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. 2021 Jul 20;16:26331055211033847. doi: 10.1177/26331055211033847

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© The Author(s) 2021

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Hypothesized mechanism explaining the anti-addictive properties of TBG. The rodent medial PFC includes the infralimbic (IL), prelimbic (PL), and anterior cingulate (AC) cortex, which exert top-down control over a number of subcortical brain regions. Addiction is characterized by atrophy of neurons in the PFC (ie, the retraction of neurites and loss of dendritic spines). TBG-induced growth of cortical neurons is predicted to enhance the excitability of these neurons, thus re-establishing top-down corticolimbic control.