Disrupted synapses: prefrontal cortex-reward circuit dysfunction in stress-induced depression-like behaviors

Read full text
Authors: Ashraf Mahmud, Mehmet Akif Karaman
Cited by: 3
References: 201

Abstract

Major depressive disorder (MDD) is a multifactorial, circuit-level disorder often triggered by chronic stress, which fundamentally disrupts the neural networks governing reward processing. Central to this pathology is the prefrontal cortex (PFC), an integration hub exerting top-down executive control over subcortical regions. Here, we synthesize translational and preclinical evidence detailing how chronic stress induces structural, functional, and molecular maladaptations within the PFC and its reward-related downstream projections. By dissecting specific neural pathways-including the PFC's connections to the nucleus accumbens (NAc), ventral tegmental area (VTA), ventral hippocampus (vHIPP), and lateral habenula (LHb)- we map how projection-specific dysregulation drives distinct depressive phenotypes. Furthermore, we examine the cellular mechanisms underlying these circuit alterations, emphasizing the roles of disrupted neuromodulation (dopamine, glutamate, and serotonin), impaired synaptic plasticity, and robust neuroinflammatory cascades. We highlight notable sex-dependent findings where relevant, illustrating how specific transcriptomic, morphological, and circuit-level responses can diverge between males and females. Finally, we discuss the necessity of moving beyond simplistic behavioral dichotomies and integrating multimodal neurobiological approaches. Ultimately, delineating these precise, circuit-specific vulnerabilities provides a critical framework for developing targeted therapeutics for stress-induced affective disorders.

Fields of Study & Subjects

Neurotransmitter Receptor Influence on Behavior Stress Responses and Cortisol Tryptophan and brain disorders

Publication details

Journal / source
Frontiers in Cellular Neuroscience
Publisher
Frontiers Media SA
Volume
20
Pages
1843871–1843871
Publication date
20 May 2026
Language
EN