Genomic glucocorticoid receptor effects guide acute stress-induced delayed anxiety and basolateral amygdala spine plasticity in rats

IF 4.3 2区 医学 Q1 NEUROSCIENCES Neurobiology of Stress Pub Date : 2023-11-10 DOI:10.1016/j.ynstr.2023.100587
Leonardo S. Novaes , Leticia M. Bueno-de-Camargo , Amadeu Shigeo-de-Almeida , Vitor A.L. Juliano , Ki Goosens , Carolina D. Munhoz
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Abstract

Anxiety, a state related to anticipatory fear, can be adaptive in the face of environmental threats or stressors. However, anxiety can also become persistent and manifest as anxiety- and stress-related disorders, such as generalized anxiety or post-traumatic stress disorder (PTSD). In rodents, systemic administration of glucocorticoids (GCs) or short-term restraint stress induces anxiety-like behaviors and dendritic branching within the basolateral complex of the amygdala (BLA) ten days later. Additionally, increased arousal-related memory retention mediated by elevated GCs requires concomitant noradrenaline (NE) signaling, both acting in the BLA. It is unknown whether GCs and NE play a role in the delayed acute stress-induced effects on behavior and BLA dendritic plasticity. Here, inhibiting corticosterone (CORT) elevation during 2 h of restraint stress prevents stress-induced increases in delayed anxiety-like behavior and BLA dendritic spine density in rats. Also, we show that the delayed acute stress-induced effects on behavior and morphological alterations are critically dependent on genomic glucocorticoid receptor (GR) actions in the BLA. Unlike CORT, the pharmacological enhancement of NE signaling in the BLA was insufficient to drive delayed anxiety-related behavior. Nonetheless, the delayed anxiety-like behavior ten days after acute stress requires NE signaling in the BLA during stress exposure. Therefore, we define the essential roles of two stress-related hormones for the late stress consequences, acting at two separate times: CORT, via GR, immediately during stress, and NE, via beta-adrenoceptors, during the expression of delayed anxiety.

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基因组糖皮质激素受体影响大鼠急性应激诱导的延迟性焦虑和杏仁核基底外侧脊柱可塑性
焦虑是一种与预期恐惧相关的状态,在面对环境威胁或压力源时可以适应。然而,焦虑也可能持续存在,表现为焦虑和压力相关的疾病,如广泛性焦虑或创伤后应激障碍(PTSD)。在啮齿类动物中,全身给予糖皮质激素(GCs)或短期约束应激可在10天后诱导杏仁核基底外侧复合体(BLA)内的焦虑样行为和树突分支。此外,由GCs升高介导的觉醒相关记忆保留的增加需要伴随去甲肾上腺素(NE)信号,两者都在BLA中起作用。目前尚不清楚GCs和NE是否在延迟急性应力诱导的行为和BLA树突可塑性的影响中发挥作用。在本研究中,抑制抑制应激2小时时皮质酮(CORT)升高可防止应激诱导的延迟性焦虑样行为和大鼠BLA树突棘密度的增加。此外,我们还表明,延迟急性应激诱导的行为和形态改变的影响严重依赖于BLA中基因组糖皮质激素受体(GR)的作用。与CORT不同,BLA中NE信号的药理增强不足以驱动延迟的焦虑相关行为。然而,急性应激后10天的延迟焦虑样行为需要应激暴露期间BLA中的NE信号。因此,我们确定了两种与压力相关的激素在后期压力后果中的重要作用,它们在两个不同的时间起作用:CORT,通过GR,在压力期间立即起作用,NE,通过β -肾上腺素受体,在延迟焦虑的表达期间起作用。
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来源期刊
Neurobiology of Stress
Neurobiology of Stress Biochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
9.40
自引率
4.00%
发文量
74
审稿时长
48 days
期刊介绍: Neurobiology of Stress is a multidisciplinary journal for the publication of original research and review articles on basic, translational and clinical research into stress and related disorders. It will focus on the impact of stress on the brain from cellular to behavioral functions and stress-related neuropsychiatric disorders (such as depression, trauma and anxiety). The translation of basic research findings into real-world applications will be a key aim of the journal. Basic, translational and clinical research on the following topics as they relate to stress will be covered: Molecular substrates and cell signaling, Genetics and epigenetics, Stress circuitry, Structural and physiological plasticity, Developmental Aspects, Laboratory models of stress, Neuroinflammation and pathology, Memory and Cognition, Motivational Processes, Fear and Anxiety, Stress-related neuropsychiatric disorders (including depression, PTSD, substance abuse), Neuropsychopharmacology.
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