• 한국동물위생학회지
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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.

• BMB Reports
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• 제28권2호
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• pp.155-161
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• 1995

A nicotinic acetylcholine receptor (nAchR) isolated from the electric tissues of Torpedo californica has been reconstituted into a vesicle comprising a bifunctional azo-ligand (Bae 1) compound, and a liposome containing phospholipids and cholesterol (1 : 1, w/w). The liposome-mediated reconstituted receptor showed a concentration-dependent response to cholinergic drugs in a lithium ion flux assay. This liposome-mediated reconstituted nAchR was immobilized onto an electrode using various synthetic polymers which were tested for their response to the cholinergic ligands. The immobilized nAchR not only exhibited a linear response to a wide range of cholinergic ligand concentrations but also retained an operational stability which lasted for longer than 6 days. Thus, this result provides a basis for application of the immobilized nAchR-based biosensor in detecting cholinergic ligands in vitro.

• Journal of Acupuncture Research
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• 제28권1호
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• pp.37-44
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• 2011

배경 및 목적 : 봉독약침요법(bee venom pharmacopuncture, BVP)은 rheumatoid arthritis(RA)의 치료에 활용되고 있으나, RA로 인한 염증성 통증에 대한 봉독약침의 진통효과와 specific mechanism은 아직까지 명확하게 밝혀지지 않았다. 이에 본 연구에서는 RA animal model로서 collagen-induced arthritis(CIA) rat model에서 봉독약침의 a1-adrenergic, 5HT-3 그리고 muscarinic cholinergic mechanism을 확인하고자 한다. 방법 : CIA를 유도하기 위하여 male Sprague-Dawley rat에 freund's incomplete adjuvant에 유화(乳化)시킨 bovine type II collagen을 주입하고 14일 후 booster injection 시행하였다. 진통효과는 tail flick latency (TFL)로 평가하였다. 결과 : 관절염의 유도 이후 염증성 통증 역치는 시간이 지나면서 낮아지며, 5주 이후로는 통증 역치에 큰 변화가 없이 유지되었다. 첫 번째 immunization으로부터 5주 경과 후 족삼리($ST_{36}$)에 봉독약침처치(0.25 mg/ kg)를 시행하여 유의한 진통효과를 관찰하였다. 또한 봉독약침의 진통효과는 ondansetron(5HT-3 receptor antagonist, 0.5mg/kg, i.p.), atropine(muscarinic cholinergic receptor antagonist, 1mg/kg, i.p.)의 전처치에 의하여 억제되었으나, prazosin(a1-adrenergic receptor antagonist, 1mg/kg, i.p.)의 전처치에 의해서는 억제되지 않았다. 결론 : 봉독약침은 CIA로 인한 염증성 통증에 유의한 진통효과를 나타내며 그 analgesic mechanism은 5HT-3와 muscarinic cholinergic receptor에 의하여 매개되며 a1-adrenergic receptor에 의하여 매개되지는 않았다.

• The Korean Journal of Physiology and Pharmacology
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• 제6권2호
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• pp.63-70
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• 2002

Cholinergic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) by the activation of muscarine receptors was investigated in mechanically dissociated rat nucleus basalis of the Meynert neurons using the conventional whole-cell patch recording configuration. Muscarine $(10{\mu}M)$ reversibly and concentration-dependently decreased mIPSC frequency without affecting the current amplitude distribution. Muscarine action on GABAergic mIPSCs was completely blocked by $1{\mu}M$ methoctramine, a selective $M_2$ receptor antagonist, but not by $1{\mu}M$ pirenzepine, a selective $M_1$ receptor antagonist. NEM $(10{\mu}M),$ a G-protein uncoupler, attenuated the inhibitory action of muscarine on GABAergic mIPSC frequency. Muscarine still could decrease GABAergic mIPSC frequency even in the $Ca^{2+}-free$ external solution. However, the inhibitory action of muscarine on GABAergic mIPSCs was completely occluded in the presence of forskolin. The results suggest that muscarine acts presynaptically and reduces the probability of spontaneous GABA release, and that such muscarine-induced inhibitory action seems to be mediated by G-protein-coupled $M_2$ receptors, via the reduction of cAMP production. Accordingly, $M_2$ receptor-mediated disinhibition of nBM neurons might play one of important roles in the regulation of cholinergic outputs from nBM neurons as well as the excitability of nBM neurons themselves.

• 생명과학회지
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• 제25권10호
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• pp.1103-1109
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• 2015

뇌 해마의 콜린성 신경분포는 학습과 기역에 연관성이 있는 것으로 알려져 있으며 이의 작용제인 carbachol 투여 시 장기기억 저하가 유도됨이 알려져 왔다. 그러나 이러한 콜린성 자극에 의한 해마 신경세포의 시냅스 내 변화기작은 완전히 알려지지 않고 있다. 본 연구에서는 아세틸콜린 수용체의 활성에 의하여 유도되는 장기기억 저하 현상에 있어 alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) 수용체가 후시냅스 표면으로부터 사라지는 현상과 이의 조절기작에 대하여 알아보고자 한다. 이를 위하여 쥐 해마의 일차세포를 추출하고 체외에서 배양한 성숙 신경세포에 carbachol 을 투여하여 장기기억 저하를 유도 하였으며, 후시냅스의 표면으로부 터 AMPA 수용체의 아단위체인 GluA2가 M1 무스카린 수용체의 길항제에 의하여 저해 되었다. 또한 콜린성 자극 에 의한 GluA2의 내재화 현상의 작용기작 연구를 위하여 쥐 해마 절편에 carbachol 투여 후 GluA2와 직접적인 상호작용을 하는 Glutam내재화 되었음을 확인하였다. 이러한 현상은 ate receptor-interacting protein 1 (GRIP1) 과 clathrine 단백질이 매개하는 세포내이입 작용을 하는 adaptin-α 단백질의 결합 변화를 관찰하였다. GluA2는 carbachol 자극에 의해 세포내이입 과정에서 adaptin-α 와의 결합이 증가하였으며 반대로 GRIP1과는 해리되었다. 이는 아세틸콜린의 수용체의 자극에 의하여 GluA2의 내제화 작용이 수반되며, 이의 작용기작으로 GluA2의 후시 냅스 표면 발현시에 결합하고 있는 GRIP1과 해리 되면서 장기기억 저하 현상이 유도됨을 의미한다.

• 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.

• Molecules and Cells
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• 제38권9호
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• pp.796-805
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• 2015

Gintonin is a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand. Oral administration of gintonin ameliorates learning and memory dysfunctions in Alzheimer's disease (AD) animal models. The brain cholinergic system plays a key role in cognitive functions. The brains of AD patients show a reduction in acetylcholine concentration caused by cholinergic system impairments. However, little is known about the role of LPA in the cholinergic system. In this study, we used gintonin to investigate the effect of LPA receptor activation on the cholinergic system in vitro and in vivo using wild-type and AD animal models. Gintonin induced $[Ca^{2+}]_i $ transient in cultured mouse hippocampal neural progenitor cells (NPCs). Gintonin-mediated $[Ca^{2+}]_i $ transients were linked to stimulation of acetylcholine release through LPA receptor activation. Oral administration of gintonin-enriched fraction (25, 50, or 100 mg/kg, 3 weeks) significantly attenuated scopolamine-induced memory impairment. Oral administration of gintonin (25 or 50 mg/kg, 1 2 weeks) also significantly attenuated amyloid-${\beta}$ protein ($A{\beta}$)-induced cholinergic dysfunctions, such as decreased acetylcholine concentration, decreased choline acetyltransferase (ChAT) activity and immunoreactivity, and increased acetylcholine esterase (AChE) activity. In a transgenic AD mouse model, long-term oral administration of gintonin (25 or 50 mg/kg, 3 months) also attenuated AD-related cholinergic impairments. In this study, we showed that activation of G protein-coupled LPA receptors by gintonin is coupled to the regulation of cholinergic functions. Furthermore, this study showed that gintonin could be a novel agent for the restoration of cholinergic system damages due to $A{\beta}$ and could be utilized for AD prevention or therapy.

• International Journal of Oral Biology
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• 제46권1호
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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.

• 대한수의학회지
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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.

• 한국동물위생학회지
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• 제18권3호
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• pp.29-35
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• 1995

The effects of prostaglandin $F_2{\alpha}$ were investigated on the uterine smooth muscle motility in the pig. The results were summarized as follows : 1. Prostaglandin $F_2{\alpha}$ caused the contraction of the porcine uterine smooth muscle and the contractile responses increased between the concentration of prostaglandine $F_2{\alpha}$ $10^{-9}$ M and $5{\times}10^{-8}$ M with a dose-dependent manner. 2. The contractile response induced by prostaglandine $F_2{\alpha}$($10^{-8}$ M) was not blocked by pre-treatment with cholinergic receptor blocker, atropine ($10^{-6}$ M). 3. The contractile response induced by prostaglandine $F_2{\alpha}$(10$^{-8}$ M) was not blocked by pretreament with ${\alpha}$-adrenergic receptor blocker, phentolamine($10^{-6}$ M) and ${\beta}$-adrenergic receptor blocker, propranolol($10^{-6}$ M). From these results, it was concluded that the effects of uterine smooth muscle by prostaglandine $F_2{\alpha}$ were only the contraction mediated by prostaglandine TEX>$F_2{\alpha}$ receptor in pig, and that it may not be related to the cholinergic and adrenergic receptor.