• Proceedings of the PSK Conference
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• 2003.04a
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• pp.126.1-126.1
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• 2003

Adrenal medullary chromaffin cells secrete catecholamines in response to nicotinic agonists (Douglas ＆ Rubin. 1961; Wakade, 1981; Amy ＆ Kirshner, 1982). Several types of voltage-dependent Ca2+ channels are present on adrenal chromaffin cells, but the role of each type in the catecholamine secretion process remains controversial. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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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)

• Annals of Clinical Neurophysiology
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• v.23 no.1
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• pp.7-16
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• 2021

Transcranial magnetic stimulation (TMS) is a safe and noninvasive tool for investigating the cortical excitability of the human brain and the neurophysiological functions of GABAergic, glutamatergic, and cholinergic neural circuits. Neurophysiological biomarkers based on TMS parameters can provide information on the pathophysiology of dementia, and be used to diagnose Alzheimer's disease and differentiate different types of dementia. This review introduces the basic principles of TMS, TMS devices and stimulating paradigms, several neurophysiological measurements, and the clinical implications of TMS for Alzheimer's disease.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.223-230
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• 2005

The purpose of the present study was to examine the effect of naltrexone, an opioid antagonist, on secretion of catecholamines (CA) evoked by cholinergic nicotinic stimulation and membrane-depolarization from the isolated perfused rat adrenal gland and to establish the mechanism of its action. Naltrexone $(3{\times}10^{-6}M)$ perfused into an adrenal vein for 60 min produced time-dependent inhibition in CA secretory responses evoked by ACh $(5.32{\times}10^{-3}M)$ , high $K^+$ $(5.6{\times}10^{-2}M)$ , DMPP ($10^{-4}$ M) and McN-A-343 $(10^{-4}M)$ . Naltrexone itself did also fail to affect basal CA output. In adrenal glands loaded with naltrexone $(3{\times}10^{-6}M)$ , the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}-ATPase$, were also inhibited. However, in the presence of met-enkephalin $(5{\times}10^{-6}M)$ , a well-known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Collectively, these experimental results demonstrate that naltrexone inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that this inhibitory effect of naltrexone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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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 Korean Biological Nursing Science
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• v.14 no.1
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• pp.25-32
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• 2012

Purpose: influence of benzodiazepine (midazolam)or cholinergic inhibitor (atropine or glycopyrrlate) on intra-operative body temperature remains unclear and controversial. This study compares intra-operative body temperature in 50 abdominal surgical patients under general anesthesia between the administration of midazolam and glycopyrrolate in combination, or glycopyrrolate alone. Methods: Patients who underwent abdominal surgery were recruited from September 2008 through October 2009 at Gachon University Gil hospital in incheon. Core body temperature was measured in the right ear using a tympanic membrane thermometer at induction of general anesthesia and at 1 hr, 2 hr, and 3 hr after induction. Results: There were no differences in core body temperature at any measurement point between either patient group (F=1.08, $p$=.377). Core body temperature decreased throughout the 3 hr after induction in both groups (F=9.22, $p$ <.001). Specially, core temperatures at induction of general anesthesia (p<.001), 1 hr (p<.001), 2 hr ($p$ <.001), and 3 hr ($p$ <.001) after induction were lower than before administration of midazolam and glycopyrrolate, or glycopyrrolate alone. Conclusion: We conclude that a cholinergic inhibitor (glycopyrrolate, 0.1 mg) therefore seems not to affect intra-operative body temperature of patients given a benzodiazepine (midazolam, 0.04 mg $kg^{-1}$), and not to increase body temperature in patients not given a benzodiazepine during the 3 hr after the induction of general anesthesia. Intra-operative warming therefore is needed to prevent hypothermia in surgical patients who receive pre-operative administration of midazolam and/or glycopyrrolate.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.217-217
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• 1996

The putative role of vasoactive intestinal polypeptide (VIP) as non-adrenergic non-cholinergic (NANC) neurotransmitter has been studied in rabbit corpus cavernosum. In the presence of atropine and guanethidine the short and prolonged electrical field stimulation (EFS, 2～16 ㎐) induced a frequency-dependent relaxation which was abolished by tetrodotoxin (0.3 ${\mu}$M), a nerve conductance blocker. The neurogenic relaxant reponses were not affected in the presence of VIP-inactivating peptidase, ${\alpha}$-chymotrypsin (2 units/$m\ell$), whereas VIP-induced relaxation were completely abolished. Inhibition of nitric oxide synthase by N$\^$G/-nitro-L-arginine (10～100 ${\mu}$M) caused concentration-dependent inhibition to the neurogenic relaxant responses and at 100 ${\mu}$M the relaxations were virtually abolished. In contrast NO (3～30 ${\mu}$M) and VIP (0.001～l ${\mu}$M)-induced relaxation were unaffected. The inhibitory effect of L-NNA was reversed in the presence of L-arginine (5 mM), the precursor of the NO biosynthesis. Hemog1obin (20～60 ${\mu}$M), sequestering NO in the extracellular space, abolished the NO-evoked relaxation and also caused a concentration-dependent inhibition to the neurogenic relaxation. These observation indicate that NANC relaxation induced by prolonged EFS of rabbit corpus cavernosum is also mediated mainly by nitric oxide as same as that of short EFS, and suggest that VIP is not involved in NANC relaxation of rabbit corpus cavernosum and NO would not be produced by VIP in this tissue.

• Biomolecules & Therapeutics
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• v.15 no.2
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• pp.108-117
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• 2007

The aim of the present study was to investigate the effect of glibenclamide, a hypoglycemic sulfonylurea, which selectively blocks ATP-sensitive K$^+$ channels, on secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused rat adrenal glands. The perfusion of glibenclamide (1.0 mM) into an adrenal vein for 90 min produced time-dependently enhanced the CA secretory responses evoked by ACh (5.32 mM), high K$^+$ (a direct membrane depolarizer, 56 mM), DMPP (a selective neuronal nicotinic receptor agonist, 100 ${\mu}$M for 2 min), McN-A-343 (a selective muscarinic M1 receptor agonist, 100 ${\mu}$M for 2 min), Bay-K-8644 (an activator of L-type dihydropyridine Ca$^{2+}$ channels, 10 ${\mu}$M for 4 min) and cyclopiazonic acid (an activator of cytoplasmic Ca$^{2+}$-ATPase, 10 ${\mu}$M for 4 min). In adrenal glands simultaneously preloaded with glibenclamide (1.0 mM) and nicorandil (a selective opener of ATP-sensitive K$^+$ channels, 1.0 mM), the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to the considerable extent of the control release in comparison with that of glibenclamide-treatment only. Taken together, the present study demonstrates that glibenclamide enhances the adrenal CA secretion in response to stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization from the isolated perfused rat adrenal glands. It seems that this facilitatory effect of glibenclamide may be mediated by enhancement of both Ca$^{2+}$ influx and the Ca$^{2+}$ release from intracellular store through the blockade of K$_{ATP}$ channels in the rat adrenomedullary chromaffin cells. These results suggest that glibenclamide-sensitive K$_{ATP}$ channels may play a regulatory role in the rat adrenomedullary CA secretion.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.1
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• pp.83-90
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• 1997

Aim of this study was to investigate if pancreatic polypeptide (PP) reduced the insulin action via the intra-pancreatic cholinergic nerves in the isolated rat pancreas. The pancreas was isolated from rats and perfused with intra-arterial infusion of modified Krebs-Henseleit solution containing 2.5 mM glucose at a flow rate of 1.2 ml/min. Simultaneous intra-arterial infusion of insulin (100 nM) resulted inpotentiation of the pancreatic flow rate and amylase output which were stimulated by cholecystokinin (CCK, 14 pM). These potentiating actions of insulin on the CCK -stimulated pancreatic exocrine secretion were completely abolished by administration of rat PP. Vesamicol, a potent inhibitor of vesicular acetylcholine storage, and tetrodotoxin (TTX) also significantly reduced the combined actions of insulin and CCK. Administration of carbamylcholine, an acetylcholine agonist, completely restored the vesamicol- or TTX-induced inhibition of the potentiation between insulin and CCK. Also rat PP failed to attenuate the restoring effect of carbamylcholine. Electrical field stimulation (15-30 V, 2 msec and 8 Hz) resulted in a significant increase in the pancreatic flow rate and amylase output in voltage-dependent manner. Effects of electrical field stimulation were augmented by endogenous insulin. Rat PP also suppressed the pancreatic exocrine secretion stimulated by electrical field stimulation. These observations strongly suggest that PP inhibits the potentiating actions of insulin on CCK -stimulated pancreatic exocrine secretion by suppression of the intra-pancreatic cholinergic activity in the isolated rat pancreas.

• The Korean Journal of Pain
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• v.11 no.1
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• pp.7-22
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• 1998

The development of the superior cervical ganglion was studied by electron microscopic method in human fetuses ranging from 40 mm to 260 mm of crown-rump length(10 to 30 weeks of gestational age). At 40 mm fetus, the superior cervical ganglion was composed of clusters of undifferentiated cell, primitive neuroblast, primitive supporting cell, and unmyelinated fibers. At 70 mm fetus, the neuroblasts and their processes were ensheated by the bodies or processes of satellite cells. The cytoplasm of the neuroblast contained rough endoplasmic reticulum, mitochondria, Golgi complex, Nissl bodies and dense-cored vesicles. As the neuroblasts grew and differentiated dense-cored vesicles moved away from perikaryal cytoplasm into developing processes. Synaptic contacts between the cholinergic axon and dendrites of postganglionic neuron and a few axosomatic synapses were first observed at 70 mm fetus. At 90 mm fetus the superior cervical ganglion consisted of neuroblasts, satellite cells, granule-containing cells, and unmyelinated nerve fibers. The ganglion cells increased somewhat in numbers and size by 150 mm fetus. Further differentiation resulted in the formation of young ganglion cells, whose cytoplasm was densely filled with cell organelles. During next prenatal stage up to 260 mm fetus, the cytoplasm of the ganglion cells contained except for large pigment granules, all intracytoplasmic structures which were also found in mature superior cervical ganglion. A great number of synaptic contact zones between the cholinergic preganglionic axon and the dendrites of the postganglionic neuron were observed and a few axosomatic synapses were also observed. Two morphological types of the granule-containing cells in the superior cervical ganglion were first identified at 90 mm fetus. Type I granule-containing cell occurred in solitary, whereas type II tended to appeared in clusters near the blood capillaries. Synaptic contacts were first found on the solitary granule-containing cell at 150 mm fetus. Synaptic contacts between the soma of type I granule-containing cells and preganglionic axon termials were observed. In addition, synaptic junctions between the processes of the granule-containing cells and dendrites of postganglionic neuron were also observed from 150 mm fetus onward. In conclusion, superior cervical ganglion cells and granule-containing cells arise from a common undifferentiated cell precursor of neural crest. The granule-containg cells exhibit a local modulatory feedback system in the superior cervical ganglion and may serve as interneurons between the preganglionic and postganglionic cells.