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Pooseh, S.

Publications and source records attributed to Pooseh, S..

3 recordsLinked to original sources

Connection Failure: Differences in White Matter Microstructure are associated with 5-HTTLPR but not with Risk-Seeking for Losses

In a previous study (Neukam, Kroemer et al. 2018), we found for the 5-HTTLPR genotype higher risk-seeking for losses in S/S vs. L/L carrier, which could not be explained by acutely changed central serotonin levels. This finding alternatively may be the result of reduced top-down control from the frontal cortex due to altered signal pathways involving the amygdala and ventral striatum. The serotonergic system is known to be involved in neurodevelopment and neuroplasticity. Therefore, the aim of this study was to investigate whether structural differences in white matter can explain the differences in risk-seeking behaviour that we observed in our previous study and whether 5-HTTLPR groups differ in their white matter microstructure. These differences can be detected using diffusion-weighted imaging (DWI). We assumed lower structural connectivity in S/S compared to L/L carrier, and a negative relationship between risk-seeking for losses and connectivity. We used DWI to compute diffusion parameters for the frontostriatal and uncinate tract in 175 individuals (39 S/S, 80 S/L, 56 L/L). Results showed no significant relationship between diffusion parameters and risk-seeking for losses. Furthermore, we did not find significant differences in diffusion parameters of the S/S vs. L/L group. There were only group differences in the frontostriatal tract showing stronger structural connectivity in the S/L group, which is also reflected in the whole brain approach. Therefore, the data do not support our hypothesis that the association between 5- HTTLPR and risk-seeking for losses is related to differences in white matter pathways implicated in decision-making.

neuroscience↗

Individual differences in dopamine function underlying the balance between model-based and model-free control

Reinforcement learning involves a balance between model-free (MF) and model-based (MB) systems. Recent studies suggest that individuals with either pharmacologically enhanced levels of dopamine (DA) or higher baseline levels of DA exhibit more MB control. However, it remains unknown whether such pharmacological effects depend on baseline DA. Here, we investigated whether effects of L-DOPA on the balance of MB/MF control depend on ventral striatal baseline DA. Sixty participants had two functional magnetic resonance imaging (fMRI) scans while performing a two-stage sequential decision-making task under 150 mg L-DOPA or placebo (counterbalanced), followed by a 4-hour 18F-DOPA positron emission tomography (PET) scan (on a separate occasion). We found an interaction between baseline DA levels and L-DOPA induced changes in MB control. Individuals with higher baseline DA levels showed a greater L-DOPA induced enhancement in MB control. Surprisingly, we found a corresponding drug-by-baseline DA interaction on MF, but not MB learning signals in the ventromedial prefrontal cortex. We did not find a significant interaction between baseline DA levels and L-DOPA effects on MF control or MB/MF balance. In sum, our findings point to a baseline dependency of L-DOPA effects on differential aspects of MB and MF control. Individual differences in DA washout may be an important moderator of L-DOPA effects. Overall, our findings complement the general notion where higher DA levels is related to a greater reliance on MB control. Although the relationship between phasic DA firing and MF learning is conventionally assumed in the animal literature, the relationship between DA and MF control is not as straightforward and requires further clarification.

neuroscience↗

L-DOPA reduces model-free control of behavior by attenuating the transfer of value to action

Dopamine is a key neurotransmitter in reinforcement learning and action control. Recent findings suggest that these components are inherently entangled. Here, we tested if increases in dopamine tone by administration of L-DOPA upregulate deliberative \"model-based\" control of behavior or reflexive \"model-free\" control as predicted by dual-control reinforcement-learning models. Alternatively, L-DOPA may impair learning as suggested by \"value\" or \"thrift\" theories of dopamine. To this end, we employed a two-stage Markov decision-task to investigate the effect of L-DOPA (randomized cross-over) on behavioral control while brain activation was measured using fMRI. L-DOPA led to attenuated model-free control of behavior as indicated by the reduced impact of reward on choice and increased stochasticity of model-free choices. Correspondingly, in the brain, L-DOPA decreased the effect of reward while prediction-error signals were unaffected. Taken together, our results suggest that L-DOPA reduces model-free control of behavior by attenuating the transfer of value to action.

neuroscience↗