• Title, Summary, Keyword: Neurotransmitter release

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

  • Jung, Nam-Chae
    • Journal of the Institute of Convergence Signal Processing
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    • v.14 no.4
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    • pp.222-230
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    • 2013
  • Retinal bipolar cells according to the light stimulus respond to potential slowly, emit neurotransmitter release(glutamine acid) to depend on membrane potential. In this paper, the several physiological information on neurotransmitter release mechanism in the presynaptic terminal of the ON-type bipolar cells are incorporated into the formula model. The source of fast components and slow components of neurotransmitter release was arranged in parallel, this model was able to reproduce the membrane potential and intracellular $Ca^{2+}$ concentration dependence of neurotransmitter release faithfully. In addition, because the fast releasable components of neurotransmitter was represented by the membrane potential dependence of trapezoid type, whereas the slow releasable components was represented by the membrane potential dependence of a bell type, $Ca^{2+}$ concentration rise in intracellular is suppressed by $Ca^{2+}$ buffer to reduce slow releasable components, it was confirmed that the membrane potential dependence of neurotransmitter release was characteristics of a trapezoid type. And, in the light response of ON type bipolar cell, the result of the simulation of the neurotransmitter release caused by the components of transient and persistent was that the start of light response occurred the fast release of neurotransmitter, it was confirmed that the transient component and persistent component of the light response occurred the slow release. It was confirmed that the later of persistent component of the light response occurred due to the continuous release by synaptic vesicle supplemented from the storage pool.

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

  • Shin, Yeon-Kyun
    • Interdisciplinary Bio Central
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    • v.1 no.1
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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.

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

  • Kim, Mi-Yeon;Kim, Mi-Young
    • YAKHAK HOEJI
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    • v.54 no.5
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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.

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

  • Lee, Yun-Sik;Park, Kie-In
    • Toxicological Research
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    • v.14 no.3
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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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Screening of active substance FS11052 as an inhibitor of neurotransmitter release from PC12 cells (PC12 세포에서 신경전달물질 방출을 저해하는 생리활성물질 FS11052의 탐색)

  • Lee, Yun-Sik;Lee, John Hwa
    • Korean Journal of Veterinary Research
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    • v.46 no.2
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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 $Ca^{2+}$.

Correlation between mEPSC Amplitude and Rise Time upon the Blockade of AMPA Receptor Desensitization at Hippocampal Synapses

  • Jung, Su-Hyun;Choi, Suk-Woo
    • The Korean Journal of Physiology and Pharmacology
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    • v.6 no.2
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    • pp.81-85
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    • 2002
  • Conventional views of synaptic transmission generally overlook the possibility of 'postfusional-control' the regulation of the speed or completeness of transmitter release upon vesicular fusion. However, such regulation often occurs in non-neuronal cells where the dynamics of fusion-pore opening is critical for the speed of transmitter release. In case of synapses, the slower the transmitter release, the smaller the size and rate-of-rise of postsynaptic responses would be expected if postsynaptic neurotransmitter receptors were not saturated. This prediction was tested at hippocampal synapses where postsynaptic AMPA-type glutamate receptors (AMPAR) were not generally saturated. Here, we found that the small miniature excitatory postsynaptic currents (mEPSCs) showed significantly slower rise times than the large mEPSCs when the sucrose-induced mEPSCs recorded in cyclothiazide (CTZ), a blocker for AMPAR desensitization, were sorted by size. The slow rise time of the small mEPSCs might result from slow release through a non-expanding fusion pore, consistent with postfusional control of neurotransmitter release at central synapses.

Rim1α and Neurexin3 Regulate Synaptosomal Dopamine Release (Rim1α와 neurexin3의 시냅토좀 도파민 분비 조절)

  • Lee, Sang-Kyeong;Shim, Joo-Cheol;Kim, Young-Hoon;Kong, Bo-Geum;Seog, Dae-Hyun
    • Journal of Life Science
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    • v.19 no.9
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    • pp.1232-1238
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    • 2009
  • Neurotransmitter release is regulated by various proteins of the active zone in the presynaptic nerve terminals. Dopamine (DA) is an essential neurotransmitter associated with the pathophysiology of diverse behavioral and mental illness such as schizophrenia and drug addiction. We measured synaptosomal DA release of knockout (KO) mice which lacked major genes related to neurotransmitter release. Synaptosomal DA uptake and release were performed and measured using [$^3H$]-DA and superfusion experiments. 3 of the 17 KO mice exhibited altered DA release compared to their littermate controls. In $Rim1{\alpha}$ KO, [$^3H$]-DA release evoked by membrane depolarization significantly decreased. Both basal (physiological buffer-evoked) and membrane depolarization-evoked DA release significantly decreased in dopaminergic conditional KO of $Rim1{\alpha}{\beta}$. Dopaminergic conditional KO of neurexin3 demonstrated a significant increase of membrane depolarization-evoked DA release. These data explain the similarities and distinctions between DA and other classical neurotransmitters such as glutamate and GABA ($\gamma$-aminobutyric acid) release. In conclusion, $Rim1{\alpha}$ and neurexin3 may be important regulators of presynaptic DA release and related to disorders of the nervous system.

Effect about Neurite Extension of S9940, and Inhibitor of Exocytosis in PC12 Cells (PC12 세포 신경전달물질 방출 저해제 S9940이 신경세포 돌기신장에 미치는 영향)

  • Lee, Yun-Sik;Park, Kie-In
    • Toxicological Research
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    • v.14 no.3
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    • pp.349-356
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    • 1998
  • We identified S9940, a novel microbial metabolite from Streptomyces spp., to inhibit the release of neurotransmitter from PC12 cells. S9940 is an inhibitor of trifiated norepinephrine ([$^{3}H$]-NE) release in high $K^+$ buffer solution containing ionomycin, indicating that S9940 inhibits neurotransmitter release after the influx of $Ca^{2+}$ ions. We also examined the effect of S9940 on $\beta-glucuronidase$ release from guinea pig neurophils and the effect on the neurite extension of PC12 cells and rat hippocampal neurons. As a result, S9940 inhibited $\beta-glucuronidase$ release: when treated with $5{\mu}g/ml$ of S9940, which prevented [$^{3}H$]-NE release, the inhibition of neurite extension for both PC12 cells and rat hippocampal neurons was observed.

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Effects of Forskolin on Endogenous Dopamine and Acetylcholine Release in Rat Neostriatal Slices

  • Kim, Hwa-Jung
    • Archives of Pharmacal Research
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    • v.19 no.6
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    • pp.520-528
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    • 1996
  • The involvement of the cyclic AMP (cAMP) effector system in the release of endogenous dopamine and acetylcholine from the rat neostriatum was assessed. Forskolin, an activator of adenylate cyclase, was used to enhance cAMP production, and the consequence of this enhancement on the spontaneous and potassium stimulated release of dopamine and acetylcholine was evaluated. Neostriatal slices were prepared from Fischer 344 rats and after a preincubation period the release of each endogenous neurotransmitter was measured from the same slice preparation. To measure acetylcholine release the slice acetylcholinesterase (AChE) activity was inhibited with physostigmine, but the release from slices with intact AChE activity was also determined (choline, instead of acetylcholine was detected in the medium). Under both conditions forskolin induced a significant dose-dependent increase in the potassium-evoked release of dopamine. In the same tissue preparations the release of neither acetylcholine (AChE inhibited) nor choline (AChE intact) was affected by forskolin. The results indicate that the CAMP second messenger system might be involved in neuronal mechanisms that enhance neostriatal dopamine release, but stimulation of this second messenger by forskolin does not further enhance neostriatal acetylcholine release.

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Involvement of the cAMP Effector System in Dopamine and Acetylcholine Release from Rat Neostriatal Slices

  • Kim, Hwa-Jung;Molly H. Weiller
    • Proceedings of the Korean Society of Applied Pharmacology
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    • pp.179-179
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    • 1996
  • The involvement of the cyclic AMP (cAMP) effector system in the release of endogenous dopamine and acetylcholine from the rat neostriatum was assessed. Forskolin, an activator of adenylate cyclase, was used to enhance CAMP production, and the consequence of this enhancement on the spontaneous and potassium stimulated release of dopamine and acetylcholine was evaluated. Neostriatal slices were prepared from Fischer 344 rats and after a preincubation period the release of each endogenous neurotransmitter was measured from the same slice preparation. To measure acetylcholine release the slice acetylcholinesterase (AChE) activity was inhibited with physostigmine, but the release from slices with intact AChE activity was also determined (choline, instead of acetylcholine was detected in the medium). Under both conditions forskolin induced a significant dose-dependent increase in the potassium-evoked release of dopamine. In the same tissue preparations the release of neither acetylcholine (AChE inhibited) nor choline (AChE intact) was affected by forskolin. The results indicate that the cAMP second messenger system is involved ill neuronal mechanisms that enhance neuronal dopamine release, but stimulation of this second messenger by forskolin does not further enhance neostriatal acetylcholine release.

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