Abstract

The stress system coordinates the adaptive reactions of the organism to stressors. Therefore, dysfunctions in this circuit may correlate to anxiety-related disorders, including depression. Comprehending the dynamics of this network may lead to a better understanding of the mechanisms that underlie these diseases. The central nucleus of the amygdala (CeA) activates the hypothalamic-pituitary-adrenal axis and brainstem nodes by triggering endocrine, autonomic and behavioral stress responses. The medial prefrontal cortex plays a significant role in regulating reactions to stressors, and is specifically important for limiting fear responses. Brain oscillations reflect neural systems activity. Synchronous neuronal assemblies facilitate communication and synaptic plasticity, mechanisms that cooperatively support the temporal representation and long-term consolidation of information. The purpose of this article was to delve into the interactions between these structures in stress contexts by evaluating changes in oscillatory activity. We particularly analyzed the local field potential in the infralimbic region of the medial prefrontal cortex (IL) in urethane-anesthetized rats after the electrical activation of the central nucleus of the amygdala by mimicking firing rates induced by acute stress. Electrical CeA activation induced a delayed, but significant, change in the IL, with prominent slow waves accompanied by an increase in the theta and gamma activities, and spindles. The phase-amplitude coupling of both slow waves and theta oscillations significantly increased with faster oscillations, including theta-gamma coupling and the nesting of spindles, theta and gamma oscillations in the slow wave cycle. These results are further discussed in neural processing terms of the stress response and memory formation.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.