• Title/Summary/Keyword: cholinergic

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Neurophysiology of Laryngopharyngeal Reflux and Brainstem Reflex (인후두역류증후군과 뇌간반사에 관한 신경생리)

  • Han, Baek Hwa;Hong, Ki Hwan
    • Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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    • v.27 no.2
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    • pp.73-77
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    • 2016
  • Laryngopharyngeal reflux disease (LPRD) is different with gastroesophageal reflux disease (GERD). The lower esophageal sphincter (LES) possesses an intrinsic nervous plexus that allows the LES to have a considerable degree of independent neural control. Sympathetic control of the LES and stomach stems from cholinergic preganglionic neurons in the intermediolateral column of the thoracic spinal cord (T6 through T9 divisions), which impinge on postganglionic neurons in the celiac ganglion, of which the catecholaminergic neurons provide the LES and stomach with most of its sympathetic supply. Sympathetic regulation of motility primarily involves inhibitory presynaptic modulation of vagal cholinergic input to postganglionic neurons in the enteric plexus. The magnitude of sympathetic inhibition of motility is directly proportional to the level of background vagal efferent input. Recognizing that the LES is under the dual control of the sympathetic and parasympathetic nervous systems, we refer the reader to other comprehensive reviews on the role of the sympathetic and parasympatetic control of LES and gastric function. The present review focuses on the functionally dominant parasympathetic control of the LES and stomach via the dorsal motor nucleus of the vagus.

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Non-adrenergic non-cholinergic relaxation and contraction in circular smooth muscle of bovine reticular groove (소(우(牛)) 식도구 윤상근의 비아드레날린 비콜린성 이완 및 수축)

  • Kang, Tong-mook;Han, Ho-jae;Yang, Il-suk
    • Korean Journal of Veterinary Research
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    • v.35 no.2
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    • pp.279-285
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    • 1995
  • To characterize non-adrenergic non-cholinergic(NANC) nerve mediated contractile responses in circular smooth muscle of bovine reticular groove, we investigated NANC relaxation and contraction induced by electric field stimulation to enteric nerves. In the presence of atropine($1{\mu}M$) and guanethidine($50{\mu}M$), electric field stimulation at frequency of 1 to 16Hz(square pulses, 0.5ms duration, 70V) evoked clear-cut relaxations through stimulations. Transient 'rebound contraction' was occured when the stimulus was switched off. All of the responses (relaxation and rebound contraction) were dose-dependently blocked by Nw-nitro-$_{\small{L}}$-arginine methyl ester(L-NAME), an inhibitor of nitric oxide synthesis, and methylene blue, and inhibitor of soluble guanylate cyclase. Tetraethyl ammonium(TEA), a potassium channel blocker, did not block the NANC relaxations.

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Anti-dementia Effects of Cornus officinalis S. et Z. extract on the Scopolamine Induced Dementia in Mouse (Scopolamine유도 치매쥐에서 산수유 추출물의 항치매 효과)

  • Sohn, Kieho;Kim, Jeongsuk
    • Korean Journal of Pharmacognosy
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    • v.48 no.4
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    • pp.304-313
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    • 2017
  • These days, as the average span of population's life increases, the number patients of dementia also increases. But Research on Korean medicine is stilled limited. The research evaluates the effect of the extract from Cornus officinalis S.et Z on cognitive impairment induced by scopolamine in mice. The mice were randomly divided into five groups of ten mice. The normal group was treated with only 0.9% saline. The control group was treated with scopolamine (5 mg/kg, i.p.). The positive control group was treated with tacrin. The C100, 200 group was treated with C. officinalis extracts 100, 200 mg/kg. Memory-related behaviors were evaluated using a morris water maze and a passive avoidance test. Protein levels of BDNF, p-CREB (ser133), immunohistochemistry staining, and cholinergic activities were measured in brain tissue. The effects of C. officinalis extract significantly increased acetylcholine concentration and decreased acetylcholinesterase activity. The C. officinalis extract affected memory formation. Also, to confirm expression of protein BDNF, p-CREB (ser133) in the hippocampus, the researchers observed that immunohistochemistry and western blot increased in C. officinalis extract. These results suggest that C. officinalis provides a significant neuroprotective effect against scopolamine-induced cholinergic system and cognitive impairment.

Brain Mechanisms Generating REM Sleep (뇌의 REM 수면 발생기전)

  • Sohn, Jin-Wook
    • Sleep Medicine and Psychophysiology
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    • v.2 no.2
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    • pp.133-137
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    • 1995
  • The author reviews current knowledge about what REM sleep is and where and how it is generated. REM sleep is the state in which our most vivid dreams occur. REM sleep is identified by the simultaneous presence of a desynchronized cortical EEG, an absence of activity in the antigravity muscles(atonia), and periodic bursts of rapid eye movements. Another characteristic phenomena of REM sleep are the highly synchronized hippocampal EEG of theta frequency and the ponto-geniculo-occipital(PGO) spike. All these phenomena can be explained in terms of changes in neuronal activity. Transection studies have determined that the pons is sufficient for generating REM sleep. Lesion studies have identified a small region in the lateral pontine tegmentum corresponding to lateral portions of the nucleus reticularis pontis oralis(RPO) and the region immediately ventral to the locus coeruleus, which is required for REM sleep. Unit recording studies have found a population of cells within this region that is selectively active in REM sleep. Cholinergic neurons of the giant cell field of pontine tegmentum(ETG), which is 'REM a sleep-on cells', has shown to be critically involved in the generation of REM sleep. Noradrenergic neurons of the locus coeruleus and serotonergic neurons of the dorsal raphe, which are called 'REM sleep-off cells', appear to act in a reciprocal manner to the cholinergic neurons. It is proposed that the periodic cessations of discharge of 'REM sleep-off cells' during REM sleep might be significant for the prevention of the desensitization of receptors of these neurons.

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Effects of Clonidine on the Negative Chronotropic Response Induced by Vagal Stimulation in the Rat

  • Hong, Sung-Cheul;Huh, Kyung-Hye;Chung, Joon-Ki;Park, Mi-Sun
    • Archives of Pharmacal Research
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    • v.11 no.1
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    • pp.65-73
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    • 1988
  • The effects of clonidine on the negative chronotropic response induced by stimulation of vagus nerve were studied in the presence of propranolol in reserpinized and anesthetized rats. When the heart rate was decreased by stimulation of the vagus nerve, clonidine significantly inhibited vagally induced heart rate decrease (negative chronotropic response) in dose dependent manner. This inhibitory effect of clonidine was virtually abolished by phentolamine, ${\alpha}_1-\;and\;{\alpha}_2-adrenoceptor$ antagonist, and partially antagonized by prazosin, ${\alpha}_1-adrenoceptor$ antagonist. On the other hand, when the heart rate was decreased by the infusion of bethanechol, a muscarinic parasympathetic stimulant, clonidine had no effect on the bethanechol-induced heart rate decrease. These results suggest that clonidine inhibits vagally induced negative chronotropic response by activation of presynaptic ${\alpha}-adrenoceptors$ located on the parasympathetic cholinergic nerve terminal in the heart and this effect of clonidine is more related to ${\alpha}_2-adrenoceptors$ than ${\alpha}_1-adrenoceptors$.

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Activation of acetylcholine receptor elicits intracellular Ca2+ mobilization, transient cytotoxicity, and induction of RANKL expression

  • Heo, Seong-Jong;Kim, Min Seuk
    • International Journal of Oral Biology
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    • v.41 no.3
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    • pp.119-123
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    • 2016
  • Acetylcholine receptors (AChR) including muscarinic and nicotinic AChR are widely expressed and mediate a variety of physiological cellular responses in neuronal and non-neuronal cells. Notably, a functional cholinergic system exists in oral epithelial cells, and nicotinic AChR (nAChR) mediates cholinergic anti-inflammatory responses. However, the pathophysiological roles of AChR in periodontitis are unclear. Here, we show that activation of AChR elicits increased cytosolic $Ca^{2+}([Ca^{2+}]_i)$, transient cytotoxicity, and induction of receptor activator of nuclear factor kappa-B ligand (RANKL) expression. Intracellular $Ca^{2+}$ mobilization in human gingival fibroblast-1 (hGF-1) cells was measured using the fluorescent $Ca^{2+}$ indicator, fura-2/AM. Cytotoxicity and induction of gene expression were evaluated by measuring the release of glucose-6-phosphate dehydrogenase and RT-PCR. Activation of AChR in hGF-1 cells by carbachol (Cch) induced $[Ca^{2+}]_i$ increase in a dose-dependent manner. Treatment with a high concentration of Cch on hGF-1 cells caused transient cytotoxicity. Notably, treatment of hGF-1 cells with Cch resulted in upregulated RANKL expression. The findings may indicate potential roles of AChR in gingival fibroblast cells in bone remodeling.

Comparison of Green Tea Extract and Epigallocatechin Gallate on Secretion of Catecholamines from the Rabbit Adrenal Medulla

  • Lim Dong-Yoon
    • Archives of Pharmacal Research
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    • v.28 no.8
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    • pp.914-922
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    • 2005
  • The present study was designed to examine the effects of green tea extract (CUMC6335) and epigallocatechin gallate (EGCG) on secretion of catecholamines (CA) in the isolated perfused rabbit adrenal gland. In the presence of CUMC6335 $(200 {\mu}g/mL)$ into an adrenal vein for 60min, CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (56 mM), DMPP $(100{\mu}M \;for\;2min)$, and Bay-K-8644 $(10{\mu}M\;for\;4min)$ from the isolated perfused rabbit adrenal glands were greatly inhibited in a time-dependent fashion. However, EGCG $(10{\mu}g/mL)$ did not affect CA release evoked by ACh, high $K^+$, and Bay-K-8644. CUMC6335 itself failed to affect basal catecholamine output. Taken together, these results demonstrate that CUMC6335 inhibits CA secretion evoked by stimulation of cholinergic nicotinic receptors, as well as the direct membrane depolarization from the isolated perfused rabbit adrenal gland. It is thought that this inhibitory effect of CUMC6335 may be due at least in part to the blocking action of the L-type dihydropyridine calcium channels in the rabbit adrenomedullary chromaffin cells, which is relevant to the cholinergic nicotinic blockade. It seems that there is a big difference in mode of action between CUMC6335 and EGCG.

Expression of neurotransmitter receptors in oral keratinocytes and their response to agonists

  • Choi, Eun Ji;Chang, Sung-Ho;Choi, Se-Young;Choi, Youngnim
    • International Journal of Oral Biology
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    • v.46 no.1
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    • pp.39-44
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    • 2021
  • This study aimed to investigate whether neurotransmitter receptors in the nervous system were also expressed in oral keratinocytes. Expressions of various neurotransmitter receptor genes in immortalized mouse oral keratinocyte (IMOK) cells were examined by reverse transcriptase polymerase chain reaction. IMOK cells expressed calcitonin gene-related peptide (CGRP) receptor subunit genes Ramp1 and Ramp3 and glutamate receptor subunit genes Grina, Gria3, Grin1, Grin2a, and Grin2d. Moreover, IMOK cells expressed Adrb2 and Chrna5 that encode beta 2 adrenergic receptor and cholinergic receptor nicotinic alpha 5 for sympathetic and parasympathetic neurotransmitters, respectively. The expression of Bdkrb1 and Ptger4, which encode receptors for bradykinin and prostaglandin E2 involved in inflammatory responses, was also observed at low levels. Expressions of Ramp1 and Grina in the mouse gingival epithelium were also confirmed by immunohistochemistry. When the function of neurotransmitter receptors expressed on IMOK cells was tested by intracellular calcium response, CGRP, glutamate, and cholinergic receptors did not respond to their agonists, but the bradykinin receptor responded to bradykinin. Collectively, oral keratinocytes express several neurotransmitter receptors, suggesting the potential regulation of oral epithelial homeostasis by the nervous system.

The Study on the Analgesic Effect and its Cholinergic Mechanism of Electroacupuncture in the Rat Model of Collagen-induced Arthritis (Collagen 유발(誘發) 관절염(關節炎) 동물모델에 대(對)한 전침자극(電鍼刺戟)의 진통효과(鎭痛效果) 및 그 기전(機轉)에 관(關)한 연구(硏究))

  • Baek, Yong-hyeon;Hong, Seong-hun;Yang, Hyung-in;Park, Dong-suk;Choi, Do-young
    • Journal of Acupuncture Research
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    • v.21 no.2
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    • pp.115-129
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    • 2004
  • Objectives : To investigate the analgesic effect and its cholinergic mechanism of electroacupuncture(EA) in the rat model of collagen-induced arthritis(CIA). Methods : Immunization of male Sprague-Dawley rats with bovine typeII (CII) collagen emulsified in Freund's incomplete adjuvant, followed by a booster injection 14 days later, leads to development of arthritis in more than 70% of rats by 21 days postinjection. After three weeks of first immunization, EA stimulation(2 Hz, 0.07 mA, 0.3 ms) was delivered into Jogsamni($ST_{36}$) for 30 minutes. Analgesic effect was evaluated by tail flick latency(TFL). We compared the analgesic effect of EA with TFLs between pretreatment of normal saline and pretreatment of Atropine (1 mg/kg, intraperitoneal) and Neostigmine ($100{\mu}g/kg$, intraperitoneal) in CIA. Results : 1. TFLs were gradually decreased in CIA as increasing severity of arthritis. 2. Jogsamni($ST_{36}$) EA stimulation in CIA increased TFLs and the effect lasted for 60 minutes. 3. Increased TFLs with Jogsamni($ST_{36}$) EA stimulation were inhibited with pretreatment of atropine in CIA 4. Increased TFLs with Jogsamni($ST_{36}$) EA stimulation did not show an obvious synergistic effect with pretreatment of neostigmine in CIA. Conclusions: Jogsamni($ST_{36}$) EA showed analgesic effects in CIA. The analgesic effects of Jogsamni($ST_{36}$) EA were inhibited by atropine pretreatment and combined application of Jogsamni(ST36) EA and neostigmine did not show an synergistic effect. These observations suggest that intrinsic muscarinic cholinergic pathways represent an important modulating system in pain perception of inflammatory pain in CIA It is suggested that, the active mechanism of analgesic effect in EA may involve the release of acetylcholine in the spinal cord.

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Ameliorating Effects of the Cognitive-Enhancing Korean Herbs on Neurotoxic-Induced Amnesia in Rats (새로운 제형의 치매치료제제의 효능연구)

  • Kim Ji Hyun;Jung Jin Yong;Chae Yoon Byung;Hahm Dae Hyun;Park Yang Jin;Lee Hye Jung;Shim Insop
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.16 no.2
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    • pp.303-310
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    • 2002
  • Ancient Korean physicians have used several oriental herbs to cure dementia and these effects were described in the Korean herbal books. Some cognitive-enhancing oriental herbs have been widely used as a herbal medicine against dementia. However, few of studies have proved their efficacy in treatment for dementia. In the present study, we investigated the effects of herbal compounds, which are mainly consisted of Uncaria sinensis, Corydalis yanhusuo and Acorus gramineus on learning and memory in Mortis water maze task and the central cholinergic system of the rats with neurotoxic medial septum lesion. In water maze test, the animals were trained to find a platform in a fixed position during 6 days and then received a 60-s probe trial in which the platform was removed from the pool on the 7th day. Ibotanic and 192 saporin lesion of the medial septum (MS) impaired the performance of maze test and degenerated choline acetyltransferase (ChAT) in the brain, which is a marker of the central cholinergic system. Daily administrations of herbal medicine (100mg/kg, p.o.) for 21 consecutive days produced significant reversals of the neurotoxic-induced deficit in learning and memory. These treatments also reduced the loss of cholinergic immunoreactive neurons in the brain induced by neurotoxin. These results demonstrated that herbal compounds ameliorated learning and memory deficits through effects on the central nervous system, partly through effect on the acetylcholine system. Our studies suggest an evidence of these herbs as treatment of Alzheimer's disease.