• 제목/요약/키워드: neurotransmitter

검색결과 368건 처리시간 0.035초

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

  • 정민정;박송자;이선희;윤재순
    • 약학회지
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    • 제34권5호
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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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Expression of neurotransmitter receptors in oral keratinocytes and their response to agonists

  • Choi, Eun Ji;Chang, Sung-Ho;Choi, Se-Young;Choi, Youngnim
    • International Journal of Oral Biology
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    • 제46권1호
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    • pp.39-44
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    • 2021
  • This study aimed to investigate whether neurotransmitter receptors in the nervous system were also expressed in oral keratinocytes. Expressions of various neurotransmitter receptor genes in immortalized mouse oral keratinocyte (IMOK) cells were examined by reverse transcriptase polymerase chain reaction. IMOK cells expressed calcitonin gene-related peptide (CGRP) receptor subunit genes Ramp1 and Ramp3 and glutamate receptor subunit genes Grina, Gria3, Grin1, Grin2a, and Grin2d. Moreover, IMOK cells expressed Adrb2 and Chrna5 that encode beta 2 adrenergic receptor and cholinergic receptor nicotinic alpha 5 for sympathetic and parasympathetic neurotransmitters, respectively. The expression of Bdkrb1 and Ptger4, which encode receptors for bradykinin and prostaglandin E2 involved in inflammatory responses, was also observed at low levels. Expressions of Ramp1 and Grina in the mouse gingival epithelium were also confirmed by immunohistochemistry. When the function of neurotransmitter receptors expressed on IMOK cells was tested by intracellular calcium response, CGRP, glutamate, and cholinergic receptors did not respond to their agonists, but the bradykinin receptor responded to bradykinin. Collectively, oral keratinocytes express several neurotransmitter receptors, suggesting the potential regulation of oral epithelial homeostasis by the nervous system.

망막 ON형 쌍극세포의 광응답에 따른 다중성분의 전달물질 방출에 관한 해석 (Analysis on Multi-Components of Neurotransmitter Release in Response to Light of Retinal ON-Type Bipolar Cells)

  • 정남채
    • 융합신호처리학회논문지
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    • 제14권4호
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    • pp.222-230
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    • 2013
  • 망막 쌍극세포는 광자극에 대하여 완만한 전위응답을 하며, 막전위에 의존하여 전달물질(glutamine 산)을 방출한다. 본 논문에서는 ON형 쌍극세포의 시냅스 앞단에서 전달물질 방출 기구에 관한 여러 가지의 생리학적 정보를 수식적 모델로 통합하였다. 전달물질 방출의 빠른 성분과 느린 성분의 공급원을 병렬로 배치한 본 모델은 전달물질 방출의 막전위 및 세포 내 $Ca^{2+}$ 농도 의존성을 충실하게 재현할 수가 있었다. 또한 전달물질의 빠른 방출 성분은 사다리꼴 모양의 막전위 의존성을 나타내는 데에 반하여, 느린 방출 성분은 종모양의 막전위 의존성을 나타내기 때문에 세포 내의 $Ca^{2+}$ 농도 상승을 $Ca^{2+}$ 완충제로 억제하여 느린 방출 성분이 감소되고, 전달 물질 방출의 막전위 의존성이 사다리꼴 모양의 특성이 되는 것을 확인하였다. 그리고 ON 형 쌍극세포의 광응답에서 일시적 성분과 지속적 성분에 의하여 발생하는 전달물질 방출을 시뮬레이션한 결과 광응답의 시작은 전달물질을 빠르게 방출하게 하였으며, 광응답의 일시적 성분과 초기의 지속적 성분은 전달물질을 느리게 방출하도록 하였다. 또한 광응답의 후기 지속적 성분은 저장 pool로부터 보충된 시냅스 소포에 의하여 지속적인 방출이 발생하기 때문이라는 것을 확인하였다.

Cholesterol, Statins, and Brain Function: A Hypothesis from a Molecular Perspective

  • Shin, Yeon-Kyun
    • Interdisciplinary Bio Central
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    • 제1권1호
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    • pp.2.1-2.3
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    • 2009
  • There is evidence that cholesterol in the brain plays an important role in the neurotransmitter release. A decrease of the cholesterol level severely hampers the activity of the membrane fusion machinery, thereby inhibiting the release. Meanwhile, the results from several clinical studies suggest that a low cholesterol level is linked to the dysfunction of some brain activities. Because the neurotransmitter release underlies the basic brain function, the combined results lead to a testable hypothesis that the cholesterol-lowering drugs may inhibit the neurotransmitter release at the synapse. Such inhibition of the release could result in impaired brain function for a limited group of people. A molecular basis for the hypothesis is discussed.

PC12 세포주에서 Translationally Controlled Tumor Protein에 의한 Mitogen-activated Protein Kinases 활성 조절 (Regulation of Mitogen-activated Protein Kinases by Translatoinally Controlled Tumor Protein in PC12 Cells)

  • 김미연;김미영
    • 약학회지
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    • 제54권5호
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    • pp.323-327
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    • 2010
  • Translationally controlled tumor protein (TCTP) activates basophils to release histamine and causes chronic inflammation. It was also reported that TCTP significantly reduced in brain of Alzheimer's Disease and Down Syndrome as compared to normal person, suggesting that TCTP might be involved in cognitive function. We wondered whether TCTP could act as a general inducer in neurotransmitters release in brain. We, therefore, investigated the role of TCTP in PC12 cell line which expressed neuronal properties. We found that TCTP could activate JNK, and the activity was inhibited by pretreatment of dicoumarol, a JNK inhibitor. However, TCTP could not activate ERK that has known to be involved in neurotransmitter release. These suggest TCTP did not participate in neurotransmitter release from PC12 cells, and TCTP might not be a general inducer in neurotransmitter release.

SSP 주파수 진폭변조가 Vasoactive Intestinal Peptide와 $\beta$-endorphin, cGMP에 미치는 영향 (Effects of frequency - amplitude electrical stimulation on sympathetic neurotransmitter and vasoactive intestinal peptide)

  • 최영덕;심규리;장문경
    • The Journal of Korean Physical Therapy
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    • 제14권4호
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    • pp.454-474
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    • 2002
  • Vasoactive intestinal peptide (VIP) is a very potent dilatator and a nonadrenergic, noncholinergic (NANC) neurotransmitter or neuromodulator in the peripheral and the central nervous systems. The mechanisms of action of VIP were examined in aortic circular and in uterine longitudinal smooth muscle strips of the rat. The effects of sympathetic neurotransmitter were investigated in gastric and aortic circular muscle strips of the mouse and the rat. The effects of silver spike point, SSP, low frequency electrical stimulations of VIP, sympathetic neurotransmitter and $\beta$-endorphin were examined in plasma, serum and 24h urine from the healthy volunteer. In gastric smooth muscle strips from the mouse, adrenergic neurotransmitter norepinephrine was inhibitory effected, followed by caused phasic and tonic contraction to the, muscrine receptor agonist carbachol and acetylcholine, respectively. In urine from the healthy volunteer, both norepinephrine and epinephrine were significantly decreased in continue type and low frequency (3 Hz) of SSP electrical stimulations. The contractile responses to S-HT in uterine longitudinal smooth muscle strips of the rats were completely decreased by a VIP 1 $\mu$M. The contractile responses to PGF2$\alpha$ were not decreased by a VIP. In plasma and serum from the healthy volunteer, both VIP and $\beta$-endorphin were significantly increased in continue type and low frequency (3 Hz) of SSP electrical stimulations. Therefore, this study demonstrate that VIP has the capacity to relax vascular or gastric smooth muscles in part by stimulating the generation of NO, and silver spike point low frequency electrical stimulation has the capacity both to decrease sympathetic neurotransmitters and to increase VIP, $\beta$-endorphin.

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PC12 세포에서 신경전달물질 방출을 저해하는 물질 S9940 물질의 탐색 (Screeing of S9940 as an Inhibitor of Neurotransmitter Release from PC12 Cells)

  • 이윤식;박기인
    • Toxicological Research
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    • 제14권3호
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    • pp.341-348
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    • 1998
  • We established an in vitro experimental system using the following procedure. We first introduced tritium-labelled norepinephrine ([3H]-NE)into PC12 cells. The [3H]-NE incorporated into PC12 cells were then stimulated by a high concentration (60 mM) of $K^+$ during 12 minutes. Then, we counted the amount of [3H]-NE release from PC12 cells with the scintillation counter. After screening fungal, Streptomyces or bacterial product using this experimental system, we obtained S9940 from Streptomyces spp. which inhibited [3H]-NE release from PC12 cells. S9940 also inhibits the release of ATP as a neurotransmitter of PC12 cells and rat cortical neurons. The inhibitory effect was seen even when the PC12 cells were treated with low $K^+$ buffer containing ionomycin $(1\muM)$ as an ionopore. This result suggests that the inhibitory action of S9940 on neurotransmitter release appeared after the influx of $Ca^{2+}$.

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

  • 이선희;신대섭;김부영
    • Biomolecules & Therapeutics
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    • 제3권1호
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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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PC12 세포에서 신경전달물질 방출을 저해하는 생리활성물질 FS11052의 탐색 (Screening of active substance FS11052 as an inhibitor of neurotransmitter release from PC12 cells)

  • 이윤식;이존화
    • 대한수의학회지
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    • 제46권2호
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    • pp.87-96
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    • 2006
  • We established an in vitro experimental system using the following procedure. We first introduced tritium-labeled norepinephrine ([$^3$H]-NE) into PC12 cells, The [$^3$H]-NE incorporated into PC12 cells were then stimulated by a high concentration (60 mM) of $K^+$ buffer during 12 minutes. Then, we collected $100{\mu}l$ supernatant and counted the amount of [$^3$H]-NE release from PC12 cells with a scintillation counter. After screening fungal, Streptomyces spp. or bacterial product using this experimental sytem, we obtained FS11052 from Streptomyces spp. which inhibited [$^3$H]-NE release from PC12 cells. FS11052 also inhibits the release of ATP as a neurotransmitter of PC12 cells and rat cortical neurons, The inhibitory effect was seen even when the PC12 cells were treated with low $K^-$ buffer containing ionomycin ($1{\mu}M$) as an ionopore. This result suggests that the inhibitory action of FS11052 on neurotransmitter release appeared after the influx of $Ca^{2+}$.

Sodium/chloride-Dependent Transporters: Elucidation of Their Properties Using the Dopamine Transporter

  • Caron, Marc G.
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 1994년도 춘계학술대회 and 제3회 신약개발 연구발표회
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    • pp.88-93
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    • 1994
  • The mechanisms controlling the intensity and duration of synaptic transmission are numerous. Once an action potential reaches a nerve terminal, the stored neurotransmitters are released in a quantum fashion into the synaptic cleft. At that point neurotransmitters can act on post-synaptic receptors to elicit an action on the post-synaptic cell or net at so-called auto-receptors that are located on the presynaptic side and which often regulate the further release of the neutotransmitter. Whereas the action of the neurotransmitter receptors is regulated by desensitization phenomenon, the major mechanism by which the intensity and duration of neurotransmitter action is presumably regulated by either its degradation or its removal from the synaptic cleft. In the central nervous system, specialized proteins located in fe plasma membrane of presynaptic terminals function to rapidly remove neurotransmitters from the synaptic cleft in a sodium chloride-dependent fashion. These proteins have been referred to as uptake sites or neurotransmitter transporters. Once taken up by the plasma membrane transporters, neurotransmitters are repackaged into secretory vesicles by distinct transporters which depend on a proton gradient.

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