• Journal of the Korean Society of Tobacco Science
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• v.27 no.2
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• pp.212-218
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• 2005

Cigarette smoking has been known to have a few beneficial effects on some neuronal diseases such as Alzheimer's disease(AD), Parkinson's disease(PD) and prion disease by scrapie agent shows many similar properties with AD. In this respect, we investigated what biological effects are exerted by cigarette smoke exposure(CSE) in the brain of mouse infected by 87V scrapie. The scrapie agent was inoculated through stereotaxic microinjection of the homogenates of the scrapie agent infected brain into the intracerebral system in the 1M mice. The inoculation into mice typically exhibits neurochemical, physiological and histopathological characteristics of prion disease: loss of neurotransmitters and induction of astrocytosis and vacuolation in brain as well as reduction of spatial movement and loss of body weight. CSE led to alleviated the loss of body weight and also improved spatial movement of the infected mice. Most interestingly, CSE attenuated astrocytosis and vacuolation caused by scrapie infection in the brain. In addition, decreased levels of dopamine in striatal and hypothalamic regions as well as serotonin level in hippocampus caused by scrapie infection were also attenuated by exposure to cigarette smoke. These findings suggest that cigarette smoke, by its inhibition of astrocytosis and vacuolation followed by its restoration of levels of some neurotransmitters, may partly contribute to suppression in the progress of neurodegeneration caused by scrapie infection.

• Biomolecules & Therapeutics
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• v.4 no.1
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• pp.36-45
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• 1996

The antihistaminic action of eighteen herbal medicines was investigated by the radioligand binding and functional assays. The hexane fractions of Trichosanthis radix, Mori cortex radicis and Evodiae fructus dosedependently inhibited [$^3$H] mepyramine binding to H$_1$, receptor in guinea-pig brain homogenates and histamine-induced contraction of isolated guinea-pig ileum. Antihistaminic action of the hexane and ethyl acetate fractions of Mori cortex radicis and the hexane fraction of Evodiae fructus was more potent than their antimuscarinic action evaluated from the inhibition of [$^3$H]QNB binding and carbachol response. The ethyl acetate and chloroform fractions from Scutellariae radix also inhibited histamine-induced contraction, but antihistaminic potencies of these fractions were almost identical with their antimuscarinic potencies. The hexane fractions of Mori cortex radicis and Evodiae fructus inhibited selectively the increase of histamine-induced cutaneous vascular Permeability in the rat dorsal skins. However, the ethyl acetate fraction from Scutellariae radix inhibited eqipotently the effects of histamine and serotonin on the vascular permeability. These results demonstrate that the hexane and ethyl acetate fractions of Mori cortex radicis and the hexane fraction of Evodiae fructus have the selective histamine H$_1$receptor blocking activity.

• 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.

• Archives of Pharmacal Research
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• v.11 no.3
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• pp.230-239
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• 1988

Thirty kinds of medicinal plants were screened to examine inhibitory activities on rat brain monoamine oxidase A, using serotonin as a substrate. As active principles, various kinds of stilbenes were isolated from Veratri Rhizoma, Reynoutriae Radix and Rhei undulati Rhizoma, and several kinds of flavonoids from Sophorae Flos, Chrisanthemi Flos and Glycine max. Among the compounds isolated, resveratrol(I) strongly inhibited MAO-A competitively, and its $IC_{50}$ and Ki values were 2 ${\mu}M$ and 2.5 ${\mu}M$, respectively. Inhibitory potencies towards MAO-A of some stilbenes and flavonoids were also compared.

• Korean Journal of Biological Psychiatry
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• v.22 no.4
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• pp.149-154
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• 2015

Mood disorder is a common psychiatric illness with a high lifetime prevalence in the general population. Many prescribed antidepressants modulate monoamine neurotransmitters including serotonin, norepinephrine and dopamine. There has been greater focus on the major excitatory neurotransmitter in the human brain, glutamate, in the pathophysiology and treatment of major depressive disorder (MDD). Recently, ketamine, an N-methyl-D-aspartate receptor antagonist, has received attention and has been investigated for clinical trials and neurobiological studies. In this article, we will review the clinical evidence for glutamatergic dysfunction in MDD, the progress with ketamine as a rapidly acting antidepressant, and other N-methyl-D-aspartate receptor antagonist for treatment-resistant depression.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.188-188
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• 1998

Extracts of 24 edible vegetables were tested concerning their action on in vitro inhibition on dopamine ${\beta}$-hydroxylase (DBH) and monoamine oxidase (MAO). All vegetables were purchased in Korean market and their common names were kept. Radish sprouts, ‘kkoch-na-mul’, ‘chong-gyong-chae’, ragwort, applemint showed strong DBH inhibitory effect when tyramine and crude bovine adrenal DBH were used as substrate and enzyme, respectively. ‘Cham-chwi’(Aster scaber), kale, ‘cham-na-mul’(Pimpinella brachycarpa), leek were found to have MAO-A inhibitory effect with serotonin and crude rat brain MAO-A. Lettuce, ‘chong-gyong-chae’, radish sprouts, beet leaves were found to have MAO-B inhibitory effect with benzyl amine and crude rat liver MAO-B.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.115-120
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• 2018

Chronic cerebral hypoperfusion (CCH), which is associated with onset of vascular dementia, causes cognitive impairment and neuropathological alterations in the brain. In the present study, we examined the neuroprotective effect of duloxetine (DXT), a potent and balanced serotonin/norepinephrine reuptake inhibitor, on CCH-induced neuronal damage in the hippocampal CA1 region using a rat model of permanent bilateral common carotid arteries occlusion. We found that treatment with 20 mg/kg DXT could attenuate the neuronal damage, the reduction of phosphorylations of mTOR and p70S6K as well as the elevations of $TNF-{\alpha}$ and $IL-1{\beta}$ levels in the hippocampal CA1 region at 28 days following CCH. These results indicate that DXT displays the neuroprotective effect against CCH-induced hippocampal neuronal death, and that neuroprotective effect of DXT may be closely related with the attenuations of CCH-induced decrease of mTOR/p70S6K signaling pathway as well as CCH-induced neuroinflammatory process.

• Journal of Nutrition and Health
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• v.22 no.4
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• pp.247-256
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• 1989

Growing male rats were allowed to have food from two dishes containing isocaloric, isoprotein 15% or 70% carbohydrate diet for 4, 8, 12 or 24 hours a day at the beginning of the dark period. Four hours of feeding were not enough to grow though the first 4 hours of intake were significantly higher than other periods. 4-hour and 8-hour feeding groups consumed significantly less carbohydrate calorie than 12-hour and ad libitum feeding groups, which hence, showed lower ratio of carbohydrate to protein in the total food consumed. The fasting brain tryptophan and serotonin levels among groups were not significantly different. It appears therefore that the manipulation of the feeding period could be valuable in suppression of carbohydrate appetitie, especially carbohydrate carving.

• Archives of Pharmacal Research
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• v.10 no.1
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• pp.50-59
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• 1987

(E)-2-Phenylcyclopropylamine ((E)-TCP), (Z)-2-Phenylacyclopropylamine ((Z)-TCP), (E)-1-methyl-2-phenylcyclopropylamine ((E)-MTCP), and (Z)-1-methyl-2-phenylcyclopropylamine ((Z)-MTCP) were synthesized and used to determine to what extent 1-methylsubstitution and stereochemistry of 2-phenycyclopropylamines affect inhibition of monoamine oxidase (MAO). Inhibition of rat brain mitochondrial MAO-A and B by the compounds were measured using serotonin and benzylamine as the substrate, respectively and $IC_{50}$ values obtianed with 95% confidence limits by the method of computation. For the inhibition of MAO-A, (E)-MTPC ($IC_{50}$ = 6.2 * $10^{-8}$M) was found to be 37 times more potent than (Z)-MTCP ($IC_{50}$ = 7.8 * $10^{-8}$M), was 7 times more potent than (Z)-MTCP($IC_{50}$= 4.7 * $10^{-7}$M) and (E)-TCP($IC_{50}$ =7.8 * $10^{-8}$M),0.6 times as potent as (Z)- TCP ($IC_{50}$ = 4.4 * $10^{-8}$M). The results suggested that while without 1-methyl group, potency of a (Z)-isomer was comparable to that of (E)-isomer, the methyl group in its (Z)-position was very unfavorable to the inhibition of MAO and that in its (E)-position, the methyl group contributed positively to the potency as found by the fact that (E)-MTCP was 1-5 times more potent than (E)-TCP. In view of the selective inhibition of MAO-A- or B over MAO-A and 1-methyl substitution as well as the stereochemical factors did not significantly influence the selectivity.

• Molecules and Cells
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• v.40 no.7
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• pp.495-502
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• 2017

The $5-HT_6R$ has been considered as an attractive therapeutic target in the brain due to its exclusive expression in the brain. However, the mechanistic linkage between $5-HT_6Rs$ and brain functions remains poorly understood. Here, we examined the effects of $5-HT_6R$-mediated cell morphological changes using immunocytochemistry, Western blot, and live-cell imaging assays. Our results showed that the activation of $5-HT_6Rs$ caused morphological changes and increased cell surface area in HEK293 cells expressing $5-HT_6Rs$. Treatment with 5-HT specifically increased RhoA-GTP activity without affecting other Rho family proteins, such as Rac1 and Cdc42. Furthermore, live-cell imaging in hippocampal neurons revealed that activation of $5-HT_6Rs$ using a selective agonist, ST1936, increased the density and size of dendritic protrusions along with the activation of RhoA-GTP activity and that both effects were blocked by pretreatment with a selective $5-HT_6R$ antagonist, SB258585. Taken together, our results show that $5-HT_6R$ plays an important role in the regulation of cell morphology via a RhoA-dependent pathway in mammalian cell lines and primary neurons.