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Disruption of dorsolateral prefrontal cortex decreases model-based in favor of model-free control in humans.

ABSTRACT: Human choice behavior often reflects a competition between inflexible computationally efficient control on the one hand and a slower more flexible system of control on the other. This distinction is well captured by model-free and model-based reinforcement learning algorithms. Here, studying human subjects, we show it is possible to shift the balance of control between these systems by disruption of right dorsolateral prefrontal cortex, such that participants manifest a dominance of the less optimal model-free control. In contrast, disruption of left dorsolateral prefrontal cortex impaired model-based performance only in those participants with low working memory capacity.

SUBMITTER: Smittenaar P

PROVIDER: S-EPMC3893454 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature

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Disruption of dorsolateral prefrontal cortex decreases model-based in favor of model-free control in humans.

Smittenaar Peter P FitzGerald Thomas H B TH Romei Vincenzo V Wright Nicholas D ND Dolan Raymond J RJ

Neuron 20131024 4

Human choice behavior often reflects a competition between inflexible computationally efficient control on the one hand and a slower more flexible system of control on the other. This distinction is well captured by model-free and model-based reinforcement learning algorithms. Here, studying human subjects, we show it is possible to shift the balance of control between these systems by disruption of right dorsolateral prefrontal cortex, such that participants manifest a dominance of the less opt ...[more]

PMID: 24206669

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Project description:BackgroundMethamphetamine (MA), is an extremely addictive stimulant that adversely affects the central nervous system. Accumulating evidence indicates that molecular mechanisms such as oxidative stress, apoptosis, and autophagy are involved in the toxicity of MA. Considering experimental animal studies exhibiting MA-induced neurotoxicity, the relevance of these findings needs to be evidently elucidated in human MA users. It is generally assumed that multiple chemical substances released in the brain following MA-induced metabolic activation are primary factors underlying damage of neural cells. Hence, this study aimed to investigate the role of autophagy and apoptosis as well as oxidative stress in the brain of postmortem MA-induced toxicity.Materials and methodsIn this study, we determine the gene expression of autophagy and apoptosis, including BECN1, MAP1ALC3, CASP8, TP53, and BAX genes in ten healthy controls and ten chronic users of MA postmortem dorsolateral prefrontal cortex (DLPFC) by real-time polymerase chain reaction. Also, we applied immunohistochemistry in formalin-fixed and paraffin-embedded human brain samples to analyze brain-derived neurotrophic factor (BDNF). Also, spectrophotometry was performed to measure glutathione (GSH) content.ResultsThe expression level of apoptotic and autophagic genes (BECN1, MAP1ALC3, CASP8, TP53, and BAX) were significantly elevated, while GSH content and BDNF showed substantial reductions in DLPFC of chronic MA users. Discussion: Our data showed that MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. Also, MA induces multiple functional and structural perturbations in the brain, determining its toxicity and possibly contributing to neurotoxicity.DiscussionOur study showed BDNF-positive cells as well as GSH amount, displayed significant declines in DLPFC of MA user. MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. However, further investigations are needed to throw light on the cellular and molecular mechanisms that act in the various regions of the addicted brain, especially in DLPFC.

Dataset Information

Disruption of dorsolateral prefrontal cortex decreases model-based in favor of model-free control in humans.

Publications

Disruption of dorsolateral prefrontal cortex decreases model-based in favor of model-free control in humans.

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