• Title/Summary/Keyword: Agonist

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Effects of Mutagenesis of Highly Conserved Tyrosine Residues on the Function of m1 Muscarinic Receptor

  • Lee, Seok-Yong;Cho, Tai-Soon
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1996.04a
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    • pp.209-209
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    • 1996
  • Muscarinic acetylcholine receptors contain two highly conserved tyrosine residues which are located within or at the extracellular border of the second transmembrane domain. These tyrosine residues are located at positions 82 and 85 of the sequence of the ml subtype of muscarinic receptors. In this wok, we studied the involvement of these two residues in ligand binding to and agonist-induced activation this receptor subtype. our data suggest an important role for these two tyrosines in these processes, with a more prominent role for the tyrosine residue located at position 82 than that located at position 85. Evidence is also provided that while the aromatic moiety of these tyrosine residues is important for antagonist binding, both this moiety and the tyrosine phenolic hydroxyl group are involved in agonist binding and receptor activation.

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INFLUENCE OF GLUCOCORTICOIDS ON NICOTINIC AND MUSCARINIC STIMULATION-INDUCED CATECHOL-AMINE SECRETION FROM THE RAT ADRENAL GLAND

  • Lim, Dong-Yoon;Lee, Jae-Joon;Park, Cheol-Hee;Ko, Suk-Tai
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1996.04a
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    • pp.242-242
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    • 1996
  • The influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K$\^$+/ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100 uM) into an adrenal vein for 20min produced relatively a dose-dependent inhibition in CA secretion evoked by ACh (5.32mM), excess K$\^$+/ (56mM), DMPP (a selective nicotinic receptor agonist, 100uM for 2min), McN-A-343 (a muscarinic receptor agonist, 100uM for 4min), Bay-K-8644 (a calcium channel activator, 10 uM for 4min) and cyclopiazonic acid (a releaser of intracellular Ca$\^$2+/, 10uM for 4min).

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Physiological Review of Weakness in Patients with Hemiparesis (편부전마비 환자에서의 근육약화에 대한 생리학적 고찰)

  • Kim, Jong-Man;Kim, Tack-Hoon
    • Physical Therapy Korea
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    • v.3 no.2
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    • pp.84-94
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    • 1996
  • This paper reviews physiological changes in the nervous system of patients with hemiparesis that may contribute to muscle weakness. The discussion includes the important role that alterations in the physiology of motor units, notably changes in firing rates and muscle fiber atrophy, play in the manifestation of muscle weakeness. This role is compared with the lesser role that spasticity of the antagonist muscle group appears to play in determining the weakness of agonist muscles. The contribution of other factors that result in mechanical restraint of the agonist by the antagonist is discussed relative to muscle weakness in patients with hemiparesis. More studies on patients with hemiparesis are required to assess what role muscle strength training should play in rehabiliting patients after a stroke.

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The Regulation of Osteoclastogenesis by L-Type Channel Agonist (L-형 칼슘 이온통로에 의한 파골세포 분화의 조절)

  • Noh, A-Long-Sae-Mi;Yim, Mi-Jung
    • YAKHAK HOEJI
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    • v.54 no.6
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    • pp.461-465
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    • 2010
  • We investigated the role of L-type $Ca^{2+}$ channel in receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclast formation. BayK 8644, a L-type $Ca^{2+}$ channel agonist, was shown to increase the RANKLinduced osteoclastogenesis and actin ring formation in mouse bone marrow-dereived macrophage (BMM) culture system. BayK 8644 stimulated RANKL-induced extracellular signal-regulated kinase (ERK) and p38 MAP kinase (MAPK) activation, which leads to increased nuclear factor of activated T cells (NFAT)c1 expression. Taken together, these data indicate that L-type $Ca^{2+}$ channel regulates osteoclast formation possibly through ERK- and p38-mediated NFATc1 expression.

횐쥐 적출 관류부신을 이용한 Catecholamine 분비작용의 검색방법

  • 고석태;임동윤
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1992.05a
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    • pp.38-38
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    • 1992
  • 횐쥐 적출 완류부신을 이용하여 neuronal nicotinic(NN) agonist인 DMPP와 M1-muscarinic agonist인 McN-A-343의 카테콜아민(CA) 분비 작용의 차이와 특성에 대해서 연구한 결과는 다음과 같다. DMPP (100 $\mu$M)와 McN-A-343(100 $\mu$M)은 부신정맥내로 투여시 유의한 카테콜아민 분비작용을 나타내었다. Mol농도로 비교시 McN-A-343의 CA분비작용은 DMPP의 약 1/5정도였다. DMPP의 CA분비작용은 chlorisondamine이나 desipramine 또는 $Ca_2$$^{2}$-free Krebs + EGTA 관류등의 전처치로 의의있게 억제되었으나, pirenzepine, ouabain 및 physostigmine등 전처치에 의해서는 영향을 받지않았다. 그러나 atropine 전처치시 DMPP의 분비작용은 오히려 증강되었다.

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Effects of Dopamine Agonists on Primary Cultured Neurons from Various Brain Regions

  • Kim, Kyeong-Man
    • Biomolecules & Therapeutics
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    • v.2 no.1
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    • pp.16-22
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    • 1994
  • Using 2 to 4 day-old postnatal rats, primary brain cell cultures were made from various brain regions (substantia nigra, hippocampus, striatum, and nucleus accumbens). Whole-cell patch clamp technique was used for electrophysiological studies. Neurons cultured from substantia nigra were characterized more in detail to test whether these cultured neurons were appropriate for physiological studies. Immunocytochemical and electrophysiological properties of these cultured neurons agreed with those from other in vivo or in vitro studies suggesting that cultured neurons maintained normal cytological and physiological conditions. Modulation of ionic channels through dopamine receptors were studied from brain areas where dopamine plays important roles on brain functions. When neurons were clamped near resting membrane potential (-74mV), R(+), R(+)-SKF 38393, a specific D$_1$receptor agonist, activated cultured striatal neurons, and dopamine itself produced biphasic responses. Responses of cultured hippocampal neurons to dopamine agonists were kinds of mirror images to those from striatal neurons; D$_1$receptor agonists inhibited hippocampal neurons but quinpirole, a D$_2$receptor agonist, activated them. Neurons cultured from nucleus accumbens were inhibited by dopamine.

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