• Biomolecules & Therapeutics
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• v.32 no.6
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• pp.659-684
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• 2024

Viral infections are increasingly recognized as triggers for depressive disorders, particularly following the SARS-CoV-2 pandemic and the rise of long COVID. Viruses such as Herpes Simplex Virus (HSV), Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) are linked to depression through complex neurobiological mechanisms. These include immune system dysregulation, chronic inflammation, and neurotransmitter imbalances that affect brain function and mood regulation. Viral activation of the immune system leads to the release of pro-inflammatory cytokines, resulting in neuroinflammation and associated depressive symptoms. Furthermore, specific viruses can disrupt neurotransmitter systems, including serotonin, dopamine, and glutamate, all of which are essential for mood stabilization. The unique interactions of different viruses with these systems underscore the need for virus-specific therapeutic approaches. Current broad-spectrum treatments often overlook the precise neurobiological pathways involved in post-viral depression, reducing their efficacy. This review emphasizes the need to understand these virus-specific interactions to create tailored interventions that directly address the neurobiological effects induced by each type of virus. These interventions may include immunomodulatory treatments that target persistent inflammation, antiviral therapies to reduce the viral load, or neuroprotective strategies that restore neurotransmitter balance. Precision medicine offers promising avenues for the effective management of virus-induced depression, providing patient-specific approaches that address the specific biological mechanisms involved. By focusing on the development of these targeted treatments, this review aims to pave the way for a new era in psychiatric care that fully addresses the root causes of depression induced by viral infections.

• Korean Journal of Biological Psychiatry
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• v.20 no.4
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• pp.129-135
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• 2013

Aggression can be defined as 'behavior intended to harm another' which can be seen both from humans and animals. However, trying to understand aggression in a simplistic view may make it difficult to develop an integrated approach. So, we tried to explain aggression in a multidisciplinary approach, affected by various factors such as neuroanatomical structures, neurotransmitter, genes, and sex hormone. Parallel with animal models, human aggression can be understood with two phenomena, offensive aggression and defensive aggression. Neurobiological model of aggression give a chance to explain aggression with an imbalance between prefrontal regulatory influences and hyper-reactivity of the subcortical areas involved in affective evaluation, finally in an aspect of brain organization. Serotonin and GABA usually inhibit aggression and norepinephrine while glutamate and dopamine precipitate aggressive behavior. As there is no one gene which has been identified as a cause of aggression, functions between gene to gene interaction and gene to environment interaction are being magnified. Contributions of sex hormone to aggression, especially molecular biologic interaction of testosterone and regulation of estrogen receptor have been emphasized during the research on aggression. This multidisciplinary approach on aggression with types, neurochemical bases, and animal models can bring integrated interpretation on aggression.

• Biomolecules & Therapeutics
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• v.30 no.3
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• pp.232-237
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• 2022

Autism spectrum disorder (ASD) having core characteristics of social interaction problems and repetitive behaviors and interests affects individuals at varying degrees and comorbidities, making it difficult to determine the precise etiology underlying the symptoms. Given its heterogeneity, ASD is difficult to treat and the development of therapeutics is slow due to the scarcity of animal models that are easy to produce and screen with. Based on the theory of excitation/inhibition imbalance in the brain with ASD which involves glutamatergic and/or GABAergic neurotransmission, a pharmacologic agent to modulate these receptors might be a good starting point for modeling. N-methyl-D-aspartic acid (NMDA) is an amino acid derivative acting as a specific agonist at the NMDA receptor and therefore imitates the action of the neurotransmitter glutamate on that receptor. In contrast to glutamate, NMDA selectively binds to and regulates the NMDA receptor, but not other glutamate receptors such as AMPA and kainite receptors. Given this role, we aimed to determine whether NMDA administration could result in autistic-like behavior in adolescent mice. Both male and female mice were treated with saline or NMDA (50 and 75 mg/kg) and were tested on various behavior experiments. Interestingly, acute NMDA-treated mice showed social deficits and repetitive behavior similar to ASD phenotypes. These results support the excitation/inhibition imbalance theory of ASD and that NMDA injection can be used as a pharmacologic model of ASD-like behaviors.

• Molecules and Cells
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• v.38 no.12
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• pp.1023-1028
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• 2015

Whole body energy balance is achieved through the coordinated regulation of energy intake and energy expenditure in various tissues including liver, muscle and adipose tissues. A positive energy imbalance by excessive energy intake or insufficient energy expenditure results in obesity and related metabolic diseases. Although there have been many obesity treatment trials aimed at the reduction of energy intake, these strategies have achieved only limited success because of their associated adverse effects. An ancient neurotransmitter, serotonin is among those traditional pharmacological targets for anti-obesity treatment because it exhibits strong anorectic effect in the brain. However, recent studies suggest the new functions of peripheral serotonin in energy homeostasis ranging from the endocrine regulation by gut-derived serotonin to the autocrine/paracrine regulation by adipocyte-derived serotonin. Here, we discuss the role of serotonin in the regulation of energy homeostasis and introduce peripheral serotonin as a possible target for anti-obesity treatment.

• Journal of Pharmacopuncture
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• v.3 no.2
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• pp.1-25
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• 2000

We were trying to study the validity of Puffer fish's poison(Tetrodotoxin- TTX) to make a traditional Korean Medical treatment. The following conclusions were made after literary studies. 1. The first record of the puffer fish dates back 2000 years ago in the Chinese text Book of Mountain and Sea and other texts from the similar period. 2. Puffer fish's poison IS known as tetrodotoxin which is an amino perhydroquinazoline compound. It has a chemical formula of $C_{11}H_{17}N_3O_8$ in the hemiacetal structure and has the molecular weight of 319. 3. Tetrodotoxin (TTX) plays a role as potent neurotransmitter blocker by blocking the $Na^+$ -gate channel which hinders the influx of $Na^+$ ion into the cell. 4. Symptoms of the puffer fish poisoning ranges from blunted sense in the lips and tongue, occasional vomiting in the first degree to sudden descending of the blood pressure, apnea, and other critical conditions in the fourth degree. Intoxication of the puffer fish poison progresses at a rapid pace as death may occur after an hour and half up to eight hours in maximum. Typical death occurs after four to six hours. 5. Ways to treat the puffer fish poisoning include gastric irrigation, induce vomiting, purgation, intravenous fluid injection, and correcting electrolytic imbalance and acidosis. In cases of dyspnea, apply oxygen inhalation and conduct artificial respiration. 6. Tetrodotoxin (TTX) may be applied in treating brain disorders, ocular pain, excess pain in the large intestine and ileum, and relieving tension of the skeletal museles, neuralgia, rheumatism, arthritis, and etc. 7. In terms of Oriental medicine, the puffer fish poison has characteristics of sweet, warm, and poisonous. It's known efficacies are to tonify weakness, dispel damp, benefit the lower back, relieve hemorrhoid, kills parasites, remove edema, and so forth. And the puffer fish eggs processed with ginger are said to be effective against tuberculosis and lung cancer, thus, it's validity must be investigated and further research should be followed.

• Journal of mucopolysaccharidosis and rare diseases
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• v.2 no.2
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• pp.43-45
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• 2016

Whole body energy balance is achieved through the coordinated regulation of energy intake and energy expenditure in various tissues including liver, muscle and adipose tissues. A positive energy imbalance by excessive energy intake or insufficient energy expenditure results in obesity and related metabolic diseases. Although there have been many obesity treatment trials aimed at the reduction of energy intake, these strategies have achieved only limited success because of their associated adverse effects. Serotonin is among those traditional pharmacological targets for anti-obesity treatment because central 5-HT functions as an anorexigenic neurotransmitter in the brain. Thus, there have been many trials aimed at increasing the activity of 5-HT in the central nervous system, and some of the developed methods are already used in the clinical setting as anti-obesity drugs. However, recent studies suggest the new functions of peripheral serotonin in energy homeostasis ranging from the endocrine regulation by gut-derived serotonin to the autocrine/paracrine regulation by adipocyte-derived serotonin. Pharmacological inhibition of 5-HT synthesis leads to inhibition of lipogenesis in epididymal white adipose tissue (WAT), induction of browning in inguinal WAT and activation of adaptive thermogenesis in brown adipose tissue (BAT). Fat specific Tph1 knock-out (Tph1 FKO) mice exhibit similar phenotypes as mice with pharmacological inhibition of 5-HT synthesis, suggesting the localized effects of 5-HT in adipose tissues. In addition, Htr3a KO mice exhibit increased energy expenditure in BAT and Htr2a KO mice exhibit the decreased lipid accumulation in WAT. These data suggest the clinical significance of the peripheral serotonergic system as a new therapeutic target for anti-obesity treatment.