• Title/Summary/Keyword: amino acid neurotransmitter

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Changes of Amino Acid Neurotransmitter Contents in Rat Brain by Toluene Inhalation (톨루엔 흡입이 뇌내 아미노산 신경전달물질 함량에 미치는 영향)

  • 이선희;신대섭;김부영
    • Biomolecules & Therapeutics
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    • v.3 no.1
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    • pp.91-96
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    • 1995
  • The effects of toluene inhalation on the contents of amino acid neurotransmitters in rat brain were investigated and blood toluene concentrations inducing changes of behavior and amino acid neurotransmitter contents in rat brain were observed. Male wistar rats were exposed to toluene vapor (single dose : 1700, 5000 and 10000 ppm for 2 hrs, repeated dose : 1700 and 5000 ppm for 2 hrs/day$\times$6 days). Toluene concentrations in blood and the inhalation chamber were assayed by GC with headspace sampler. HPLC method following PITC derivatization was used to measure the amino acid contents in brain tissues such as frontal cortex, caudate, hippocampus, cerebellum and brain stem. Glutamic acid and aspartic acid levels were increased by single inhalation of toluene (5000 ppm) in all the brain areas assayed in this experiment. In caudate and cerebellum, taurine levels were decreased by single inhalation of low dose toluene (1700 ppm), but increased by repeated administration. At high blood toluene concentration, GABA levels were increased in all the brain areas assayed in this experiment and the increasing extents of inhibitory amino acid contents measured in caudate and hippocampus were greater than those of excitatory amino acids. These results suggest that the changes of amino acid neurotransmitter contents in brain by exposure to toluene may modulate toluene-induced behaviors.

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The Effect of Carbon Monoxide Intoxication on the Changes in Contents of Amino Acid Neurotransmitter of Rat Brain (일산화탄소 중독이 뇌내 아미노산 신경전달물질 함량변화에 미치는 영향)

  • Jung, Min-Jung;Park, Son-Ja;Lee, Sun-Hee;Yun, Jae-Soon
    • YAKHAK HOEJI
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    • v.34 no.5
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    • pp.323-333
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    • 1990
  • To study influence of carbonmonoxide (CO) poisoning on the content of amino acid neurotransmitter in brain, male rat was exposed to CO 5000 ppm for 30 minutes (60-75% HbCO). Aspartic acid and glutamic acid level in the cerebral cortex and aspartic acid level in the striatum were significantly decreased. GABA level in the cerebral cortex was significantly increased after the 30 and 60 minutes of CO intoxication. Taurine level in both the cerebral cortex and the striatum was increased although nonsignificant. Consequently, the CO-induced hypoxia brain showed lower level of excitatory neurotransmitter, aspartic acid and glutamic acid and higher level of inhibitory neurotransmitter, GABA and taurine. These results suggest that the change in content of amino acid neurotransmitter in the rat brain may be concerned with several CO poisoning symptoms.

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Efect of Herbal Medicinal Preparations Containing Ginseng on Learning and Memory in Kainate-induced Seizures

  • Park, Jin-Kyu;Jin, Sung-Ha;Park, Kum-Hee;Ko, Ji-Hun;Ki yeul Nam;Yang, Deok-Chun;Park, Eun-Kyung
    • Proceedings of the Plant Resources Society of Korea Conference
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    • pp.84-95
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    • 2000
  • Panax ginseng and the herbal medicinal mixtures containing ginseng have been widely used as a traditional medicinal prescriptions. In order to develop more efficient and protective prescriptions on seizures and subsequent memory deterioration, we investigated the biochemical and ethopharmacological effects of ginsenosides and fractions from the natural medicinal plant products related to control convulsions. In this studies we show results improving spatial teaming and memory deficits induced by kainic acid, a potent neurotoxic and neuroexcitatory analogue of the amino acid neurotransmitter glutamate.

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Measurements of Extracellular Excitatory Amino Acid Neurotransmitter Levels in Corpus Striatum of Toluene Inhaled Rat by Microdialysis (톨루엔 흡입 흰쥐의 선조체에서 미세투석법을 이용한 세포외성 흥분성 아미노산 신경전달물질의 측정)

  • Baeck, Seung-Kyung;Kim, Hae-Kyu;Kim, Cheol-Min
    • YAKHAK HOEJI
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    • v.42 no.1
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    • pp.95-100
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    • 1998
  • Male Sprague-Dawley rats were exposed to the toluene at 3,000${\pm}$200ppm via inhalation for two hours (single inhalation group), three weeks by two hours per day, six days per wee k (repeated inhalation group). We examined the level of excitatory amino acids of the extracellular neurotransmitter within the corpus striatum of rats by using in vivo microdialysis. Aspartate (Asp) and glutamate (Glu) of excitatory amino acid neurotransmitters were generally decreased in the inhalation groups compared with the control group, and more significantly decreased in the repeated inhalation group than in the single inhalation group except that Asp was increased from 60 min after the beginning of the inhalation to 30 min after the termination.

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Alterations of Amino Acid Level in Depressed Rat Brain

  • Yang, Pei;Li, Xuechun;Ni, Jian;Tian, Jingchen;Jing, Fu;Qu, Changhai;Lin, Longfei;Zhang, Hui
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.5
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    • pp.371-376
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    • 2014
  • Amino-acid neurotransmitter system dysfunction plays a major role in the pathophysiology of depression. Several studies have demonstrated the potential of amino acids as a source of neuro-specific biomarkers could be used in future diagnosis of depression. Only partial amino acids such as glycine and asparagine were determined from certain parts of rats' brain included hippocampi and cerebral cortex in previous studies. However, according to systematic biology, amino acids in different area of brain are interacted and interrelated. Hence, the determination of 34 amino acids through entire rats' brain was conducted in this study in order to demonstrate more possibilities for biomarkers of depression by discovering other potential amino acids in more areas of rats' brain. As a result, 4 amino acids (L-aspartic acid, L-glutamine, taurine and ${\gamma}$-amino-n-butyric acid) among 34 were typically identified as potentially primary biomarkers of depression by data statistics. Meanwhile, an antidepressant called Fluoxetine was employed to verify other potential amino acids which were not identified by data statistics. Eventually, we found L-${\alpha}$-amino-adipic acid could also become a new potentially secondary biomarker of depression after drug validation. In conclusion, we suggested that L-aspartic acid, L-glutamine, taurine, ${\gamma}$-amino-n-butyric acid and L-${\alpha}$-amino-adipic acid might become potential biomarkers for future diagnosis of depression and development of antidepressant.

Apoptotic Process is Involved in the L-Glutamate-Induced PC12 Cell Death (L-Glutamate에 의한 PC12 세포의 고사성 사망)

  • Sung, Ki-Wug;Jung, Kyung-Heui;Kim, Seong-Yun;Kang, Jung-Hyae;Lee, Sang-Bok
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.6
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    • pp.699-705
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    • 1997
  • Although it is known that neuronal cell death during development occurs by apoptosis, the mechanisms underlying excitatory amino acid-induced neuronal cell death remain poorly understood. In this study we have examined the mechanism by which L-glutamate, an excitatory amino acid neurotransmitter, induces cell death in PC12 cell lines. To characterize cell death, we employed sandwich enzyme-linked immunosorbent assay(ELISA) method for cellular DNA fragmentation, DNA agarose gel electrophoresis and chromatin staining by acridine orange and ethidium bromide after treating the PC12 cells with L-glutamate. L-Glutamate caused dose-dependent cell death with a maximum at 24 hrs after the treatment. These cellular fragmentation was blocked by pretreatment of MK-801, a noncompetitive N-methyl-D-aspartic acid(NMDA) receptor antagonist, and nerve growth factor(NGF). Analysis of DNA integrity from L-glutamate-treated cells revealed cleavage of DNA into regular sized fragments, a biochemical hallmark of apoptosis. The PC12 cells that were induced to die by L-glutamate treatment exhibited classical chromatin condensation under the light microscopy after acridine orange and ethidium bromide staining. These results suggest that apoptosis is one of the key features that are involved in L-glutamate-induced excitotoxic cell death in PC12 cells, and these cell death are mediated by NMDA receptor and depend on NGF.

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The neuroprotective effect of Acori graminei rhizoma extract against cerebral ischemia in rats (석창포(石菖蒲)가 뇌허혈(腦虛血)을 유발(誘發)시킨 백서(白鼠)에서의 뇌신경보호효과(腦神經保護效果))

  • Keum, Hyeon-Su;Jeon, Yeon-Yi;Lee, Eun-Ju;Park, Chi-Sang;Park, Chang-Gook;Heo, Jin-Hwa;Yang, Chae-Ha;Cho, Jung-Sook;Kang, Seoung-Jun
    • The Journal of Internal Korean Medicine
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    • v.22 no.3
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    • pp.341-351
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    • 2001
  • Object: Acori graminei rhizoma(AGR) extract is clinically used to treat the cerebral ischemia in Korea. The present study was undertaken to study the neuroprotective effect of AGR extract in middle cerebral artery occlusion(MCAO) rats. Methods: Changes of extracellular levels of glutamate, aspartate, GABA, glycine, taurine, tyrosine, alanine in striatum were collected at 20 minutes interval by in vivo microdialysis and then analyzed by HPLC(high performance liquid chromatography) in rats subjected to permanent focal cerebral ischemia induced by 2 hours of MCAO. AGR extract was orally administrated before MCAO. Different animals were used for measurement of cerebral infarction volume induced by 24 hours of MCAO with TTC staining and image analysis. Result : The infarction volume was decreased and focal cerebral ischemia - induced increase of extracellular glutamate, aspartate, and tyrosine were inhibited after the treatment of AGR extract. On the other hand, the increase of glycine and alanine not but GABA and taurine were enhenced after the treatment of AGR extract. Conclusion: These results suggest that AGR extract can playa role in protecting against cerebral ischemia by regulating extracellular levels of excitatory and inhibitory amino acid neurotransmitters.

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Preliminary Phantom Experiments to Map Amino Acids and Neurotransmitters Using MRI

  • Oh, Jang-Hoon;Kim, Hyug-Gi;Woo, Dong-Cheol;Rhee, Sun Jung;Lee, Soo Yeol;Jahng, Geon-Ho
    • Progress in Medical Physics
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    • v.29 no.1
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    • pp.29-41
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    • 2018
  • The objective of this study was to evaluate the chemical exchange saturation transfer (CEST) effect of amino acids and neurotransmitters, which exist in the human brain, depending on the concentration, pH, and amplitude of the saturation radiofrequency field. Phantoms were developed with asparagine (Asn), ${\gamma}-aminobutyric$ acid (GABA), glutamate (Glu), glycine (Gly), and myoinositol (MI). Each chemical had three different concentrations of 10, 30, and 50 mM and three different pH values of 5.6, 6.2, and 7.4. Full Z-spectrum CEST images for each phantom were acquired with a continuous-wave radiofrequency (RF) saturation pulse with two different $B_1$ amplitudes of $2{\mu}T$ and $4{\mu}T$ using an animal 9.4T MRI system. A voxel-based CEST asymmetry was mapped to evaluate exchangeable protons based on amide (-NH), amine ($-NH_2$), and hydroxyl (-OH) groups for the five target molecules. For all target molecules, the CEST effect was increased with increasing concentration and B1 amplitude; however, the CEST effect with varying pH displayed a different trend depending on the characteristics of the molecule. On CEST asymmetric maps, Glu and MI were well visualized around 3.0 and 0.9 ppm, respectively, and were well separated macroscopically at a pH of 7.4. The exchange rates of Asn, Glu, BABA, and Gly usually decreased with increasing pH. The CEST effect was dependent on the concentration, acidity of the target molecules, and B1 amplitude of the saturation RF pulse. The CEST effect for Asn can be observed in a 9.4T MRI system. The results of this study are based on applying the CEST technique in patients with neurodegenerative diseases when proteins in the brain are increased with disease progression.