• 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.

• 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.

• International Journal of Oral Biology
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• v.34 no.3
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• pp.123-129
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• 2009

Taste is associated with hedonic evaluation as well as recognition of quality and intensity. Taste information is sent to the cortical gustatory area in a chemotopical manner to be processed for discrimination of taste quality. It is also conveyed to the reward system and feeding center via the prefrontal cortices. The amygdala, which receives taste inputs, also influences reward and feeding. In terms of neuroactive substances, palatability is closely related to benzodiazepine derivatives and $\beta$-endorphin, both of which facilitate consumption of food and fluid. The reward system contains the ventral tegmental area, nucleus accumbens and ventral pallidum and finally sends information to the lateral hypothalamic area, the feeding center. The dopaminergic system originating from the ventral tegmental area mediates the motivation to consume palatable food. The actual ingestive behavior is promoted by the orexigenic neuropeptides from the hypothalamus. Even palatable food can become aversive and avoided as a consequence of postingestional unpleasant experience such as malaise. The brain mechanism of these aspects of taste is elucidated.

• Molecules and Cells
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• v.41 no.5
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• pp.454-464
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• 2018

Crosstalk between G-protein signaling and glutamatergic transmission within the brain reward circuits is critical for long-term emotional effects (depression and anxiety), cravings, and negative withdrawal symptoms associated with opioid addiction. A previous study showed that Regulator of G-protein signaling 4 (RGS4) may be implicated in opiate action in the nucleus accumbens (NAc). However, the mechanism of the NAc-specific RGS4 actions that induce the behavioral responses to opiates remains largely unknown. The present study used a short hairpin RNA (shRNA)-mediated knock-down of RGS4 in the NAc of the mouse brain to investigate the relationship between the activation of ionotropic glutamate receptors and RGS4 in the NAc during morphine reward. Additionally, the shRNA-mediated RGS4 knock-down was implemented in NAc/striatal primary-cultured neurons to investigate the role that striatal neurons have in the morphine-induced activation of ionotropic glutamate receptors. The results of this study show that the NAc-specific knock-down of RGS4 significantly increased the behaviors associated with morphine and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc. Furthermore, the knock-down of RGS4 enhanced the phosphorylation of the GluR1 and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous morphine withdrawal. These findings show a novel molecular mechanism of RGS4 in glutamatergic transmission that underlies the negative symptoms associated with morphine administration.

• Molecules and Cells
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• v.26 no.2
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• pp.121-130
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• 2008

Methamphetamine, a commonly used addictive drug, is a powerful addictive stimulant that dramatically affects the CNS. Repeated METH administration leads to a rewarding effect in a state of addiction that includes sensitization, dependence, and other phenomena. It is well known that susceptibility to the development of addiction is influenced by sources of reinforcement, variable neuroadaptive mechanisms, and neurochemical changes that together lead to altered homeostasis of the brain reward system. These behavioral abnormalities reflect neuroadaptive changes in signal transduction function and cellular gene expression produced by repeated drug exposure. To provide a better understanding of addiction and the mechanism of the rewarding effect, it is important to identify related genes. In the present study, we performed gene expression profiling using microarray analysis in a reward effect animal model. We also investigated gene expression in four important regions of the brain, the nucleus accumbens, striatum, hippocampus, and cingulated cortex, and analyzed the data by two clustering methods. Genes related to signaling pathways including G-protein-coupled receptor-related pathways predominated among the identified genes. The genes identified in our study may contribute to the development of a gene modeling network for methamphetamine addiction.

• Korean Journal of Biological Psychiatry
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• v.22 no.3
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• pp.113-117
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• 2015

Psychiatry has progressed with neurobiological basis, providing individually tailored treatment, preventing mental illness, and managing public mental health. Foundational knowledge that may contribute to the development of psychiatry and neuroscience has been attained through continual national and international investment in research. However, this knowledge obtained from neurobiological research is not being applied to clinical practice proactively. This may be due to a lack of support for translational research connecting neuroscience with clinical practice, and a lack of development and availability of educational programs for clinical psychiatrists. To solve these problems, it is essential to support translational research conducted by clinicians and to establish an appropriate reward system. Considering the direction of progress in psychiatry and the demand from clinicians, appropriate investment in research and education programs that provide neurobiological knowledge applicable to clinical practice is required. Researchers and educators must also communicate and collaborate to deliver neurobiological findings effectively.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.1-11
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• 1998

Ameliorating mechanisms of red ginseng on learning deficits were investigated in the following 3 experiments; its effects on 1) place learning deficits in aged rats and in young rats with selective hippocampal lesions (behavioral study), 2) long-term potentiation in the hippocampal formation (neuro- physiological study), and 3) ChAT (choline acetyl transferase) activity in various brain regions of aged rats (pharmacological study). In the behavioral study, first, performance in the place learning tasks were compared among 3 groups of young and aged rats; control young intact rats (10-12 week old) treated with water, aged rats (28-32 month old) treated with water, and aged rats (28-32 month old) treated with red ginseng (100 mghglday) suspended in water. Second, performance in the place learning tasks was compared among 3 groups of young rats; control intact rats treated with water, rats with bilateral hippocampal lesions treated with water, and rats with bilateral hippocampal lesions treated with red ginseng (100 mg/kg/day). Each rat in these 2 behavioral experiments was tested with the 3 types of the place learning tasks in a circular open field using intracranial self-stimulation (ICSS) as reward. The ICSS reward was delivered if the rat (1) moved distance of 100-160 cm (DMT): (2) entered an experiment-determined reward place within the open field, and this place was randomly varied in sequential trials (RRPST); or (3) entered 2 specific places, and did a shuttle behavior between the 2 places (PLT). Performance of the aged rats in the ginseng group was not significantly different from that of control young rats in ICSS (current intensity, bar press rates), DMT and RRPST. However, treatment with red ginseng significantly ameliorated place-navigation learning deficits in aged rats in the PLT. Similarly, red ginseng ameliorated learning and memory deficits in young rats with hippocampal lesions in the same tasks. In the neurophysiological study using young rats, perfusion of hippocampal slices with non-sapon in fraction of red ginseng significantly enhanced magnitudes of the long-term potentiation (LfP) in the CA3 subfield. In the pharmacological study, treatment with red ginseng did not affect ChAT activity in aged rat brain including the hippocampal formation. These results strongly suggest that red ginseng ameliorates learning and memory deficits in aged rats through actions on the CA3 subfield of the hippocampal formation, which were independent of the presynaptic components of the cholinergic system

• 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.

• Science of Emotion and Sensibility
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• v.17 no.2
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• pp.45-54
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• 2014

In recent years, advancing technology and growing interest in neuromarketing and neurobranding have led to foundational research that facilitates a better understanding of consumers' affective responses and unconscious information processing. However, the areas of aesthetics and design have remained largely unaffected by such advances and implications. The purpose of this study is to present a systematic review of the neuroscientific evidence aimed at sensible design for design and marketing researchers interested in exploring neuroaesthetics, an interdisciplinary area by nature. Sciencedirect, EBSCO, and the Google Scholar database were searched in February 2014 to select and review previous studies of aesthetics involving neuroscience. Twenty-eight studies were reviewed and divided into two categories: reward system and emotion. In addition to discussions on previous approaches, future research directions focusing on the process of aesthetic judgments (e.g., design elements, marketing stimuli) are proposed.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.5
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• pp.307-312
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• 2022

It is well known that dopamine transmission from the ventral tegmental area (VTA) modulates motivated behavior and reinforcement learning. Although dopaminergic neurons are the major type of VTA neurons, recent studies show that a significant proportion of the VTA contains GABAergic and type 2 vesicular glutamate transporter (VGLUT2)-positive neurons. The non-dopaminergic neurons are also critically involved in regulating motivated behaviors. Some VTA neurons appear to co-release two different types of neurotransmitters. They are VGLUT2-DA neurons, VGLUT2-GABA neurons and GABA-DA neurons. These co-releasing neurons show distinct features compared to the neurons that release a single neurotransmitter. Here, we review how VTA cell populations wire to the other brain regions and how these projections differentially contribute to motivated behavior through the distinct molecular mechanism. We summarize the activities, projections and functions of VTA neurons concerning motivated behavior. This review article discriminates VTA cell populations related to the motivated behavior based on the neurotransmitters they release and extends the classical view of the dopamine-mediated reward system.