Reward-Related Learning in Alcoholism

2011 ◽  
Vol 26 (S2) ◽  
pp. 2014-2014
Author(s):  
A. Heinz ◽  
A. Beck ◽  
S.Q. Park ◽  
L. Deserno ◽  
F. Schlagenhauf
Keyword(s):  
Reversal Learning ◽  
Ventral Striatum ◽  
Imaging Study ◽  
Brain Activation ◽  
Dopamine Synthesis ◽  
Healthy Controls ◽  
Reward Seeking ◽  
Positron Emission ◽  
Dorsolateral Prefrontal ◽  
Alcohol Dependent

The disposition and maintenance of alcohol addiction has been associated with dysfunctional learning, particularly with increased salience attribution to alcohol-associated stimuli and Pavlovian-to-instrumental transfer, which establishes an effect of alcohol-associated cues on operant alcohol seeking and consumption. Previous imaging studies showed that dopamine dysfunction in the ventral striatum is associated with increased brain activation elicited by alcohol-associated cues in brain areas associated with attention. Furthermore, brain activation elicited by non-alcohol (e.g. monetary) reward was decreased in detoxified alcohol-dependent patients. Neuroadaptation following addiction therefore seems to augment neuronal responses to well-established, drug-associated stimuli while interfering with the learning of new, reward-seeking behaviour patterns. Using functional magnetic resonance imaging (fMRI) we showed that in detoxified alcoholics, reward-dependent reversal learning is impaired compared to healthy controls, and that this impairment correlates with reduced functional connectivity between the ventral striatum and the dorsolateral prefrontal cortex. Furthermore, we will present first data from a multimodal imaging study combining fMRI and positron-emission-tomography (PET) to measure the association between dopamine synthesis reduction and impaired functional brain activation during reversal learning in detoxified alcohol-dependent patients compared with healthy controls.

scholarly journals O5.1. STRIATAL DOPAMINE AND REDUCED REWARD PREDICTION ERROR SIGNALING IN UNMEDICATED SCHIZOPHRENIA PATIENTS

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S11-S11
Author(s):  
Teresa Katthagen ◽  
Jakob Kaminski ◽  
Andreas Heinz ◽  
Ralph Buchert ◽  
Florian Schlagenhauf
Keyword(s):  
Prediction Error ◽  
Negative Symptoms ◽  
Ventral Striatum ◽  
Striatal Dopamine ◽  
Dopamine Synthesis ◽  
Positive Symptoms ◽  
Healthy Controls ◽  
Reward Prediction Error ◽  
Reward Prediction ◽  
Significant Difference

Abstract Background Increased striatal dopamine synthesis capacity (DSC) has consistently been reported in patients with schizophrenia (Sz). However, the functional mechanism translating this into behavior and symptoms remains unclear. It has been proposed that heightened striatal dopamine may blunt dopaminergic reward prediction error (RPE) signaling during reinforcement learning. Methods In this study, we investigated striatal DSC and RPEs and their association in unmedicated Sz and healthy controls. 23 healthy controls (HC) and 20 unmedicated Sz took part in an FDOPA-PET scan measuring DSC and underwent fMRI scanning, where they performed a reversal learning paradigm. We compared groups regarding DSC und neural RPE signals and probed the respective correlation (23 HC and 16 Sz for both measures). Results There was no significant difference between HC and Sz in DSC. Taking into account comorbid alcohol abuse revealed that only patients without such abuse showed elevated DSC in the associative and sensorimotor striatum, while those with abuse did not differ from HC. Patients performed worse during learning, accompanied by a reduced RPE signal in the ventral striatum. In HC, the DSC in the limbic striatum correlated with higher RPE signaling, while there was no significant association in patients. DSC in the associative striatum correlated with higher positive symptoms, and blunted RPE signaling was associated with negative symptoms. Discussion Our results suggest that dopamine modulation of RPE is impaired in schizophrenia. Furthermore, we observed a dissociation with elevated DSC in the associative and sensorimotor striatum contributing to positive symptoms and blunted RPE in the ventral striatum to negative symptoms.

scholarly journals Striatal Dopamine and Reward Prediction Error Signaling in Unmedicated Schizophrenia Patients

2020 ◽  
Vol 46 (6) ◽  
pp. 1535-1546
Author(s):  
Teresa Katthagen ◽  
Jakob Kaminski ◽  
Andreas Heinz ◽  
Ralph Buchert ◽  
Florian Schlagenhauf
Keyword(s):  
Reversal Learning ◽  
Prediction Error ◽  
Negative Symptoms ◽  
Ventral Striatum ◽  
Striatal Dopamine ◽  
Dopamine Synthesis ◽  
Positive Symptoms ◽  
Prediction Errors ◽  
Reward Prediction Error ◽  
Reward Prediction

Abstract Increased striatal dopamine synthesis capacity has consistently been reported in patients with schizophrenia. However, the mechanism translating this into behavior and symptoms remains unclear. It has been proposed that heightened striatal dopamine may blunt dopaminergic reward prediction error signaling during reinforcement learning. In this study, we investigated striatal dopamine synthesis capacity, reward prediction errors, and their association in unmedicated schizophrenia patients (n = 19) and healthy controls (n = 23). They took part in FDOPA-PET and underwent functional magnetic resonance imaging (fMRI) scanning, where they performed a reversal-learning paradigm. The groups were compared regarding dopamine synthesis capacity (Kicer), fMRI neural prediction error signals, and the correlation of both. Patients did not differ from controls with respect to striatal Kicer. Taking into account, comorbid alcohol abuse revealed that patients without such abuse showed elevated Kicer in the associative striatum, while those with abuse did not differ from controls. Comparing all patients to controls, patients performed worse during reversal learning and displayed reduced prediction error signaling in the ventral striatum. In controls, Kicer in the limbic striatum correlated with higher reward prediction error signaling, while there was no significant association in patients. Kicer in the associative striatum correlated with higher positive symptoms and blunted reward prediction error signaling was associated with negative symptoms. Our results suggest a dissociation between striatal subregions and symptom domains, with elevated dopamine synthesis capacity in the associative striatum contributing to positive symptoms while blunted prediction error signaling in the ventral striatum related to negative symptoms.

scholarly journals Striatal dopamine dissociates methylphenidate effects on value-based versus surprise-based reversal learning

2021 ◽  
Author(s):  
Ruben van den Bosch ◽  
Britt Lambregts ◽  
Jessica Määttä ◽  
Lieke Hofmans ◽  
Danae Papadopetraki ◽  
...  
Keyword(s):  
Reversal Learning ◽  
Learning Task ◽  
Striatal Dopamine ◽  
Emission Tomography ◽  
Sensory Cortex ◽  
Dopamine Synthesis ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Large Variability ◽  
Positron Emission

Abstract Psychostimulants such as methylphenidate are widely used for their cognitive enhancing effects, but there is large variability in the direction and extent of these effects, and there are concerns about the potential for abuse. We tested the hypothesis that methylphenidate enhances or impairs reward/punishment-based reversal learning depending on baseline striatal dopamine levels and corticostriatal gating of reward/punishment-related representations in stimulus-specific sensory cortex. Young healthy adults were scanned with functional magnetic resonance imaging during a reward/punishment reversal learning task, after intake of methylphenidate or the selective D2/3-receptor antagonist sulpiride. Striatal dopamine synthesis capacity was indexed with [18F]DOPA positron emission tomography. Reward versus punishment learning signals were boosted to a greater degree in participants with higher dopamine synthesis capacity. By contrast, striatal and stimulus-specific sensory surprise signals were boosted in participants with lower dopamine synthesis. These results unravel the mechanisms by which methylphenidate modulates reward and attention, impacting our understanding of how it can both enhance attention and mitigate reward-related compulsivity.

scholarly journals Acute acetate administration increases endogenous opioid levels in the human brain: A [11C]carfentanil molecular imaging study

2021 ◽  
pp. 026988112096591
Author(s):  
Abhishekh H Ashok ◽  
Jim Myers ◽  
Gary Frost ◽  
Samuel Turton ◽  
Roger N Gunn ◽  
...  
Keyword(s):  
Human Brain ◽  
Sodium Acetate ◽  
Statistical Significance ◽  
Imaging Study ◽  
Pet Scan ◽  
Endogenous Opioid ◽  
Reference Tissue ◽  
Healthy Human ◽  
Fourfold Increase ◽  
Positron Emission

Introduction: A recent study has shown that acetate administration leads to a fourfold increase in the transcription of proopiomelanocortin (POMC) mRNA in the hypothalamus. POMC is cleaved to peptides, including β-endorphin, an endogenous opioid (EO) agonist that binds preferentially to the µ-opioid receptor (MOR). We hypothesised that an acetate challenge would increase the levels of EO in the human brain. We have previously demonstrated that increased EO release in the human brain can be detected using positron emission tomography (PET) with the selective MOR radioligand [11C]carfentanil. We used this approach to evaluate the effects of an acute acetate challenge on EO levels in the brain of healthy human volunteers. Methods: Seven volunteers each completed a baseline [11C]carfentanil PET scan followed by an administration of sodium acetate before a second [11C]carfentanil PET scan. Dynamic PET data were acquired over 90 minutes, and corrected for attenuation, scatter and subject motion. Regional [11C] carfentanil BPND values were then calculated using the simplified reference tissue model (with the occipital grey matter as the reference region). Change in regional EO concentration was evaluated as the change in [11C]carfentanil BPND following acetate administration. Results: Following sodium acetate administration, 2.5–6.5% reductions in [11C]carfentanil regional BPND were seen, with statistical significance reached in the cerebellum, temporal lobe, orbitofrontal cortex, striatum and thalamus. Conclusions: We have demonstrated that an acute acetate challenge has the potential to increase EO release in the human brain, providing a plausible mechanism of the central effects of acetate on appetite in humans.

scholarly journals 11C- and 18F-Radiotracers for In Vivo Imaging of the Dopamine System: Past, Present and Future

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 108
Author(s):  
Michael R. Kilbourn
Keyword(s):  
Pet Imaging ◽  
In Vivo Imaging ◽  
Dopamine Synthesis ◽  
Dopamine System ◽  
Synaptic Release ◽  
Positron Emission ◽  
The Central Nervous System ◽  
Pet Radiotracers ◽  
Selection Of

The applications of positron emission tomography (PET) imaging to study brain biochemistry, and in particular the aspects of dopamine neurotransmission, have grown significantly over the 40 years since the first successful in vivo imaging studies in humans. In vivo PET imaging of dopaminergic functions of the central nervous system (CNS) including dopamine synthesis, vesicular storage, synaptic release and receptor binding, and reuptake processes, are now routinely used for studies in neurology, psychiatry, drug abuse and addiction, and drug development. Underlying these advances in PET imaging has been the development of the unique radiotracers labeled with positron-emitting radionuclides such as carbon-11 and fluorine-18. This review focuses on a selection of the more accepted and utilized PET radiotracers currently available, with a look at their past, present and future.

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