ArticleMolecular psychiatry2026
Transcranial direct current stimulation restores addictive behavior via prefrontal-striatal circuit.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Dependence on methamphetamine (METH) is a severe brain disorder characterized by high relapse rates and cognitive decline following detoxification. Recent research suggests that transcranial direct current stimulation (tDCS) may treat addiction, but the underlying neural mechanisms remain unknown. Here, we employed METH-conditioned place preference (CPP) paradigm integrated with fMRI, electrophysiology, chemogenetics, in vivo fiber photometry recordings and a novel rodent tDCS model to examine the neural circuit underlying tDCS modulation on METH-induced addictive behavior. We demonstrated that tDCS targeted at the medial prefrontal cortex (mPFC) prevents relapse. Specifically, tDCS enhanced the activity of neurons in both the infralimbic cortex (IL) and the nucleus accumbens shell (NAcSh) simultaneously. Furthermore, chemogenetic inhibition of the IL-NAcSh circuit eliminated the modulatory effects of tDCS, while activation of the IL-NAcSh circuit was sufficient to suppress the relapse. These findings reveal that the IL-NAcSh pathway functions as a descending regulatory circuit mediating the therapeutic outcomes of tDCS in the treatment of substance use disorder, offering new insights into circuit-based neuro-modulatory treatments for addiction.
Indexed as
Identifiers
41136747What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.