Chronic Stressor Exposure Impairs Extinction of Fear in Adolescent Rats and Has Associated Effects on Perineuronal Nets and Parvalbumin Interneurons

被引:2
|
作者
Virakorn, Elizabeth A. [1 ]
Richardson, Rick [1 ]
Baker, Kathryn D. [1 ,2 ]
机构
[1] UNSW Sydney, Sch Psychol, Sydney, Australia
[2] La Trobe Univ, Sch Psychol & Publ Hlth, Dept Psychol Counselling & Therapy, Melbourne, Vic 3086, Australia
基金
英国医学研究理事会; 澳大利亚研究理事会;
关键词
adolescent; fear extinction; parvalbumin; stress; perineuronal net; CORTICOSTERONE EXPOSURE; PREFRONTAL CORTEX; BRAIN; ANXIETY; AMYGDALA; BDNF; EXPRESSION; MEMORY; PLASTICITY; REACTIVITY;
D O I
10.1037/bne0000592
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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.
引用
收藏
页码:383 / 396
页数:14
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