Pharmacology Biochemistry and Behavior最新文献

{"title":"Prenatal serotonin depletion persistently disrupts social behavior and modulates ΔFosB and SERT expression in mice","authors":"María Carolina Fabio ,&nbsp;María Victoria Mujica ,&nbsp;Elisa Fogliatti ,&nbsp;María Victoria Aguilar ,&nbsp;Alicia Laura Degano ,&nbsp;Ricardo Marcos Pautassi","doi":"10.1016/j.pbb.2025.174043","DOIUrl":"10.1016/j.pbb.2025.174043","url":null,"abstract":"<div><div>Embryonic fluctuations in serotonin (5-HT) levels during pregnancy have been associated with maternal depression and linked to social deficits and neuropsychiatric disorders in offspring. This preclinical study examined the long-term effects of transient prenatal 5-HT depletion on social, anxiety-like, and depressive-like behaviors across development, and evaluated associated changes in serotonergic markers and neuronal activity in key brain regions.</div><div>Pregnant C57BL/6 mice were administered the 5-HT synthesis inhibitor para-chlorophenylalanine (PCPA), or its vehicle, from gestational day 12.5 to 14.5. Maternal affect and caregiving behavior were assessed postnatally, and offspring of both sexes were evaluated for social interaction, compulsive behavior, locomotion, ultrasonic vocalizations, and helplessness during infancy, adolescence, and adulthood. Immunohistochemistry was performed in the offspring to assess serotonin transporter (SERT) and ΔFosB expression in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc).</div><div>PCPA administration did not significantly alter depressive- or anxiety-like behavior in the dams, nor did it significantly affect maternal caregiving. The offspring prenatally exposed to PCPA exhibited reduced social interaction and increased non-social behaviors compared to controls during adolescence and adulthood. Prenatal serotonin depletion also led to decreased SERT and ΔFosB expression in the mPFC and NAc, indicating disrupted serotonergic signaling and altered neuronal activity in mood- and reward-related brain regions.</div><div>The findings suggest that even brief disruptions of serotonergic signaling during gestation can induce lasting social deficits and neurobiological alterations relevant to the pathophysiology of neurodevelopmental disorders.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"253 ","pages":"Article 174043"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199842","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":"Astrocyte gap junction dysfunction activates JAK2-STAT3 pathway to mediate inflammation in depression","authors":"Xue-Ying Yang ,&nbsp;Hui-Qin Wang ,&nbsp;Meng-Zhang ,&nbsp;Ai-Ping Chen ,&nbsp;Xin-Mu Li ,&nbsp;Zan Xing ,&nbsp;Hong Jiang ,&nbsp;Xu Yan ,&nbsp;Shi-Feng Chu ,&nbsp;Zhen-Zhen Wang ,&nbsp;Nai-Hong Chen","doi":"10.1016/j.pbb.2025.173987","DOIUrl":"10.1016/j.pbb.2025.173987","url":null,"abstract":"<div><div>Connexin 43 (Cx43) is highly expressed in astrocytes and forms gap junctions that maintain intercellular communication. Dysfunctional gap junctions in astrocytes exacerbate depressive symptoms, which has been implicated in the pathogenesis of depression. Inflammatory responses occur in the brains of most people with depression. However, it is unclear whether dysfunctional astrocyte gap junctions mediate the onset of the inflammatory response in the brains of depressed patients. Transporter protein (TSPO), the most common neuroinflammatory marker and a novel target of antidepressants identified in recent years, is mainly expressed by glial cells in the brain and is abnormally upregulated during inflammatory activation. We found that in a mouse model of chronic unpredictable stress (CUS), astrocyte gap junctions in the prefrontal cortex are impaired and the JAK2-STAT3 signaling pathway is activated, leading to an increase in the inflammatory marker TSPO. Based on this finding, we further verified using Cx43 transgenic mice that conditional knockdown of Cx43 in prefrontal cortex astrocytes also activated the JAK2-STAT3 inflammatory signaling pathway, with concomitant elevated levels of the inflammatory marker TSPO, and the mice developed depressive-like behavior. In contrast, impaired corticosterone (CORT)-induced gap junction function and increased TSPO were ameliorated by the JAK2-STAT3 inhibitor protosappanin A (PTA). Thus, targeting astrocyte Cx43 attenuates the inflammatory response in depression and improves depressive symptoms. This provides a new perspective on the pathogenesis of depression and a new therapeutic target for antidepressant research.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 173987"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586601","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":"Postnatal propionic acid exposure disrupts hippocampal agmatine homeostasis leading to social deficits and cognitive impairment in autism spectrum disorder-like phenotype in rats","authors":"Manasi Tadas ,&nbsp;Nitu Wankhede ,&nbsp;Pranali Chandurkar ,&nbsp;Nandkishor Kotagale ,&nbsp;Milind Umekar ,&nbsp;Raj Katariya ,&nbsp;Akash Waghade ,&nbsp;Dadasaheb Kokare ,&nbsp;Brijesh Taksande","doi":"10.1016/j.pbb.2025.174030","DOIUrl":"10.1016/j.pbb.2025.174030","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by a range of symptoms including impaired social interaction and cognitive deficits. Although the exact pathogenesis of ASD is not well established, recent clinical findings suggest a decline in levels of biogenic amine agmatine in autistic patients. The present study was designed to investigate the impact of postnatal propionic acid (PPA) exposure on hippocampal agmatine homeostasis in male rat pups and to explore a new therapeutic intervention for ASD using agmatine as a biological target. PPA is commonly used in experimental models of ASD due to its ability to induce social deficits, cognitive impairments, and stereotyped behaviors, which closely resemble key characteristics of ASD. Male rat pups were administered with PPA via the intrahippocampal route bilaterally (25 μg/0.25 μl per side) on PND-21 to simulate the ASD phenotype, and its subsequent effect on the endogenous agmatinergic system. The influence of agmatine treatment and its endogenous modulation on ASD-like phenotypes was also investigated. Behavioral assessments revealed that PPA exposure reduced sociability and social preference, caused learning and memory impairment in the Morris water maze, increased anxiety-like behavior in the elevated plus maze, and reduced exploratory behavior in the hole board test. Neurochemical analyses showed a decrease in agmatine concentration and an increase in its degrading enzyme agmatinase in the hippocampus. PPA treatment altered the content of GABA, glutamate, TNF-α, IL-6, BDNF, and also resulted in increased astrogliosis and neurotoxicity within the hippocampus. Chronic agmatine treatment and its endogenous modulation ameliorated the behavioral and biochemical disruptions induced by PPA exposure. This study highlights the critical role of hippocampal agmatinergic pathway in the etiopathogenesis of ASD, positioning agmatine as a promising therapeutic target for its treatment.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174030"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911623","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":"Schizophrenia-like phenotypes and long-term synaptic plasticity impairment in GluN2A-transgenic mice","authors":"Huan Zhang ,&nbsp;Wen Si ,&nbsp;Bo Wang ,&nbsp;Jiao Han ,&nbsp;Fan Ding ,&nbsp;Qingsheng Xue ,&nbsp;Xiaohua Cao","doi":"10.1016/j.pbb.2025.174026","DOIUrl":"10.1016/j.pbb.2025.174026","url":null,"abstract":"<div><div>While <em>N</em>-methyl-<span>d</span>-aspartate receptor (NMDAR) hypofunction has been suggested as a hallmark of schizophrenia, the role of subunit-specific dysregulation such as GluN2A overexpression remains poorly understood. The present study comprehensively investigated the impact of GluN2A overexpression on behavioral phenotypes, cognitive functions, and synaptic plasticity in transgenic mice with forebrain-specific overexpression of the GluN2A subunit (GluN2A-TG). Behavioral assessments revealed schizophrenia-like phenotypes, including prolonged stereotypic movement duration, impaired sensorimotor gating, reduced social interaction, and diminished nest-building activity in GluN2A-TG mice. Consistently, GluN2A-TG mice exhibited not only deficits in spatial working memory and olfactory working memory but also impaired associative learning. In addition, both long-term potentiation and long-term depression were significantly attenuated in the prefrontal cortex (PFC) of GluN2A-TG mice. Furthermore, electrophysiological analysis of NMDAR-mediated excitatory postsynaptic currents in PFC neurons revealed altered kinetics characterized by a faster decay time and significantly increased amplitude in GluN2A-TG mice. Collectively, these findings suggest that GluN2A overexpression may induce schizophrenia-like phenotypes via impairing NMDAR-dependent long-term synaptic plasticity in the PFC, likely due to altered NMDAR subunit composition leading to disrupted calcium signaling dynamics. These results provide critical insights into the pathological role of GluN2A in schizophrenia.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174026"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886798","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":"Crisugabalin, a ligand for the α2δ subunit of voltage-gated calcium channels, exhibits no obvious abuse potential in rodents","authors":"Xiaoli Gou ,&nbsp;Yijiang Liu ,&nbsp;Qidi Ye ,&nbsp;Lingzhi He ,&nbsp;Ying Chen ,&nbsp;Yansheng Dong ,&nbsp;Qingyuan Meng ,&nbsp;Zongjun Shi ,&nbsp;Yao Li ,&nbsp;Yao Lu ,&nbsp;Ju Wang ,&nbsp;Linggao Zeng","doi":"10.1016/j.pbb.2025.174015","DOIUrl":"10.1016/j.pbb.2025.174015","url":null,"abstract":"<div><div>Crisugabalin, a novel third-generation ligand targeting the <em>α2δ</em> subunit of voltage-gated calcium channels, has been approved in China for the treatment of pain associated with diabetic peripheral neuropathy and postherpetic neuralgia. Existing research suggests that ligands for the <em>α2δ</em> subunit of voltage-gated calcium channels may carry a risk of abuse. To evaluate the abuse potential of crisugabalin, five well-recognized animal models were utilized in these preclinical studies. Firstly, an intravenous self-administration paradigm was implemented in rats that were self-administering propofol to assess the reinforcing effects of crisugabalin. Secondly, a rat drug discrimination study was employed to determine the pharmacological similarity between crisugabalin and the training drug midazolam. Then, a conditioned place preference (CPP) paradigm in rats was utilized to evaluate the rewarding properties of crisugabalin. After that, a spontaneous withdrawal study was conducted in rats chronically treated with crisugabalin to examine the liability of developing physical dependence. Finally, a mouse pentylenetetrazol-induced convulsion model was used following chronic exposure to crisugabalin to assess its potential for physical dependence. The results indicated that crisugabalin showed no positive reinforcing effects and did not display midazolam-like discriminative stimulus effects. Moreover, crisugabalin did not induce significant CPP in rats and there was no risk of physical dependence in the pentylenetetrazol-induced convulsion model. In the rat spontaneous withdrawal study, crisugabalin demonstrated a very low level of physical dependence. These findings suggest that crisugabalin has minimal to no potential for abuse, thereby establishing itself as a safer option relative to pregabalin and mirogabalin.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174015"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906643","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":"Prenatal maternal stress induces increased avoidance behavior in adolescent mice offspring","authors":"Xueyong Yin ,&nbsp;Rui Jiang ,&nbsp;Xiaoyu Liu ,&nbsp;Yiran Liu ,&nbsp;Xiao Liu ,&nbsp;Fei Zhou ,&nbsp;Xi Yu ,&nbsp;Shu Yan ,&nbsp;Yunluo Li ,&nbsp;Yuru Du ,&nbsp;Youdong Li ,&nbsp;Kaoqi Lian ,&nbsp;Ye Zhao ,&nbsp;Haishui Shi","doi":"10.1016/j.pbb.2025.174029","DOIUrl":"10.1016/j.pbb.2025.174029","url":null,"abstract":"<div><div>Defensive behavior is an instinctive response to potential or actual threats, crucial for the survival and reproduction of species. It is influenced by both genetic and environmental factors and undergoes continuous changes throughout an individual's development. Stress, as a significant environmental factor, has a profound and enduring impact on reshaping an individual's behavior, particularly when experienced during early life. However, the effects of early life stress on defensive behavior remain unclear. In this study, defensive behaviors were evaluated in adolescent mice offspring exposed to prenatal stress. Serum corticosterone and neural dendritic spine density were measured. Behaviors results showed that prenatal stress significantly increased anxiety-like and avoidance behaviors in male offspring mice. Enzyme-linked immunosorbent assay (ELISA) results indicated that prenatal stress led to a significant increase in serum corticosterone levels in male offspring following predator odor exposure. Golgi staining analysis revealed a decrease in neural dendritic spine density in the medial prefrontal cortex (mPFC) of offspring. These findings suggest that behavioral changes in offspring mice caused by prenatal stress may be related to alterations in corticosterone levels and neuronal structure. However, the causation and specific mechanisms require further investigation.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174029"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906596","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":"Pre-exposure to eutylone attenuates its own aversive effects but has no impact on cocaine or MDMA: A possible role of eutylone's hybrid pharmacology","authors":"Negar G. Ardabili,&nbsp;Shira Tan,&nbsp;Anthony L. Riley","doi":"10.1016/j.pbb.2025.174013","DOIUrl":"10.1016/j.pbb.2025.174013","url":null,"abstract":"<div><div>Previous research has reported that pre-exposure to a variety of drugs of abuse can impact (reduce) the aversive effects of themselves and other abused compounds, often as a function of their shared pharmacological activity. In this context, the present series of studies investigated the effects of history with the synthetic cathinone eutylone on the aversive effects of cocaine, MDMA, and itself in adult, male Sprague-Dawley rats. Given eutylone's structural similarities with its parent compound methylone, it was predicted that its ability to attenuate cocaine- and MDMA-induced taste avoidance would parallel the effects of methylone pre-exposure in this design (cocaine &gt; MDMA). In Experiment 1, male Sprague-Dawley rats were exposed to eutylone (20 mg/kg, IP) or equivolume saline every other day for five exposures followed by taste avoidance conditioning with 20 mg/kg cocaine (SC) or 1.8 mg/kg MDMA (SC). Both cocaine and MDMA induced significant taste avoidance that developed over repeated conditioning trials. Cocaine and MDMA-induced avoidance were unaffected by eutylone history. To assess the general ability of eutylone pre-exposure to attenuate taste avoidance conditioning in the pre-exposure design, in Experiment 2, an additional set of male Sprague-Dawley rats was injected with 20 mg/kg eutylone (IP) prior to taste avoidance conditioning with eutylone (20 mg/kg (IP). Under these conditions, eutylone-induced avoidance was attenuated by eutylone pre-exposure. Given that eutylone history attenuated eutylone-induced avoidance argues that the failure to affect cocaine or MDMA was not a function of eutylone in this preparation. The inability of eutylone to attenuate the aversive effects of cocaine and MDMA despite sharing pharmacological activity suggests that eutylone's hybrid pharmacology may create a unique interoceptive effect different than that produced by either drug.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174013"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859029","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":"Drosophila model of depression-like behavior: systematic investigation of external stress parameters and intrinsic susceptibility","authors":"Wenhao Zhang ,&nbsp;Zhifu Ai ,&nbsp;Genhua Zhu ,&nbsp;Ming Yang ,&nbsp;Yali Liu ,&nbsp;Huanhua Xu ,&nbsp;Qin Zheng ,&nbsp;Yonggui Song ,&nbsp;Dan Su","doi":"10.1016/j.pbb.2025.174014","DOIUrl":"10.1016/j.pbb.2025.174014","url":null,"abstract":"<div><div>Currently, <em>Drosophila</em> is widely used to study brain diseases. Unfortunately, <em>Drosophila</em> still lacks a mature and stable model for research on depression. This study addressed this issue by systematically exploring external stress and intrinsic susceptibility factors (<em>Drosophila</em> strains, adult/larval forms) that may influence the establishment and reproducibility of the stress-induced model. On this basis, the parameters are optimized. The results indicate <em>Drosophila</em> strains and forms are critical factors influencing model establishment, while external stress is the primary cause affecting the model's mortality rate. Compared with the other four strains, Canton-S are the most susceptible to chronic unpredictable mild stress (CUMS). Larval forms exhibit lower reactivity to external stress compared to adults. Parameter variations greatly influence model mortality rates from cold/heat/starvation stress. The model methodology validation study conducted subsequently through assessments of face, construct, and predictive validity demonstrates that the model exhibits face (neurobehavioral differences), structural (neurotransmitter changes in the <em>Drosophila</em> brain), and predictive (behavioral changes after fluoxetine treatment) validity. Additionally, spatial behavior experiments in <em>Drosophila</em> provide more realistic activity patterns compared to planar behavior, minimizing potential errors in interpreting lateral movements of the <em>Drosophila</em>, and it is recommended that this metric be included in model evaluation. This study presents a comprehensive set of methods for establishing and evaluating a depression-like behavior model and offers greater convenience for research on the pathogenesis of depression, as well as the screening, efficacy evaluation, and mechanistic studies of antidepressant drugs.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174014"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859028","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":"N-acetylcysteine enhances the antipsychotic effect of aripiprazole in the neurodevelopmental rat model of schizophrenia","authors":"Zofia Rogóż ,&nbsp;Kinga Kamińska ,&nbsp;Agnieszka Wąsik","doi":"10.1016/j.pbb.2025.174028","DOIUrl":"10.1016/j.pbb.2025.174028","url":null,"abstract":"<div><div>Symptoms of schizophrenia are well characterized, but the mechanism underlying the pathogenesis of the disease still remains unknown. In addition, therapy of negative symptoms and cognitive deficits in schizophrenic patients is a serious clinical problem. Some clinical studies have shown that the atypical antipsychotic drug aripiprazole (ARI), and the antioxidant <em>N</em>-acetylcysteine (NAC) are effective in reducing positive and negative symptoms of schizophrenia in patients. The aim of the present study was to evaluate the influence of repeated co-treatment with low doses of ARI and NAC on the schizophrenia-like behavior in adult rats. The schizophrenia-like behavior was induced in Sprague-Dawley male pups in the neonatal days p5-p16 by repeated administration of the glutathione synthesis inhibitor L-butionine-(<em>S,R</em>)-sulfoximine (BSO) given together with the dopamine reuptake inhibitor 1-[2-[Bis-4(fluorophenyl)methoxy]ethyl]-4–3-(3-phenylpropyl) (GBR 12909). Adult rats received repeated co-treatment with ARI (0.1 mg/kg) and NAC (10 mg/kg) for 21 days, and their effects on schizophrenia-like behavior were assessed (on p90–91) using the social interaction test and novel object recognition test. The present data indicated that the studied drugs at higher doses: ARI (0.3 mg/kg but not 0.1 mg/kg) and NAC (30 mg/kg but not 10 mg/kg) reversed schizophrenia-like symptoms in the tested model. Moreover, repeated co-treatment with low doses of ARI with NAC also reversed schizophrenia-like behavior in the neurodevelopmental rat model of schizophrenia. The above results indicated that NAC enhanced the action of ARI in the used neurodevelopmental rat model of schizophrenia, and the mechanism of action of the used drugs in this model is discussed.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174028"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906644","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 ventral hippocampus mediates experience-dependent social modulation of fear in rats","authors":"Dan Tao ,&nbsp;Cuijie Shi ,&nbsp;Zhihao Song ,&nbsp;Jing Wen ,&nbsp;Yujun Gao ,&nbsp;Yixiao Luo ,&nbsp;Haishui Shi ,&nbsp;Shihao Huang","doi":"10.1016/j.pbb.2025.174016","DOIUrl":"10.1016/j.pbb.2025.174016","url":null,"abstract":"<div><div>Fear Conditioning by Proxy (FCbP) is a form of socially mediated fear learning, in which no-conditioned rodents acquire fear memories through social interactions with fear-conditioned rodents. This study investigates the impact of prior similar experiences on the transmission of contextual fear memories in FCbP and explores the role of the ventral hippocampus (vHPC) in the social transmission of fear. Observers were divided into two groups: those with contextual experience (D/O) and those without contextual experience- naïve (O). These rats were exposed to fear-conditioned demonstrators (D) through social interaction, and their responses to fear contexts were observed. Additionally, the effect of vHPC inactivation on fear memory transmission was examined by injecting lidocaine into the vHPC. Fear was transmitted through social interaction among experienced rats but not among naive rats. Furthermore, lidocaine injection into the vHPC inhibited the social transmission of fear memories among experienced rats. This study demonstrates that contextual fear memories can be transmitted through social interaction among experience-dependent rats but not among naive rats. That inactivation in the vHPC blocks the social transmission of contextual fear memories.</div></div>","PeriodicalId":19893,"journal":{"name":"Pharmacology Biochemistry and Behavior","volume":"252 ","pages":"Article 174016"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143877165","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}