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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Stress impacts corticoamygdalar connectivity in an age-dependent manner

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Author(s):
Uliana, Daniela L. [1, 2] ; Gomes, Felipe V. [1, 2, 3] ; Grace, Anthony A. [1, 2]
Total Authors: 3
Affiliation:
[1] Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 - USA
[2] Univ Pittsburgh, Dept Psychiat & Psychol, Pittsburgh, PA 15260 - USA
[3] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Ribeirao Preto, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: NEUROPSYCHOPHARMACOLOGY; v. 46, n. 4 OCT 2020.
Web of Science Citations: 0
Abstract

Stress is a socio-environmental risk factor for the development of psychiatric disorders, with the age of exposure potentially determining the outcome. Several brain regions mediate stress responsivity, with a prominent role of the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) and their reciprocal inhibitory connectivity. Here we investigated the impact of stress exposure during adolescence and adulthood on the activity of putative pyramidal neurons in the BLA and corticoamygdalar plasticity using in vivo electrophysiology. 155 male Sprague-Dawley rats were subjected to a combination of footshock/restraint stress in either adolescence (postnatal day 31-40) or adulthood (postnatal day 65-74). Both adolescent and adult stress increased the number of spontaneously active putative BLA pyramidal neurons 1-2 weeks, but not 5-6 weeks post stress. High-frequency stimulation (HFS) of BLA and mPFC depressed evoked spike probability in the mPFC and BLA, respectively, in adult but not adolescent rats. In contrast, an adult-like BLA HFS-induced decrease in spike probability of mPFC neurons was found 1-2 weeks post-adolescent stress. Changes in mPFC and BLA neuron discharge were found 1-2 weeks post-adult stress after BLA and mPFC HFS, respectively. All these changes were transient since they were not found 5-6 weeks post adolescent or adult stress. Our findings indicate that stress during adolescence may accelerate the development of BLA-PFC plasticity, probably due to BLA hyperactivity, which can also disrupt the reciprocal communication of BLA-mPFC after adult stress. Therefore, precocious BLA-mPFC connectivity alterations may represent an early adaptive stress response that ultimately may contribute to vulnerability to adult psychiatric disorders. (AU)

FAPESP's process: 18/17597-3 - The impact of stress on the dopamine system depends on the state of the critical period of neuroplasticity: implications for depression and schizophrenia and for the study of new drug targets
Grantee:Felipe Villela Gomes
Support Opportunities: Research Grants - Young Investigators Grants