂,并在不同复杂度的刺激下完成 Go/Nogo 任务。在第一次约见之前,对患者调节θ波段活动的能力进行了测量。记录的脑电图数据通过时间分解和多变量模式分析(MVPA)进行了分析:结果:哌醋甲酯效应和θ波段活动的自主可调控性对不同 Nogo 条件下的误报率有交互影响。MVPA显示,哌醋甲酯效应与θ波段活动的自愿可调控性在刺激加工层面上相互作用,而在反应选择过程中,哌醋甲酯效应与Nogo条件的复杂性相互作用:研究结果表明,个体的θ波段可调控性会影响个体儿茶酚胺能系统对药物调控的反应性。因此,对儿茶酚胺能系统的药理调控对认知控制的影响很可能取决于现有的自我调节能力,而自我调节能力又是药理调控所针对的认知过程的基础。
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引用次数: 0
MiR-182-5p: A Novel Biomarker in the Treatment of Depression in CSDS-Induced Mice. MiR-182-5p:一种治疗csds诱导小鼠抑郁的新型生物标志物
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2024-01-01 DOI: 10.1093/ijnp/pyad064
Ya-Bin Zheng, Xiao-Ming Sheng, Xiang Jin, Wei Guan

Background: Depression is a neuropsychiatric disease with a high disability rate and mainly caused by the chronic stress or genetic factors. There is increasing evidence that microRNAs (miRNAs) play a critical role in the pathogenesis of depression. However, the underlying molecular mechanism for the pathophysiology of depression of miRNA remains entirely unclear so far.

Methods: We first established a chronic social defeat stress (CSDS) mice model of depression, and depression-like behaviors of mice were evaluated by a series of behavioral tests. Next, we detected several abundantly expressive miRNAs suggested in previous reports to be involved in depression and found miR-182-5p was selected as a candidate for analysis in the hippocampus. Then western blotting and immunofluorescence were used together to examine whether adeno-associated virus (AAV)-siR-182-5p treatment alleviated chronic stress-induced decrease in hippocampal Akt/GSK3β/cAMP-response element binding protein (CREB) signaling pathway and increase in neurogenesis impairment and neuroinflammation. Furthermore, CREB inhibitor was adopted to examine if blockade of Akt/GSK3β/CREB signaling pathway abolished the antidepressant actions of AAV-siR-182-5p in mice.

Results: Knockdown of miR-182-5p alleviated depression-like behaviors and impaired neurogenesis of CSDS-induced mice. Intriguingly, the usage of agomiR-182-5p produced significant increases in immobility times and aggravated neuronal neurogenesis damage of mice. More importantly, it suggested that 666-15 blocked the reversal effects of AAV-siR-182-5p on the CSDS-induced depressive-like behaviors in behavioral testing and neuronal neurogenesis within hippocampus of mice.

Conclusions: These findings indicated that hippocampal miR-182-5p/Akt/GSK3β/CREB signaling pathway participated in the pathogenesis of depression, and it might give more opportunities for new drug developments based on the miRNA target in the clinic.

背景:抑郁症是一种致残率高的神经精神疾病,主要由慢性应激或遗传因素引起。越来越多的证据表明,mirna在抑郁症的发病机制中起着至关重要的作用。然而,到目前为止,miRNA抑制病理生理的潜在分子机制仍然完全不清楚。方法:首先建立慢性社会失败应激(CSDS)小鼠抑郁模型,通过一系列行为测试评估小鼠的抑郁样行为。接下来,我们检测了几个在以前的报道中被认为参与抑郁的高表达mirna,并发现miR-182-5p被选为海马的候选分析,然后使用western blotting和免疫荧光一起检测AAV-siR-182-5p治疗是否缓解了慢性应激诱导的海马Akt/GSK3β/CREB信号通路的减少以及神经发生损伤和神经炎症的增加。此外,我们采用camp反应元件结合蛋白(CREB)抑制剂来检测阻断Akt/GSK3β/CREB信号通路是否会消除小鼠AAV-siR-182-5p的抗抑郁作用。结果:miR-182-5p敲低可减轻csds诱导小鼠的抑郁样行为和神经发生受损。有趣的是,agomiR-182-5p的使用显著增加了小鼠的静止时间,加重了神经元神经发生损伤。更重要的是,666-15阻断了AAV-siR-182-5p在行为学测试中对csds诱导的抑郁样行为和海马内神经元神经发生的逆转作用。结论:这些发现提示海马miR-182-5p/Akt/GSK3β/CREB信号通路参与了抑郁症的发病机制,临床中基于miRNA靶点的新药开发可能会有更多的机会。
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引用次数: 0
Integrative Analyses of scRNA-seq, Bulk mRNA-seq, and DNA Methylation Profiling in Depressed Suicide Brain Tissues. 抑郁症自杀性脑组织scRNA-seq、大块信使核糖核酸-seq和DNA甲基化谱的综合分析。
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2023-12-18 DOI: 10.1093/ijnp/pyad057
Yalan Zhou, Lan Xiong, Jianhua Chen, Qingzhong Wang

Background: Suicidal behaviors have become a serious public health concern globally due to the economic and human cost of suicidal behavior to individuals, families, communities, and society. However, the underlying etiology and biological mechanism of suicidal behavior remains poorly understood.

Methods: We collected different single omic data, including single-cell RNA sequencing (scRNA-seq), bulk mRNA-seq, DNA methylation microarrays from the cortex of Major Depressive Disorder (MDD) in suicide subjects' studies, as well as fluoxetine-treated rats brains. We matched subject IDs that overlapped between the transcriptome dataset and the methylation dataset. The differential expression genes and differentially methylated regions were calculated with a 2-group comparison analysis. Cross-omics analysis was performed to calculate the correlation between the methylated and transcript levels of differentially methylated CpG sites and mapped transcripts. Additionally, we performed a deconvolution analysis for bulk mRNA-seq and DNA methylation profiling with scRNA-seq as the reference profiles.

Results: Difference in cell type proportions among 7 cell types. Meanwhile, our analysis of single-cell sequence from the antidepressant-treated rats found that drug-specific differential expression genes were enriched into biological pathways, including ion channels and glutamatergic receptors.

Conclusions: This study identified some important dysregulated genes influenced by DNA methylation in 2 brain regions of depression and suicide patients. Interestingly, we found that oligodendrocyte precursor cells (OPCs) have the most contributors for cell-type proportions related to differential expression genes and methylated sites in suicidal behavior.

背景:由于自杀行为给个人、家庭、社区和社会带来的经济和人力成本,自杀行为已成为全球严重的公共卫生问题。然而,自杀行为的潜在病因和生物学机制仍知之甚少。方法:我们从自杀受试者研究的MDD皮层以及氟西汀治疗的大鼠大脑中收集了不同的单组学数据,包括scRNA-seq、大块信使核糖核酸seq、DNA甲基化微阵列。我们匹配了转录组数据集和甲基化数据集之间重叠的受试者ID。通过两组比较分析计算差异表达基因(DEGs)和差异甲基化区(DMRs)。进行交叉组学分析以计算差异甲基化CpG位点和定位转录物的甲基化和转录物水平之间的相关性。此外,我们对大量信使核糖核酸序列和DNA甲基化谱进行了去卷积分析,并将scRNA-seq作为参考谱。结果:最终发现17个关键基因在不同的组学和组织中有共同的变化,7种细胞类型中少突胶质细胞前体细胞(OPCs)的细胞类型比例存在显著差异。同时,我们对抗抑郁药治疗大鼠的单细胞序列的分析发现,药物特异性差异表达基因富集到生物途径中,包括离子通道和谷氨酸能受体。结论:本研究在抑郁症和自杀患者的两个大脑区域发现了一些受DNA甲基化影响的重要失调基因。有趣的是,我们发现OPCs对自杀行为中与差异表达基因和甲基化位点相关的细胞类型比例贡献最大。
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引用次数: 0
Differential Roles of Oxytocin Receptors in the Prefrontal Cortex and Nucleus Accumbens on Cocaine Self-Administration and Reinstatement of Cued Cocaine Seeking in Male Rats. 雄性大鼠前额叶皮质和伏隔核催产素受体在可卡因自我给药和可卡因寻找线索恢复中的差异作用。
IF 4.8 2区 医学 Q1 Medicine Pub Date : 2023-12-18 DOI: 10.1093/ijnp/pyad059
Rachel D Penrod, Makoto Taniguchi, Angela M Kearns, Jordan L Hopkins, Carmela M Reichel

Background: Little is known about the specific roles of cortical and accumbal oxytocin receptors in drug use disorders. To better understand the importance of the endogenous oxytocin system in cocaine relapse behavior, we developed an adeno-associated viral vector-expressing short hairpin (sh) RNAs to selectively degrade the rat oxytocin receptor (OxyR) mRNA in vivo.

Methods: Male (Sprague-Dawley) rats received bilateral infusions of the shRNA for the oxytocin receptor (shOxyR) or an shRNA control virus into the prefrontal cortex (PFC) or the nucleus accumbens core (NAc). Rats self-administered cocaine on an escalating FR ratio for 14 days, lever responding was extinguished, and rats were tested for cued and cocaine-primed reinstatement of drug seeking.

Results: OxyR knockdown in the PFC delayed the acquisition of lever pressing on an fixed ratio 1 schedule of reinforcement. All rats eventually acquired the same level of lever pressing and discrimination, and there were no differences in extinction. OxyR knockdown in the NAc had no effect during acquisition. In both the PFC and NAc, the shOxyR decreased cued reinstatement relative to shRNA control virus but was without effect during drug-primed reinstatement. OxyR knockdown in the PFC increased chamber activity during a social interaction task.

Conclusions: This study provides critical new information about how endogenous OxyRs function to affect drug seeking in response to different precipitators of relapse. The tool developed to knockdown OxyRs in rat could provide important new insights that aid development of oxytocin-based therapeutics to reduce return-to-use episodes in people with substance use disorder and other neuropsychiatric disorders.

背景:关于皮质和accumbal催产素受体在药物使用障碍中的具体作用知之甚少。为了更好地理解内源性催产素系统在可卡因复发行为中的重要性,我们开发了一种表达短发夹(sh)RNA的腺相关病毒载体(AAV),以在体内选择性降解大鼠OxyR mRNA。方法:雄性(Sprague-Dawley)大鼠接受双侧向前额叶皮层(PFC)或伏隔核(NAc)输注催产素受体shRNA(shOxyR)或shRNA对照病毒(shCntrl)。大鼠以不断上升的FR比率自行服用可卡因14天,杠杆反应消失,大鼠接受提示和可卡因引发的药物寻求恢复测试。结果:PFC中的OxyR击倒延迟了FR1强化计划中杠杆按压的获得。所有大鼠最终都获得了相同水平的杠杆按压和辨别能力,灭绝没有差异。在采集期间,NAc中的OxyR敲低没有影响。在PFC和NAc中,相对于shCntrl,shOxyR降低了提示性恢复,但在药物引发的恢复过程中没有效果。PFC中的OxyR敲低增加了社交任务中的室活动。结论:本研究提供了关于内源性OxyRs如何影响药物寻求以应对不同复发诱因的关键新信息。为降低大鼠体内的OxyRs而开发的工具可以提供重要的新见解,有助于开发基于催产素的治疗方法,以减少物质使用障碍和其他神经精神障碍患者的再次使用事件。
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引用次数: 0
期刊
International Journal of Neuropsychopharmacology
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