Elizabeth A Virakorn, Rick Richardson, Kathryn D Baker
{"title":"慢性压力暴露会损害青春期大鼠的恐惧消退能力,并对神经元周围网和副神经元产生相关影响。","authors":"Elizabeth A Virakorn, Rick Richardson, Kathryn D Baker","doi":"10.1037/bne0000592","DOIUrl":null,"url":null,"abstract":"<p><p>Adolescents, both human and nonhuman, exhibit impairments in the extinction of learned fear, an effect that is exacerbated, at least in rodents, by exposure to chronic stress. However, we have little understanding of the mechanisms underlying this effect. Therefore, here, we examined whether corticosterone exposure, a model of chronic stress, alters the expression of inhibitory neurons expressing parvalbumin (PV) in the basolateral amygdala and prefrontal cortex, two brain regions that have been implicated in fear extinction memories, in adolescent rats. We also examined the expression of perineuronal nets (PNNs), extracellular matrix structures that encompass inhibitory interneurons, in these two regions. These structures might render fear memories resistant to extinction by applying a structural \"brake\" on the plasticity of fear memories. Corticosterone-exposed adolescent rats exhibited poor extinction retention, as in past work, and were also found to have reduced percentage of PV-positive cells surrounded by PNNs in the basolateral amygdala. PV cells and PNNs were unaffected by corticosterone exposure in the prefrontal cortex. Our results suggest that the altered function of amygdala interneurons may be associated with the impaired extinction performance in stress-exposed adolescent rats. (PsycInfo Database Record (c) 2024 APA, all rights reserved).</p>","PeriodicalId":8739,"journal":{"name":"Behavioral neuroscience","volume":null,"pages":null},"PeriodicalIF":1.6000,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Chronic stressor exposure impairs extinction of fear in adolescent rats and has associated effects on perineuronal nets and parvalbumin interneurons.\",\"authors\":\"Elizabeth A Virakorn, Rick Richardson, Kathryn D Baker\",\"doi\":\"10.1037/bne0000592\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Adolescents, both human and nonhuman, exhibit impairments in the extinction of learned fear, an effect that is exacerbated, at least in rodents, by exposure to chronic stress. However, we have little understanding of the mechanisms underlying this effect. Therefore, here, we examined whether corticosterone exposure, a model of chronic stress, alters the expression of inhibitory neurons expressing parvalbumin (PV) in the basolateral amygdala and prefrontal cortex, two brain regions that have been implicated in fear extinction memories, in adolescent rats. We also examined the expression of perineuronal nets (PNNs), extracellular matrix structures that encompass inhibitory interneurons, in these two regions. These structures might render fear memories resistant to extinction by applying a structural \\\"brake\\\" on the plasticity of fear memories. Corticosterone-exposed adolescent rats exhibited poor extinction retention, as in past work, and were also found to have reduced percentage of PV-positive cells surrounded by PNNs in the basolateral amygdala. PV cells and PNNs were unaffected by corticosterone exposure in the prefrontal cortex. Our results suggest that the altered function of amygdala interneurons may be associated with the impaired extinction performance in stress-exposed adolescent rats. (PsycInfo Database Record (c) 2024 APA, all rights reserved).</p>\",\"PeriodicalId\":8739,\"journal\":{\"name\":\"Behavioral neuroscience\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2024-07-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Behavioral neuroscience\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1037/bne0000592\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BEHAVIORAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Behavioral neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1037/bne0000592","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BEHAVIORAL SCIENCES","Score":null,"Total":0}
Chronic stressor exposure impairs extinction of fear in adolescent rats and has associated effects on perineuronal nets and parvalbumin interneurons.
Adolescents, both human and nonhuman, exhibit impairments in the extinction of learned fear, an effect that is exacerbated, at least in rodents, by exposure to chronic stress. However, we have little understanding of the mechanisms underlying this effect. Therefore, here, we examined whether corticosterone exposure, a model of chronic stress, alters the expression of inhibitory neurons expressing parvalbumin (PV) in the basolateral amygdala and prefrontal cortex, two brain regions that have been implicated in fear extinction memories, in adolescent rats. We also examined the expression of perineuronal nets (PNNs), extracellular matrix structures that encompass inhibitory interneurons, in these two regions. These structures might render fear memories resistant to extinction by applying a structural "brake" on the plasticity of fear memories. Corticosterone-exposed adolescent rats exhibited poor extinction retention, as in past work, and were also found to have reduced percentage of PV-positive cells surrounded by PNNs in the basolateral amygdala. PV cells and PNNs were unaffected by corticosterone exposure in the prefrontal cortex. Our results suggest that the altered function of amygdala interneurons may be associated with the impaired extinction performance in stress-exposed adolescent rats. (PsycInfo Database Record (c) 2024 APA, all rights reserved).