Physiologic studies revealed that neurons in the dopaminergic midbrain of non-human primates encode reward prediction errors. It was furthermore shown that reward prediction errors are adaptively scaled with respect to the range of possible outcomes, enabling sensitive encoding for a large range of reward values. Congruently, neuroimaging studies in humans demonstrated that BOLD-responses in the ventral striatum encode reward prediction errors in similar fashion as dopaminergic midbrain neurons, suggesting that these BOLD-responses may be driven by dopaminergic midbrain activity. However, neuroimaging results are ambiguous with respect to the adaptive scaling of reward prediction errors, leading to the conjecture that under certain circumstances other than dopaminergic midbrain input may drive ventral striatal BOLD-responses. The goal of this study was to substantiate whether BOLD-responses in the ventral striatum rather respond to adaptively scaled reward prediction errors or absolute reward magnitude. In addition, we aimed to identify neuronal structures modulating activity in the ventral striatum. Sixteen healthy participants played a wheel of fortune game, where they could win three differently valued rewards while being scanned. BOLD-responses increased after gaining rewards; this gain was however independent of the absolute reward magnitude. In contrast BOLD-responses upon reward omission decreased with reward magnitude. A psychophysiological interaction analysis identified a cluster in the brainstem in proximity of the dorsal raphe nucleus, a cluster in the lateral orbitofrontal cortex, and a cluster in the rostral cingulate zone. These clusters changed their connectivity with the ventral striatum in relation to the absolute reward magnitude in reward omission trials.
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http://dx.doi.org/10.1016/j.brainres.2011.07.019 | DOI Listing |
J Psychiatr Res
January 2025
Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, 52246, USA; Iowa Neuroscience Institute, University of Iowa, Iowa City, IA, 52246, USA; Yale Child Study Center, Yale School of Medicine, New Haven, CT, 06510, USA. Electronic address:
Prenatal stress is a risk factor for neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD). However, how early stress modification of brain development contributes to this pathophysiology is poorly understood. Ventral forebrain regions such as dorsal striatum are of particular interest: dorsal striatum modulates movement and cognition, is altered in NDDs, and has a primarily GABAergic population.
View Article and Find Full Text PDFPharmacol Res Perspect
February 2025
New Drug Development Center, Daegu, Korea.
Oxidation of dopamine can cause various side effects, which ultimately leads to cell death and contributes to Parkinson's disease (PD). To counteract dopamine oxidation, newly synthesized dopamine is quickly transported into vesicles via vesicular monoamine transporter 2 (VMAT2) for storage. VMAT2 expression is reduced in patients with PD, and studies have shown increased accumulation of dopamine oxidation byproducts and α-synuclein in animals with low VMAT2 expression.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Pediatrics, Children's Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, USA.
The orbitofrontal cortex (OFC) is a large cortical structure, expansive across anterior-posterior axes. It is essential for flexibly updating learned behaviors, and paradoxically, also implicated in inflexible and compulsive-like behaviors. Here, we investigated mice bred to display inflexible reward-seeking behaviors that are insensitive to action consequences.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
January 2025
Department of Child and Adolescent Psychiatry, Faculty of Medicine, TUD Dresden University of Technology, German Center for Child and Adolescent Health (DZKJ), partner site Leipzig/Dresden, Dresden, Germany.
Objective: Conduct disorder (CD) is associated with deficits in the use of punishment for reinforcement learning (RL) and subsequent decision-making, contributing to reckless, antisocial, and aggressive behaviors. Here, we used functional magnetic resonance imaging (fMRI) to examine whether differences in behavioral learning rates derived from computational modeling, particularly for punishment, are reflected in aberrant neural responses in youths with CD compared to typically-developing controls (TDCs).
Methods: 75 youths with CD and 99 TDCs (9-18 years, 47% girls) performed a probabilistic RL task with punishment, reward, and neutral contingencies.
J Neurochem
January 2025
Department of Pathology, School of Veterinary Medicine, University of São Paulo, Sao Paulo, Brazil.
Autism spectrum disorder (ASD) is a complex developmental disorder characterized by several behavioral impairments, especially in socialization, communication, and the occurrence of stereotyped behaviors. In rats, prenatal exposure to valproic acid (VPA) induces autistic-like behaviors. Previous studies by our group have suggested that the autistic-like phenotype is possibly related to dopaminergic system modulation because tyrosine hydroxylase (TH) expression was affected.
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