• BMB Reports
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• v.46 no.11
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• pp.519-526
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• 2013

Dopamine (DA) regulates emotional and motivational behavior through the mesolimbic dopaminergic pathway. Changes in DA signaling in mesolimbic neurotransmission are widely believed to modify reward-related behaviors and are therefore closely associated with drug addiction. Recent evidence now suggests that as with drug addiction, obesity with compulsive eating behaviors involves reward circuitry of the brain, particularly the circuitry involving dopaminergic neural substrates. Increasing amounts of data from human imaging studies, together with genetic analysis, have demonstrated that obese people and drug addicts tend to show altered expression of DA D2 receptors in specific brain areas, and that similar brain areas are activated by food-related and drug-related cues. This review focuses on the functions of the DA system, with specific focus on the physiological interpretation and the role of DA D2 receptor signaling in food addiction.

• Science of Emotion and Sensibility
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• v.20 no.4
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• pp.113-126
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• 2017

The purpose of the study was to find grey matter (GM) and white matter (WM) volume reduction in the brain reward system among patients with alcohol dependency. This study investigated regional GM and WM in chronic alcoholic patients, focusing primarily on the reward system, including principal components of the mesocorticolimbic reward circuit as well as cortical areas with modulating and oversight functions. Sixteen abstinent long-term chronic alcoholic men and demographically matched 16 healthy control men participated in the study. Morphometric analysis was performed on magnetic resonance brain scans using voxel-based morphometry (VBM)-diffeomorphic Anatomical Registration through Exponentiated Liealgebra (DARTEL). We derived GM and WM volumes from total brain and cortical and subcortical reward-related structures. Morphometric analyses that revealed the total volume of GM and WM was reduced and cerebrospinal fluid (CSF) was increased in the alcohol group compared to control group. The pronounced volume reduction in the reward system was observed in the GM and WM of the nucleus accumbens (NAc), GM of the amygdala, GM and WM of the hippocampus, WM of the thalamus, GM and WM of the insula, GM of the dorsolateral prefrontal cortex (DLPFC), GM of the orbitofrontal cortex (OFC), GM of the cingulate cortex (CC), GM and WM of the parahippocampal gyrus in the alcohol group. We identified volume reductions in WM as well as GM of reward system in the patients with alcohol dependency. These structural deficits in the reward system elucidate underlying impairment in the emotional and cognitive processing in alcoholism.

• Journal of Veterinary Science
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• v.25 no.5
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• pp.63.1-63.12
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• 2024

Importance: Glutamic acid decarboxylase 67 (GAD67) is a gamma-aminobutyric acid (GABA) synthesis enzyme associated with the function of other neurotransmitter receptors, such as the N-methyl-D-aspartate (NMDA) receptor and cannabinoid receptor 1. However, the role of GAD67 in the development of different abused drug-induced reward behaviors remains unknown. In order to elucidate the mechanisms of substance use disorder, it is crucial to study changes in biomarkers within the brain's reward circuit induced by drug use. Objective: The study was designed to examine the effects of the downregulation of GAD67 expression in the dorsal striatum on reward behavior development. Methods: We evaluated the effects of GAD67 knockdown on depression-like behavior and anxiety using the forced swim test and elevated plus maze test in a mouse model. We further determined the effects of GAD67 knockdown on ketamine- and JWH-018-induced conditioned place preference (CPP). Results: Knockdown of GAD67 in the dorsal striatum of mice increased depression-like behavior, but it decreased anxiety. Moreover, the CPP score on the NMDA receptor antagonist ketamine was increased by GAD67 knockdown, whereas the administration of JWH-018, a cannabinoid receptor agonist, did not affect the CPP score in the GAD67 knockdown mice group compared with the control group. Conclusions and Relevance: These results suggest that striatal GAD67 reduces GABAergic neuronal activity and may cause ketamine-induced NMDA receptor inhibition. Consequently, GAD67 downregulation induces vulnerability to the drug reward behavior of ketamine.

• Journal of Korea Multimedia Society
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• v.5 no.6
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• pp.704-711
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• 2002

Multimedia communication systems are characterized by supporting three different typer of services such as circuit switched services, and packet switched real Lime and non real time services. The wireless channels in a cell ate allocated by calls of these different service classes and the different service requirements have to be met. SRN is an extension of stochastic Petri nets and provides compact Modeling facilities for system analysis. To get the performance index, appropriate reward rates are assigned to its SRN. In this paper, we present a SRN model for performance analysis of channel allocation of multimedia mobile communication systems. The key contribution of this paper constitutes the Petri nets modeling techniques instead of complicate numerical analysis of Markov chains and easy way of performance analysis for channel allocations under SRN rewards concepts.

• Korean Journal of Biological Psychiatry
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• v.20 no.3
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• pp.74-79
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• 2013

Objectives This paper aims to understand the emotional-biological pathogenesis of eating disorders, and translate the understanding into new brain directed treatments. Methods The first part of the review sets the eating behavior into the context of what is now understood about the central control of appetite and molecular biology. The second part of the review sees how emotion relates to the brain circuit involving eating disorders. Results In general, patients with anorexia nervosa restricting type were less sensitive to reward, whereas patients with bulimia nervosa and anorexia nervosa binge purging type were more sensitive to it. The emotional life of people with eating disorders centers on food, weight, and shape. The abnormalities in social and emotional functioning both precede and persist outside of eating disorders. Conclusions Research into understanding the biological framework of the brain in eating disorders suggests that abnormalities may exist in emotional and information processing. This aspect can be translated into novel brain-directed treatments, particularly in anorexia nervosa.

• Molecules and Cells
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• v.40 no.6
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• pp.379-385
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• 2017

Drug addiction is a severe psychiatric disorder characterized by the compulsive pursuit of drugs of abuse despite potential adverse consequences. Although several decades of studies have revealed that psychostimulant use can result in extensive alterations of neural circuits and physiology, no effective therapeutic strategies or medicines for drug addiction currently exist. Changes in neuronal connectivity and regulation occurring after repeated drug exposure contribute to addiction-like behaviors in animal models. Among the involved brain areas, including those of the reward system, the striatum is the major area of convergence for glutamate, GABA, and dopamine transmission, and this brain region potentially determines stereotyped behaviors. Although the physiological consequences of striatal neurons after drug exposure have been relatively well documented, it remains to be clarified how changes in striatal connectivity underlie and modulate the expression of addiction-like behaviors. Understanding how striatal circuits contribute to addiction-like behaviors may lead to the development of strategies that successfully attenuate drug-induced behavioral changes. In this review, we summarize the results of recent studies that have examined striatal circuitry and pathway-specific alterations leading to addiction-like behaviors to provide an updated framework for future investigations.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.23 no.2
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• pp.49-56
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• 2012

Methylphenidate is a widely used stimulant for treatment of attention-deficit hyperactivity disorder (ADHD). In addition to core symptoms of attention and behavioral symptoms, methylphenidate is even effective for executive functions. However, abuse and misuse of stimulants, including methylphenidate, for the purpose of cognitive enhancement is an issue of concern worldwide. Some prejudices and misunderstandings against methylphenidate are popular ; however, little attention has been given to the neuropsychiatric evidence of methylphenidate for enhancement of cognitive function among healthy populations. In this article, our aim was to conduct a review of previous studies investigating the effect of methylphenidate in healthy populations. Findings from several recent studies have demonstrated the effectiveness of methylphenidate for enhancement of cognitive function in healthy populations. The mechanisms of cognitive enhancement are thought to be associated with motivation and the reward circuit in the brain. However, when considering the risk to benefit, an official discussion of the use of methylphenidate among healthy members of the population would be premature. Instead, investigation of epidemiological studies of the prevalence of misuse of stimulants among healthy members of the population, particularly adolescents and college students, is needed. In addition, based on achievements reported in previous studies, investigation of the effect of an approach using non-pharmacological enhancing motivation, which will in turn result in increased cognitive function would be helpful.

• Molecules and Cells
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• v.44 no.2
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• pp.63-67
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• 2021

The bed nucleus of the stria terminalis (BNST)-a key part of the extended amygdala-has been implicated in the regulation of diverse behavioral states, ranging from anxiety and reward processing to feeding behavior. Among the host of distinct types of neurons within the BNST, recent investigations employing cell type- and projection-specific circuit dissection techniques (such as optogenetics, chemogenetics, deep-brain calcium imaging, and the genetic and viral methods for targeting specific types of cells) have highlighted the key roles of glutamatergic and GABAergic neurons and their axonal projections. As anticipated from their primary roles in excitatory and inhibitory neurotransmission, these studies established that the glutamatergic and GABAergic subpopulations of the BNST oppositely regulate diverse behavioral states. At the same time, these studies have also revealed unexpected functional specificity and heterogeneity within each subpopulation. In this Minireview, we introduce the body of studies that investigated the function of glutamatergic and GABAergic BNST neurons and their circuits. We also discuss unresolved questions and future directions for a more complete understanding of the cellular diversity and functional heterogeneity within the BNST.