Commentary - (2025) Volume 11, Issue 1
Received: 28-Jan-2025, Manuscript No. cdp-25-165814;
Editor assigned: 30-Jan-2025, Pre QC No. P-165814;
Reviewed: 13-Feb-2025, QC No. Q-165814;
Revised: 20-Feb-2025, Manuscript No. R-165814;
Published:
27-Feb-2025
, DOI: 10.37421/2572-0791.2025.11.156
Citation: Mitchlle, Nedal. "Frontal Cortex Modulation via tDCS in Patients with Anhedonia: Targeting the Reward Circuitry in Depression." Clin Depress 11 (2025): 156.
Copyright: © 2025 Mitchlle N. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
tDCS involves the application of a low-intensity, continuous electrical current via electrodes placed on the scalp. Typically, anodal stimulation increases cortical excitability, while cathodal stimulation decreases it. This modulation of neural excitability is believed to influence synaptic plasticity and alter functional connectivity within and between key brain networks. In the treatment of depression, tDCS most often targets the Dorsolateral Prefrontal Cortex (DLPFC), especially the left hemisphere, which is implicated in executive control, emotion regulation, and goal-directed behavior. In individuals with MDD and pronounced anhedonia, the DLPFC is frequently hypoactive, while regions involved in negative affect and internal mentation, such as the subgenual anterior cingulate cortex and default mode network (DMN), show hyperconnectivity. These imbalances contribute to diminished top-down regulation of the reward system, impairing the motivational salience of rewarding stimuli [2].
By increasing activity in the left DLPFC, tDCS may help restore balance in prefrontal-limbic interactions and enhance reward responsiveness. Studies employing behavioral and neuroimaging paradigms suggest that tDCS can improve reward-related processing by influencing dopaminergic pathways and modulating striatal activity indirectly [3,4]. This is particularly relevant for anhedonia, which has been associated with blunted responses in the nucleus accumbens and ventral tegmental areaâ??regions critical for coding reward prediction and hedonic impact. Although tDCS does not directly stimulate subcortical structures, its influence on cortical regions that project to the striatum may facilitate downstream effects on dopamine release and reward anticipation. Several trials have explored this hypothesis by examining the impact of repeated anodal tDCS over the left DLPFC in patients with MDD and elevated anhedonic symptoms. Findings suggest that this approach can lead to measurable improvements in reward sensitivity, motivation, and engagement in pleasurable activities, though variability in outcomes persists.
From a mechanistic standpoint, tDCS-induced changes in cortical excitability can lead to alterations in neuroplasticity, including enhanced long-term potentiation (LTP)-like effects, increased expression of brain-derived neurotrophic factor (BDNF), and improved functional connectivity within frontostriatal networks. These changes are not immediate but accumulate over time with repeated stimulation sessions. This time-dependent nature of tDCS is consistent with the slow development of therapeutic effects and highlights the importance of treatment adherence and protocol optimization. Moreover, the state-dependency of tDCS effects implies that concurrent cognitive or emotional engagement during stimulation may enhance its impact. For instance, coupling tDCS with reward-based tasks or behavioral activation strategies may facilitate targeted neuroplasticity within the desired neural circuits, increasing the salience and reinforcing value of positive experiences [5].
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