Disruption of dorsolateral prefrontal cortex decreases model-based in favor of model-free control in humans.
Ontology highlight
ABSTRACT:
SUBMITTER: Smittenaar P
PROVIDER: S-EPMC3893454 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Many studies have discussed the neural basis of asset bubbles. They found that the dorsolateral prefrontal cortex (DLPFC) played an important role in bubble formation, but whether a causal relationship exists and the mechanism of the effect of the DLPFC on bubbles remains unsettled. Using transcranial direct current stimulation (tDCS), we modulated the activity of the DLPFC and investigated the causal relationship between the DLPFC and the asset bubble in the classical learning-to-forecast experiment. 126 subjects were randomly divided into three groups and received different stimulations (left anodal/right cathodal, right anodal/left cathodal, or sham stimulation), respectively. We also conducted a 2-back task before and after stimulation to measure changes in subjects' cognitive abilities and explore in detail the cognitive mechanism of the effect of DLPFC stimulation on asset bubbles. Based on our results, we found that the bubble of the left anodal/right cathodal stimulation group was significantly smaller than that of the sham stimulation group. In the meantime, subjects performed significantly better in the 2-back task after left anodal/right cathodal stimulation but not right anodal/left cathodal or sham stimulation, which is consistent with their performance in the learning-to-forecast experiment, supporting the cognitive mechanism to some extent. Furthermore, we examined different forecasting rules across individuals and discovered that the left anodal/right cathodal stimulation group preferred the adaptive learning rule, while the sham and right anodal/left cathodal stimulation groups adopted a pure trend-following rule that tended to intensify market volatility aggressively.
| S-EPMC6521735 | biostudies-literature
Project description:The objective of this study was to test the feasibility of using the dorsolateral prefrontal cortex as a signal source for brain-computer interface control in people with severe motor impairment. We implanted two individuals with locked-in syndrome with a chronic brain-computer interface designed to restore independent communication. The implanted system (Utrecht NeuroProsthesis) included electrode strips placed subdurally over the dorsolateral prefrontal cortex. In both participants, counting backwards activated the dorsolateral prefrontal cortex consistently over the course of 47 and 22 months, respectively. Moreover, both participants were able to use this signal to control a cursor in one dimension, with average accuracy scores of 78?±?9% (standard deviation) and 71?±?11% (chance level: 50%), respectively. Brain-computer interface control based on dorsolateral prefrontal cortex activity is feasible in people with locked-in syndrome and may become of relevance for those unable to use sensorimotor signals for control.
| S-EPMC7508852 | biostudies-literature
Project description:Drug-related cues induce craving, which may perpetuate drug use or trigger relapse in addicted individuals. Craving is also under the influence of other factors in daily life, such as drug availability and self-control. Neuroimaging studies using drug cue paradigms have shown frontal lobe involvement in this contextual influence on cue reactivity, but have not clarified how and which frontal area accounts for this phenomenon. We explored frontal lobe contributions to cue-induced drug craving under different intertemporal drug availability conditions by combining transcranial magnetic stimulation and functional magnetic resonance imaging in smokers. We hypothesized that the dorsolateral prefrontal cortex (DLPFC) regulates craving during changes in intertemporal availability. Subjective craving was greater when cigarettes were immediately available, and this effect was eliminated by transiently inactivating the DLPFC with transcranial magnetic stimulation. Functional magnetic resonance imaging demonstrated that the signal most proportional to subjective craving was located in the medial orbitofrontal cortex across all contexts, whereas the DLPFC most strongly encoded intertemporal availability information. The craving-related signal in the medial orbitofrontal cortex was attenuated by inactivation of the DLPFC, particularly when cigarettes were immediately available. Inactivation of the DLPFC also reduced craving-related signals in the anterior cingulate and ventral striatum, areas implicated in transforming value signals into action. These findings indicate that DLPFC builds up value signals based on knowledge of drug availability, and support a model wherein aberrant circuitry linking dorsolateral prefrontal and orbitofrontal cortices may underlie addiction.
| S-EPMC3600476 | biostudies-literature
Project description:Anxious individuals consistently fail in controlling emotional behavior, leading to excessive avoidance, a trait that prevents learning through exposure. Although the origin of this failure is unclear, one candidate system involves control of emotional actions, coordinated through lateral frontopolar cortex (FPl) via amygdala and sensorimotor connections. Using structural, functional, and neurochemical evidence, we show how FPl-based emotional action control fails in highly-anxious individuals. Their FPl is overexcitable, as indexed by GABA/glutamate ratio at rest, and receives stronger amygdalofugal projections than non-anxious male participants. Yet, high-anxious individuals fail to recruit FPl during emotional action control, relying instead on dorsolateral and medial prefrontal areas. This functional anatomical shift is proportional to FPl excitability and amygdalofugal projections strength. The findings characterize circuit-level vulnerabilities in anxious individuals, showing that even mild emotional challenges can saturate FPl neural range, leading to a neural bottleneck in the control of emotional action tendencies.
| S-EPMC10423291 | biostudies-literature
Project description:Continuous theta-burst stimulation (cTBS), a non-invasive brain stimulation technique, can induce long-lasting changes in synaptic plasticity, vital for memory reconsolidation. For this study, a total of 170 participants completed four experiments by a randomized controlled design. Succeeding fear conditioning, the subjects received cTBS over the right dorsolateral prefrontal cortex (dlPFC) or vertex (control) with or without exposure to the conditioned stimulus to reactivate the original fear memory, and then underwent fear response tests. Compared with cTBS over the vertex and without memory reactivation, only cTBS over the right dlPFC after reactivation decreased the fear response for both recent and remote fear memories. This procedure was effective only during the reconsolidation window. The disruptive effect of cTBS over the right dlPFC on fear memory reconsolidation was delay-dependent. These findings demonstrate that cTBS time-dependently and delay-dependently prevents the return of fear and may have clinical potential for treating fear-related disorders.
| S-EPMC8786637 | biostudies-literature
Project description:It is generally assumed that choice between different actions reflects the difference between their action values yet little direct evidence confirming this assumption has been reported. Here we assess whether the brain calculates the absolute difference between action values or their relative advantage, that is, the probability that one action is better than the other alternatives. We use a two-armed bandit task during functional magnetic resonance imaging and modelled responses to determine both the size of the difference between action values (D) and the probability that one action value is better (P). The results show haemodynamic signals corresponding to P in right dorsolateral prefrontal cortex (dlPFC) together with evidence that these signals modulate motor cortex activity in an action-specific manner. We find no significant activity related to D. These findings demonstrate that a distinct neuronal population mediates action-value comparisons, and reveals how these comparisons are implemented to mediate value-based decision-making.
| S-EPMC4124863 | biostudies-literature
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.
| S-EPMC9016412 | biostudies-literature
Project description:BackgroundDorsal (DLPFC) and ventral (VLPFC) subregions in lateral prefrontal cortex play distinct roles in episodic memory, and both are implicated in schizophrenia. We test the hypothesis that schizophrenia differentially impairs DLPFC versus VLPFC control of episodic encoding.MethodsCognitive control was manipulated by requiring participants to encode targets and avoid encoding non-targets based upon stimulus properties of test stimuli. The more automatic encoding response (target versus non-target) was predicted to engage VLPFC in both groups. Conversely, having to overcome the prepotent encoding response (non-targets versus targets) was predicted to produce greater DLPFC activation in controls than in patients. Encoding occurred during event-related fMRI in a sample of 21 individuals with schizophrenia and 30 healthy participants. Scanning was followed by recognition testing outside the scanner.ResultsPatients were less successful differentially remembering target versus non-target stimuli, and retrieval difficulties correlated with more severe disorganized symptoms. As predicted, the target versus non-target contrast activated the VLPFC and correlated with retrieval success in both groups. Conversely, the non-target versus target contrast produced greater DLPFC activation in controls than in patients, and DLPFC activation correlated with performance only in controls.ConclusionIndividuals with schizophrenia can successfully engage the VLPFC to provide control over semantic encoding of individual items, but are specifically impaired at engaging the DLPFC to main context for task-appropriate encoding and thereby generate improved memory for target versus non-target items. This extends previous cognitive control models based on response selection tasks to the memory domain.
| S-EPMC4639631 | biostudies-literature
Project description:BackgroundPsychosis is common in bipolar disorder (BD) and is related to more severe cognitive impairments. Since the molecular mechanism of BD psychosis is elusive, we conducted this study to explore the proteomic differences associated with BD psychosis in the dorsolateral prefrontal cortex (DLPFC; BA9).MethodsPostmortem DLPFC gray matter tissues from five pairs of age-matched male BD subjects with and without psychosis history were used. Tissue proteomes were identified and quantified by label-free liquid chromatography tandem mass spectrometry and then compared between groups. Statistical significance was set at q < 0.40 and Log2 fold change (Log2FC) ≥ |1|. Protein groups with differential expression between groups at p < 0.05 were subjected to pathway analysis.ResultsEleven protein groups differed significantly between groups, including the reduction of tenascin C (q = 0.005, Log2FC = -1.78), the elevations of synaptoporin (q = 0.235, Log2FC = 1.17) and brain-specific angiogenesis inhibitor 1-associated protein 3 (q = 0.241, Log2FC = 2.10) in BD with psychosis. The between-group differences of these proteins were confirmed by Western blots. The top enriched pathways (p < 0.05 with ≥ 3 hits) were the outgrowth of neurons, neuronal cell proliferation, growth of neurites, and outgrowth of neurites, which were all predicted to be upregulated in BD with psychosis.LimitationsSmall sample size and uncertain relationships of the observed proteomic differences with illness stage and acute psychosis.ConclusionsThese results suggested BD with psychosis history may be associated with abnormalities in neurodevelopment, neuroplasticity, neurotransmission, and neuromodulation in the DLPFC.
| S-EPMC7234814 | biostudies-literature
Project description:total RNA-sequencing on dlPFC neurons from 19 human cocaine addicts (1-19) and 17 healthy controls (21-40)
2018-01-01 | GSE99349 | GEO