Autor(es)

Juliano, Vitor A. L. ; Shigeo-de-Almeida, Amadeu ; Cruz-Nascimento, Taynara ; Sampaio, Lucas L. ; Cruz, Fabio C. ; Novaes, Leonardo S. ; Munhoz, Carolina D.

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF NEUROSCIENCE; v. 45, n. 32, p. 13-pg., 2025-08-06.

Resumo

Stress is a critical risk factor for the development of psychological disorders, including anxiety and post-traumatic stress disorder. Key brain regions, including the basolateral amygdala (BLA) and the infralimbic medial prefrontal cortex (IL-mPFC), play crucial roles in fear regulation. Our previous research demonstrated that neuronal genomic activity of glucocorticoid receptors in the BLA during a 2 h acute restraint stress (ARS) is essential for inducing anxiety-like behavior 10 d later. Additionally, blocking BLA (3-adrenergic signaling during the elevated plus maze is crucial for preventing this stress-induced delayed anxiety-like behavior. Here, we utilized adult male Wistar rats to expand on these findings, revealing that a single ARS session increases the activity of BLA neurons and their projections to the IL-mPFC while decreasing the activity of IL-mPFC neurons and their projections to the BLA during fear extinction. This finding highlights the key role of the BLA <-> IL-mPFC circuitry in fear extinction and its susceptibility to acute stress-induced changes. Notably, the delayed stress-induced fear extinction deficit and decreased IL-mPFC activity during fear extinction depend on the stress-responsive BLA neuronal ensemble and BLA (3-adrenergic signaling during contextual fear conditioning (CFC) 10 d poststress. Our findings demonstrate the significance of BLA (3-adrenergic signaling during CFC, as it induces delayed stress-induced impairments in extinction and regulates IL-mPFC activity during fear extinction. Furthermore, this study indicates that the BLA is a pivotal regulator of delayed stress effects at both the circuitry and behavioral levels, thus shedding new light on the mechanisms underlying stress-related psychiatric conditions. (AU)

• Processo FAPESP: 22/08766-1 - Sinalização dos glicocorticoides na hiperexcitabilidade neuronal do complexo basolateral da amígdala e seus efeitos sobre a ansiedade e a extinção de memórias aversivas.
• Beneficiário: Taynara da Cruz Nascimento
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 18/19599-3 - O papel dos glicocorticoides e das aferências do nervo vago na modulação da atividade neuronal e da plasticidade de circuitos centrais e suas implicações na ansiedade induzida por estresse em ratos
• Beneficiário: Leonardo Santana Novaes
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado