• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.783-796
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• 1997

The relaxation induced by stimulation of the inhibitory non-adrenergic, non-cholinergic (iNANC) nerve is mediated by the release of iNANC neurotransmitters such as nitric oxide (NO), vasoactive intestinal peptide (VIP) and adenosine triphosphate (ATP). The mechanisms of NO, VIP or ATP-induced relaxation have been partly determined in previous studies, but the detailed mechanism remains unknown. We tried to identify the nature of iNANC neurotransmitters in the smooth muscle of guinea pig ileum and to determine the mechanism of the inhibitory effect of nitric oxide. We measured the effect of NO-donors VIP and ATP on the intracellular $Ca^{2+}$ concentration$([Ca^{2+}]_i)$, by means of a fluorescence dye(fura 2) and tension simultaneously in the isolated guinea pig ileal smooth muscle. Following are the results obtained. 1. Sodium nitroprusside $(SNP:10^{-5}\;M)$ or S -nitro-N-acetyl-penicillamine $(SNP:10^{-5}\;M)$ decreased resting $[Ca^{2+}]_i$ I and tension of muscle. SNP or SNAP also inhibited rhythmic oscillation of $[Ca^{2+}]_i$ and tension. In 40mM $K^+$ solution or carbachol ($(CCh:10^{-6}\;M)$-induced precontracted muscle, SNP decreased muscle tension. VIP did not change $[Ca^{2+}]_i$ and tension in the resting or precontracted muscle, but ATP increased resting $[Ca^{2+}]_i$ and tension in the resting muscle. 2. 1H-[1,2,4]oxadiazol(4,3-a)quinoxalin-1-one $(ODQ:1\;{\mu}M)$, a specific inhibitor of soluble guanylate cyclase, limited the inhibitory effect of SNP 3. Glibenclamide $(10\;{\mu}M)$, a blocker of $K_{ATP}$ channel, and 4-aminopyridine (4-AP:5 mM), a blocker of delayed rectifier K channel, apamin $(0.1\;{\mu}M)$, a blocker of small conductance $K_{Ca}$ channel had no effect on the inhibitory effect of SNP. Iberiotoxin $(0.1\;{\mu}M)$, a blocker of large conductance $K_{Ca}$ channel, significantly increased the resting $[Ca^{2+}]_i$, and tension, and limited the inhibitory effect of SNP. 4. Nifedipine $(1\;{\mu}M)$ or elimination of external $Ca^{2+}$ decreased not only resting $[Ca^{2+}]_i$ and tension but also oscillation of $[Ca^{2+}]_i$ and tension. Ryanodine $(5\;{\mu}M)$ and cyclopiazonic acid $(10\;{\mu}M)$ decreased oscillation of $[Ca^{2+}]_i$ and tension. 5. SNP decreased $Ca^{2+}$ sensitivity of contractile protein. In conclusion, these results suggest that 1) NO is an inhibitory neurotransmitter in the guinea pig ileum, 2) the inhibitory effect of SNP on the $[Ca^{2+}]_i$ and tension of the muscle is due to a decrease in $[Ca^{2+}]_i$ by activation of the large conductance $K_{Ca}$ channel and a decrease in the sensitivity of contractile elements to $Ca^{2+}$ through activation of G-kinase.

• Korean Journal of Veterinary Research
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• v.34 no.3
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• pp.493-500
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• 1994

The purpose of this study was to investigate the effects of neurotransmitters and the source of $Ca^{2+}$ in the effects of neurotransmitters on the motility of pig oviductal isthmic smooth muscle. The motility of the isolated smooth muscle was recorded by using physiological recording system. The results were summarized as follows; Acetylcholine, norepinephrine, histamine and prostaglandin $F_{2{\alpha}}(PGF_{2{\alpha}})$ caused the contraction and the contractile responses were increased in a dose-dependent manner from the concentration of $10^{-7}$ to $10^{-4}M$. The maximum contractility of acetylcholine, norepinephrine, histamine and $PGF_{2{\alpha}}$ was 65.99, 28.66, 83.99 and 47.33% of 100 mM K contraction, respectively. The contractile response induced by acetylcholine$(10^{-6}M)$ was completely blocked by the pretreatment with cholinergic receptor blocker, atropine$(10^{-6}M)$, the contractile response induced by norepinephrine$(10^{-5}M)$ was blocked by the pretreatment with ${\alpha}$-adrenergic receptor blocker, phentolamine$(10^{-6}M)$ but was not blocked and rather increased by the pretreatment with ${\beta}$-adrenergic receptor blocker. propranolol$(10^{-6}M)$, the contractile response induced by histamine$(10^{-6}M)$ was completely blocked by the pretreatment with $H_1$-histaminergic receptor blocker, pyrilamine$(10^{-6}M)$ but was increased by the pretreatment with $H_2$-histaminergic receptor blocker, cimetidine$(10^{-6}M)$. The contractile response induced by acetylcholine$(10^{-6}M)$, norepinephrine$(10^{-5}M)$ and histamine$(10^{-6}M)$ was weakly contracted response in $Ca^{2+}$-free medium, but the contractile response induced by $PGF_{2{\alpha}}(10^{-6}M)$ was disappeared. The contractile response induced by acetylcholine$(10^{-6}M)$, norepinephrine$(10^{-5}M)$ and histamine$(10^{-6}M)$ was powerfully depressed by the pretreatment with $Ca^{2+}$-channel blocker, verapamil$(10^{-5}M)$ but the contractile response induced by $PGF_{2{\alpha}}(10^{-6}M)$ was completely inhibited.

• Journal of the Korea Convergence Society
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• v.8 no.11
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• pp.461-476
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• 2017

The purpose of this study was to investigate the existing theories related to overtraining syndrome and to examine the mechanism of overtraining syndrome from the viewpoint of brain science by examining domestic and foreign literature related to the relationship between overtraining syndrome and brain neurotransmitter. The aim of this paper is to provide basic data that can improve the understanding of the mechanism of overtraining syndrome and the role of neurotransmitters and neuromodulators. The results of this study and a number of hypotheses about the overtraining syndrome were proposed, each with strengths and weaknesses. Similar symptoms that occur when the concentration of serotonin in the neurotransmitter increases are related to signs and symptoms of overtraining syndrome. However, it has not been validated to date because it can not distinguish the mechanism of the mediator between the central nervous system and the peripheral nerves. This study suggests that the mechanism of overtraining syndrome will provide important basic information to understand the complex causes of overtraining syndrome through the interaction of existing theory and brain neurotransmitter. Although there has been a lack of studies on the mechanism of overtraining syndrome and brain neurotransmitters so far, we hope that this study will provide an opportunity for more and more people to broaden their understanding of overtraining syndromes.

• Journal of Korean Ophthalmic Optics Society
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• v.20 no.3
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• pp.391-396
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• 2015

Purpose: The objective of this study was to investigate the visual system of the greater horseshoe bat (Rhinolophus ferrumequinum) by location analysis of some major neurotransmitters glutamate, ${\gamma}$-aminobutyric acid (GABA), acetylcholine, and their receptors, and $m{\ddot{u}}ller$ glial cells in retina. Methods: Standard immunocytochemical techniques were used after vibratome section of retinal tissues of adult greater horseshoe bat for this study. Immnoreactions in immunofluorescence images were analyzed using confocal microscope. Results: Anti-glutamate-immunoreactive neurons were mainly localized in the ganglion cell layer (GCL). The majority of anti-GABA-immunoreactive cells distributed in the inner nuclear layer (INL), and GABAA receptors were localized in the inner plexiform layer (IPL). Anti-choline acetyltransferase-immuoreactive cholinergic neurons were mainly located in the INL and GCL, and most of nicotinic acetylcholine receptors were localized in the IPL. The $m{\ddot{u}}ller$ cells in the retina of the greater horseshoe bat stretched theirs range from the GCL to outer nuclear layer (ONL). Conclusions: This study revealed that the retinas of the greater horseshoe bats contain the same major neurotransmitters and receptors, and glial cell in visually functional mammalian retinas. The present results may suggest that the greater horseshoe bats have the functional retinas for visual analysis through the organized retinal neural circuits.

• 한국체육학회지인문사회과학편
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• v.58 no.4
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• pp.447-459
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• 2019

This study was conducted to investigate the differences between emotional responses and neurotransmitters in moderate-intensity continuous exercise (MICE) and high-intensity interval exercise (HIIE) in 30 low-active women. Both groups performed a designed acute treadmill exercise and repeated the same exercise three times at intervals of one week. MICE performed a 25-minute continuous exercise at 90% VT(ventilation threshold) after a 5-minute warm-up session at 50% VT and then cooled down for 5 minutes at 50% VT level. The HIIE was repeated 6 times for 2 minutes at 115% VT level, and the intermediate active recovery was repeated 4 times for 2 minutes at 85% VT level. The results of the statistical analysis are as follows. MICE was showed positive effect for feeling scale and PACES after exercise in the first experiment, but negative effect in the third experiment. Conversely, HIIE was showed negative effect for feeling scale and PACES after exercise in the first experiment, but positive effect in the third experiment. Neurotransmitters were significantly increased in all three groups after 10 minutes of exercise compared to before exercise. In summary, HIIE exercise may be a strategy to increase exercise compliance for low-active women.

• Korean Journal of Biological Psychiatry
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• v.20 no.2
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• pp.29-30
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• 2013

First-line therapy of depression is a pharmacological treatment. Many prescribed antidepressants modulate monoamine neurotransmitters including serotonin, norepinephrine and dopamine. Recently, Ketamine, an N-methyl-D-aspartate receptor antagonist, has received attention and has been investigated for clinical trials and neurobiological studies. Here, I introduce ketamine as a rapid-acting antidepressant.

• Journal of Photoscience
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• v.10 no.1
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• pp.37-48
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• 2003

A review of the background and development of the p-hydroxyphenacyl group (pHP) as a photoprotecting group for biological substrates is chronicled. The pHP group has promise as an efficient, rapid phototrigger for the study of very fast biological processes. Applications include the release of neurotransmittors and second messengers, enzyme switches and nucleotides.

• Anxiety and mood
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• v.2 no.1
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• pp.3-8
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• 2006

Anxiety has been suggested to be related to many neurotransmitters in brain, such as norepinephrine, serotonin, dopamine, cholecystokinin, and gamma-amino butyric acid. There are many studies to examine the relationship between anxiety and norepinephrine, and norepinephrine seems to be clearly related to the development of anxiety. We suggest that future studies to explore the pathophysiology of anxiety should be necessary, which include studies on antianxiety drugs, genetic studies, animal model studies, and brain imaging studies.

• Proceedings of the PSK Conference
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• 2000.04a
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• pp.106.2-107
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• 2000

• Clinical and Experimental Pediatrics
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• v.51 no.12
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• pp.1290-1294
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• 2008

Seizures are a frequent symptom in metabolic disorders, although metabolic disorders are rarely found to be the cause of epilepsy. A precise diagnosis might not only influence treatment, but it might also call for counseling of the family, even if there are no direct therapeutic consequences. We review the main characteristics of epilepsy in metabolic disorders with regard to energy metabolism, toxic effects, neurotransmitters, and vitamins.