• 한국생명과학회:학술대회논문집
• /
• 한국생명과학회 2007년도 제48회 학술심포지움 및 추계국제학술대회
• /
• pp.126.2-126.2
• /
• 2007

See Full Text

• 대한약리학회지
• /
• 제19권1호
• /
• pp.85-92
• /
• 1983

Intestine is innervated by an interconnected plexus of both sympathetic and parasympathetic nerve fibers. Sympathetic influence causes inhibition of intestinal motility mediated by both ${\alpha}-\;and\;{\beta}-adrenergic$ receptors. The mechanism of intestinal relaxation by ${\beta}-receptors$ has been extensively studied, but the function of ${\alpha}-receptors$ in intestinal motility is still unclear. Although it is suggested that catecholamine reduces acetylcholine release and this may play an important role in ${\alpha}-receptor$ mediated intestinal relaxation, there is no definite evidences about the mechanism and site of action of ${\alpha}-receptor$ mediated relaxation. In this experiment, therefore, the effect and site of action of ${\alpha}-receptor$ agonists were investigated in the guinea pig ileum using electrical field stimulation. The results are summarized as follows : 1) Electrical field stimulation elicited tonic contraction in isolated guinea pig ileum ana this contraction was completely inhibited by the pretreatment of tetrodotoxin or atropine. 2) Norepinephrine, epinephrine and dopamine inhibited the contraction induced by electrical field stimulation but methoxamine and phenylephrine had little effects. 3) Inhibitory effects of norepinephrine and dopamine was partially blocked by yohimbine and phentolamine pretreatment. But haloperidol and propranolol pretreatment cause no effects on the electrical field stimulation induced contraction. Inhibitory effect of dopamine was completely blocked by both haloperidol and yohimbine pretreatment. 4) Inhibitory effects of norepinephrine and dopamine were little affected by the pretreatment with hexamethonium. It is suggested that electrical field stimulation causes tonic contraction of guinea pig ileum by releasing acetylcholine from postganglionic fiber, and this release is blocked by presynaptic ${\alpha}-receptor$ activation.

• The Korean Journal of Physiology and Pharmacology
• /
• 제2권2호
• /
• pp.147-154
• /
• 1998

It was attempted to clarify the participation of $K^+-channels$ in the post-receptor mechanisms of the muscarinic and $A_1-adenosine$ receptor- mediated control of acetylcholine (ACh) release in the present study. Slices from the rat hippocampus were equilibrated with $[^3H]$choline and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 V/cm, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Oxotremorine (Oxo, $0.1{\sim}10\;{\mu}M$), a muscarinic agonist, and $N^6-cyclopentyladenosine$ (CPA, $1{\sim}30\;{\mu}M$), a specific $A_1-adenosine$ agonist, decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. 4-aminopyridine (4AP), a specific A-type $K^+-channel$ blocker ($1{\sim}100\;{\mu}M$), increased the evoked ACh release in a dose-related fashion, and the basal rate of release is increased by 3 and $100\;{\mu}M$. Tetraethylammonium (TEA), a non-specific $K^+-channel$ blocker ($0.1{\sim}10\;{\mu}M$), increased the evoked ACh release in a dose-dependent manner without affecting the basal release. The effects of Oxo and CPA were not affected by $3\;{\mu}M$ 4AP co-treatment, but 10 mM TEA significantly inhibited the effects of Oxo and CPA. 4AP ($10\;{\mu}M$)- and TEA (10 mM)-induced increments of evoked ACh release were completely abolished in Ca^{2+}-free$ medium, but these were recoverd in low Ca^{2+}$ medium. And the effects of $K^+-channel$ blockers in low Ca^{2+}$ medium were inhibited by $Mg^{2+}$ (4 mM) and abolished by $0.3\;{\mu}M$ tetrodotoxin (TTX). These results suggest that the changes in TEA-sensitive potassium channel permeability and the consequent limitation of Ca^{2+}$ influx are partly involved in the presynaptic modulation of the evoked ACh-release by muscarinic and $A_1-adenosine$ receptors of the rat hippocampus.

• 한국자기공명학회:학술대회논문집
• /
• 한국자기공명학회 2002년도 International Symposium on Magnetic Resonance
• /
• pp.86-86
• /
• 2002

• 한국자기공명학회:학술대회논문집
• /
• 한국자기공명학회 2002년도 International Symposium on Magnetic Resonance
• /
• pp.55-55
• /
• 2002

• 한국막학회:학술대회논문집
• /
• 한국막학회 1998년도 춘계 총회 및 학술발표회
• /
• pp.31-35
• /
• 1998

1. INTRODUCTION : Recognition and binding of organic substrates by biological molecules are of vital importance in biophysics and biophysical chemistry. Most studies of the application focused on the development of biosensors, which detected reaction products generated by the binding between enzymes and substrates. Other types of biosensors in which membrane proteins (e.g., nicotinic acetylcholine receptor, auxin receptor ATPase, maltose bining protein, and glutmate receptor) were utilized as a receptor function were also developed. In the previous study[1], the shifts in membrane potential, caused by the injection of substrates into a permeation cell, were measured using immobilized glucose oxidase membranes. It was suggested that the reaction product was not the origin of the potential shifts, but the changes in the charge density in the membrane due to the binding between the enzyme and the substrates generated the potential shifts. In this study, $\gamma$-globulin was immobilized (entrapped) in a poly($\gamma$-amino acid) network, and the shifts in the membrane potential caused by the injection of some amino acids were investigated.

• 대한약학회:학술대회논문집
• /
• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
• /
• pp.84.1-84.1
• /
• 2003

Methamphetamine is a powerful stimulant that appears to produce locomotor activity and behavioral sensitization. Previous study has indicated that dopaminergic receptors are implicated in the behavioral responses of methamphetamine. Recently, it has been reported that other receptors, especially, M1 muscarinic acetylcholine receptor (M1R) plays an important role in the regulation of behavioral responses, and this receptor is abundantly expressed in brain regions, including the cerebral cortex, striatum, and the hippocampus of the animal. (omitted)

• BMB Reports
• /
• 제47권10호
• /
• pp.552-557
• /
• 2014

The main purpose of this study was to investigate whether type 3 muscarinic acetylcholine receptor (M3R) dysfunction induced vascular hyperpermeability. Transwell system analysis showed that M3R inhibition by selective antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) and small interfering RNA both increased endothelial permeability. Using coimmunoprecipitation and Western blot assay, we found that M3R inhibition increased VE-cadherin and ${\beta}$-catenin tyrosine phosphorylation without affecting their expression. Using PTP1B siRNA, we found that PTP1B was required for maintaining VE-cadherin and ${\beta}$-catenin protein dephosphorylation. In addition, 4-DAMP suppressed PTP1B activity by reducing cyclic adenosine monophosphate (cAMP), but not protein kinase $C{\alpha}$ ($PKC{\alpha}$). These data indicate that M3R preserves the endothelial barrier function through a mechanism potentially maintaining PTP1B activity, keeping the adherens junction proteins (AJPs) dephosphorylation.

• 대한수의학회지
• /
• 제39권1호
• /
• pp.55-61
• /
• 1999

The present experiments were performed to examine the effects of acetylcholine (ACh) and carbachol (CC) on thyroxine ($T_4$) release and any possible relation between inhibition of $T_4$ release and signaling pathway in guinea pig thyroids. The thyroids were incubated in the medium containing the test agents, samples of the medium were assayed for $T_4$ by EIA kits. ACh and CC inhibited the TSH-stimulated $T_4$ release. These inhibition were reversed by atropine, but not by d-tubocurarine. The inhibitory effects of ACh on $T_4$ release were prevented by $M_{1^-}$ and $M_{3^-}$muscarinic antagonists and its inhibition was also slightly reversed by $M_{2^-}$ and $M_{4^-}$muscarinic antagonists. R59022, like ACh and CC, also inhibited the TSH-stimulated $T_4$ release. This inhibition was reversed by protein kinase C inhibitor and $Ca^{2+}$ channel blocker. The present study suggests that cholinergic inhibition of $T_4$ release from thyroids can be induced mainly by activation of the $M_{1^-}$ or $M_{3^-}$ receptors and that it is mediated through the muscarinic receptorstimulated protein kinase C activation.

• 대한수의학회지
• /
• 제46권1호
• /
• pp.71-73
• /
• 2006

A 7-month-old female Shih-tzu dog was presented with intermittent trembling, dyspnea, generalized muscle weakness, and unconsciousness after exercise. No remarkable findings were shown in the complete blood counts and the radiographic examination. On serum biochemical profiles, alkaline phosphatase and creatine phosphokinase were mildly elevated. Based on history takings, physical examination, and neurological findings, presumptive diagnosis was made as a myasthenia gravis (MG). Clinical signs of this patient were dramatically improved after administration of neostigmine. The result of acetylcholine receptor antibody test in serum was 0.89 nmol/L and the histopathology of muscle were normal. Clinical sign of the patient evaluated in this study is stabilized with long-term administration of pyridostigmine at this time. This case report here describes clinical and clinicopathological findings of a juvenile onset acquired MG in a Shih-tzu dog.