• Korean Journal of Veterinary Service
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• 제17권3호
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• pp.247-254
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• 1994

To elucidate the action of the cholinergic nerve on the isolated uterine smooth muscle of the pig, effects of electrical transmural nerve stimulation and acetylcholine were investigated on the pretreatment of the physostigmine ; cholinestrase inhibitor and atropine ; cholinergic receptor blocker from physiograph. 1. The contractile response induced by acetylcholine was responsed in the concentration of 10^{-8}$ M at first and the maximum contractility was concentration of $10^{-6}$ M. 2. The contractile response induced by electrical transmural nerve stimulation(20 V, 0.5 Msec, 20 sec) was the frequency(2-64 Hz) -dependent manner. 3. The contractile response induced by acetylcholine was completely blocked by the pretreatment with cholinergic receptor blocker, atropine and was increased by the pretrement of cholinestrase inhibitor, physostigmine. 4. The contractile response induced by electrical transmural nerve stimulation was completely blocked by the pretreatment with cholinergic receptor blocker, atropine, and was increased by the pretretment of cholinestrase inhibitor, physostigmine. These findings suggest that it was powerful excitatory action by cholinergic nerve on uterine smooth muscle of the pig.

• Biomolecules & Therapeutics
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• 제8권4호
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• pp.338-348
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• 2000

The present study was attempted to determine the effect of 5'-(N'-ethylcarboxamido) adenosine (NECA), which is an potent $A_2$-adenosine receptor agonist, on catecholamine (CA) secretion evoked by cholinergic stimulation, membrane depolarization and calcium mobilization from the isolated perfused rat adrenal gland. NECA (20 nM) perfused into the adrenal vein for 60 min produced a time-related inhibition in CA secretion evoked by ACh (5.32x10$^{-3}$ M), high $K^{+}$(5.6x10$^{-2}$ M), DMPP (10$^{-4}$ M for 2 min), McN-A-343 (10$^{-4}$ M for 2 min), cyclopiazonic acid (10$^{-5}$ M for 4 min) and Bay-K-8644 (10$^{-5}$ M for 4 min). Also, in the presence of $\beta$,${\gamma}$-methylene adenosine-5'-triphosphate (MATP), which is also known to be a selective $P_{2x}$-purinergic receptor agonist, showed a similar inhibition elf CA release evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid. However, in adrenal glands preloaded with 20$\mu$M NECA for 20 min under the presence of 20$\mu$M 3-isobutyl-1-methyl-xanthine (IBMX), an adenosine receptors antagonist, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were much recovered in comparison to the case of NECA-treatment only. Taken together, these results indicate that NECA causes the marked inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization. This inhibitory effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells through the adenosine receptor stimulation. Therefore, it is suggested that the inhibitory mechanism of adenosine receptor stimulation may play a modulatory role in regulating CA secretion.n.n.

• Korean Journal of Veterinary Research
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• 제39권3호
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• pp.472-477
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• 1999

To elucidate the action of the cholinergic and adrenergic nerve on isolated gastric fundus smooth muscle of rabbit, the effects of electrical transmural stimulation were investigated in the presence of atropine, cholinergic receptor blocker; phentolamine, nonselective ${\alpha}$-adrenergic receptor blocker; propranolol, nonselective ${\beta}$-adrenergic receptor blocker and L-arginine from the isometric contraction of physiological recording system. 1. The contractile response induced by electrical transmural stimulation was increased as the frequency(1~32Hz)-dependent manner on the isolated gastric fundus smooth muscle. 2. The contractile response induced by electrical transmural stimulation was markedly inhibited by the pretreatment of atropine($1{\mu}M$). 3. The contractile response induecd by electrical transmutal stimulation was inhibited by the pretreatment of phentolamine($1{\mu}M$). 4. The relaxative response induced by electrical transmural stimulation on presence of atropine ($1{\mu}M$) was inhibited by the pretreatment of propranolol($1{\mu}M$). 5. The relaxative responses on precontraction induced by histamine($10{\mu}M$) with guanethidine ($50{\mu}M$) and atropine($1{\mu}M$) by electrical transmural stimulation were increased by L-arginine (1mM). These findings suggest that it was the excitatory action of cholinergic and ${\alpha}$-adrenergic nerve, and the inhibitory action of ${\beta}$-adrenergic nerve and nonadrenergic noncholinergic nerve on the isolated gastric fundus smooth muscle of rabbit.

• Korean Journal of Veterinary Research
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• 제33권2호
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• pp.211-216
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• 1993

To elucidate the action of the cholinergic and ${\alpha}_2$-adrenergic nerve on the isolated ileal smooth muscle of the dog, effect a of electrical field stimulation were investigated on the pretreatment of the physostigmine; cholinestrase inhibitor, yohimbine; ${\alpha}_2$-adrenoceptor blocker, atropine ; cholinergic receptor blocker and phentolamine; non-selective $\alpha$-adrenoceptor blocker from physiograph. 1. The contractile response induced by electrical field stimulation was the frequency (2-40 Hz)-dependent manner. 2. The contractile response induced by electrical field stimulation was markedly increased by the pretreatment of physostigmine$(1{\mu}M)$; cholinestrase inhibitor. 3. The contractile response induced by electrical field stimulation was increased by the pretreatment of yohimbine$(1{\mu}M)$; ${\alpha}_2$-adrenoceptor blocker. These finding suggest that it was powerful excitatory action by cholinergic nerve and inhibitory action by ${\alpha}_2$-adrenergic nerve on ileal smooth muscle of the dog.

• Korean Journal of Veterinary Research
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• 제35권2호
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• pp.237-243
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• 1995

The effects of various autonomic blocking agents to perivascular nerve stimulation were investigated on isolated coronary artery of pig. 1. The magnitude of contractile response to perivascular nerve stimulation increased with increasing frequency(280Hz) of stimulation. 2. The contractions to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) were increased by pretreatment of the cholinestrase inhibitor, physostigmine. 3. The contraction to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) was antagonised by the muscarinic antagonist, atropine. 4. The contraction to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) was blocked by the neural blocker, tetrodotoxin. 5. The contractions to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) were not significantly affected by the ${\alpha}$-adrenergic antagonist, phentolamine or ${\beta}$-adrenergic antagonist, propranolol. 6. The contractile response by the acetylcholine was increased by the pretreatment of cholinestrase inhibitor, physostigmine. This findings suggest that the powerful excitatory action by the perivascular nerve stimulation may be linked to muscarinic receptor by cholinergic nerve excitation in coronary artery of pig.

• The Journal of Korean Physical Therapy
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• 제13권1호
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• pp.61-71
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• 2001

The purpose oi this study is to identify clearly the physiologic significance of autonomic nervous system. This study is to find the loose of endogenous neurotransmitter while using the neural response of the neural excitatory action which is distributed to the perivascular smooth muscle through the electrical stimulation of the smooth muscle of coronary artery of pig. The effects of perivascular nerve stimulation were investigated on isolated coronary artery of pig.1 . The magnitude of contractile response to perivascular nerve stimulation increased with increasing frequency (2-80 Hz) of stimulation. 2. The contractions to perivascular nerve stimulation(40V, 40Hz. 0.5msec, 1 min) were increased greatly by pretreatment of the cholinestrase inhibitor physostigmine. 3. The contraction to perivascular nerve stimulation(40V,40Hz, 0.5msec, 1min) was antagonised markedly by the muscarinic antagonist atropine. 4. The contraction to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1 min) was blocked by the neural blocker tetrodotoxin. 5. The contractions to perivascular nerve stimulation(40V. 40Hz, 0.5msec, 1 min) were not affected significantly by the -adrenergic antagonist phentolamine or - adrenergic antagonist propranolol. 6. The contractile response by the acetylcholine was increased by the pretreatment of cholinestrase inhibitor physostigmine. The finding suggest that it is powerful excitatory action linked to muscarinic receptor by cholinergic nerve in coronary artery of pig.

• The Korean Journal of Physiology and Pharmacology
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• 제2권2호
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• pp.173-184
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• 1998

The present study was undertaken to examine 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\;{\mu}M$) into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), excess K^+$ (a membrane-depolarizor 56 mM), DMPP (a selective nicotinic receptor agonist, 100\;{\mu}M$ for 2 min), McN-A-343 (a muscarinic receptor agonist, 100\;{\mu}M$ for 4 min), Bay-K-8644 (a calcium channel activator, 10\;{\mu}M$ for 4 min) and cyclopiazonic acid (a releaser of intracellular $Ca^{2+}$, 10\;{\mu}M$ for 4 min). Similarly, the preperfusion of hydrocortisone (30\;{\mu}M$) for 20 min also attenuated significantly the secretory responses of CA evoked by nicotinic and muscarinic receptor stimulation as well as membrane-depolarization, $Ca^{2+}$ channel activation and the release of intracellular $Ca^{2+}$. Furthermore, even in the presence of betamethasone (30{\mu}M$), CA secretion evoked by ACh, excess K^+$, DMPP and McN-A-343 was also markedly inhibited. Taken together, the present results suggest that glucocorticoids cause the marked inhibition of CA secretion evoked by both cholinergic nicotinic and muscarinic receptor stimulation from the isolated perfused rat adrenal gland, indicating strongly that this inhibitory effect may be mediated by inhibiting influx of extracellular calcium as well as the release of intracellular calcium in the rat adrenomedullary chromaffin cells.

• Journal of Yeungnam Medical Science
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• 제12권2호
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• pp.246-259
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• 1995

This study aimed to investigate the mechanism of action of baclofen on the detrusor muscle isolated from rat. Rats (Sprague-Dawley) were sacrificed by decapitation and exsanguination. Horizontal muscle strips of $2mm{\times}15mm$ were prepared for isometric myography in isolated muscle chamber bubbled with 95% / 5%-$O_2$ / $CO_2$ at $37^{\circ}C$, and the pH was maintained at 7.4. Detrusor strips contracted responding to the electrical field stimulation (EFS) by 2 Hz, 20 msec, monophasic square wave of 60 VDC. The initial peak of EFS-Induced contraction was tended to be suppresed by ${\alpha},{\beta}$-methylene-adenosine 5'-triphosphate (mATP), a partial agonist of purinergic receptor, and baclofen, a $GABA_B$ receptor agonist (statistically nonsignificant). The late sustained contraction by EFS was suppressed significantly (p < 0.05) by additions of atropione, a cholinergic muscarinic receptor antagonist and baclofen. The adenosine 5'-triphosphate-induced contraction was completely abolished by mA TP but not by baclofen. In the presence of atropine, the subsequent addition of acetylcholine could not contract the muscle strips: but the addition of acetylcholine in the presence of baclofen evoked a contraction to a remarkable extent. These results suggest that in the condition of present study, the cholinergic innervation may play a more important role than the purinergic one, and baclofen suppresses the contractility of rat detrusor by the stimulation of the $GABA_B$ receptors to inhibit the release of neurotransmitter from the cholinergic nerve ending.

• Proceedings of the PSK Conference
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.75.2-75.2
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• 2003

The present study was designed to compare the effects of conotoxin GVIA, a selective blocker of N-type voltage-dependent calcium channels (VDCC) and cilnidipine, a blocker of both L- and N-type VDCC, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal gland, and also to establish the mechanism of action. 1. The inhibition of the CA secretory response evoked by acetylcholine (5.32 x 10$\^$-3/ ${\mu}$M) was stronger in cilnidipine-treated glands than in conotoxin GVIA-treated glands. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• 제24권6호
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• pp.517-527
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• 2020

Layer 2/3 pyramidal neurons (L2/3 PyNs) of the cortex extend their basal dendrites near the soma and as apical dendritic tufts in layer 1, which mainly receive feedforward and feedback inputs, respectively. It is suggested that neuromodulators such as serotonin and acetylcholine may regulate the information flow between brain structures depending on the brain state. However, little is known about the dendritic compartment-specific induction of synaptic transmission in single PyNs. Here, we studied layer-specific serotonergic and cholinergic induction of long-term synaptic plasticity in L2/3 PyNs of the agranular insular cortex, a lateral component of the orbitofrontal cortex. Using FM1-43 dye unloading, we verified that local electrical stimulation to layers 1 (L1) and 3 (L3) activated axon terminals mostly located in L1 and perisomatic area (L2/3). Independent and AMPA receptor-mediated excitatory postsynaptic potential was evoked by local electrical stimulation of either L1 or L3. Application of serotonin (5-HT, 10 μM) induced activity-dependent longterm depression (LTD) in L2/3 but not in L1 inputs. LTD induced by 5-HT was blocked by the 5-HT₂ receptor antagonist ketanserin, an NMDA receptor antagonist and by intracellular Ca²⁺ chelation. The 5-HT₂ receptor agonist α-me-5-HT mimicked the LTD induced by 5-HT. However, the application of carbachol induced muscarinic receptor-dependent LTD in both inputs. The differential layer-specific induction of LTD by neuromodulators might play an important role in information processing mechanism of the prefrontal cortex.