• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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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.

• YAKHAK HOEJI
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• v.38 no.4
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• pp.401-409
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• 1994

The cholinergic activity of dammarane glycosides of Panax ginseng was examined both morphologically and chemically on primary cultures of chicken embryonic brain cells. When primary cultured chicken embryonic cells were treated with $50\;{\mu}g/ml$ of total dammarane glycosides of Panax ginseng followed by the exposure to 10mM atropine for 48 hr, lactate dehydrogenase levels within the cells remained at 36% of untreated control values while atropine-treated controls fell to 0% lactate dehydrogenase. It was found that cholinergic activity was mainly exerted by the panaxadiol glycosides. The treatment of the cells with $50\;{\mu}g/ml$ of panaxadiol glycosides followed by the exposure to atropine, lactate dehydrogenase levels within the cells remained at 60% of untreated control values. Ginsenoside $Rb_1$, a component of panaxadiol glycosides, was found to exert the cholinergic activity keeping the lactate dehydrogenase levels within the cells at 70% of untreated control values. The cholinergic activity of ginsenoside $Rb_1$ seems to be exerted through acting on the $Ca^{2+}$ channel in cultured brain cells.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.3
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• pp.169-174
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• 2003

${\gamma}$-Aminobutyric acid (GABA) has been reported to enhance exocrine secretion evoked not only by secretagogues but also by intrinsic neuronal excitation in the pancreas. The pancreas contains cholinergic neurons abundantly that exert a stimulatory role in exocrine secretion. This study was undertaken to examine effects of GABA on an action of cholinergic neurons in exocrine secretion of the pancreas. Intrinsic neurons were excited by electrical field stimulation (EFS; 15 V, 2 msec, 8 Hz, 45 min) in the isolated, perfused rat pancreas. Tetrodotoxin or atropine was used to block neuronal or cholinergic action. Acetylcholine was infused to mimic cholinergic excitation. GABA $(30{\mu}M)$ and muscimol $(10{\mu}M)$, given intra-arterially, did not change spontaneous secretion but enhanced cholecystokinin (CCK; 10 pM)-induced secretions of fluid and amylase. GABA (3, 10, $30{\mu}M$) further elevated EFS-evoked secretions of fluid and amylase dose-dependently. GABA (10, 30, $100{\mu}M$) also further increased acetylcholine $(5{\mu}M)$-induced secretions of fluid and amylase in a dose-dependent manner. Bicuculline $(10{\mu}M)$ effectively blocked the enhancing effects of GABA $(30{\mu}M)$ on the pancreatic secretions evoked by either EFS or CCK. Both atropine $(2{\mu}M)$ and tetrodotoxin $(1{\mu}M)$ markedly reduced the GABA $(10{\mu}M)$-enhanced EFS- or CCK-induced pancreatic secretions. The results indicate that GABA enhances intrinsic cholinergic neuronal action on exocrine secretion via the $GABA_A$ receptors in the rat pancreas.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.185-192
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• 1998

A role of endogenous somatostatin in pancreatic exocrine secretion induced by intrapancreatic cholinergic activation was studied in the isolated rat pancreas perfused with modified Krebs-Henseleit solution. Intrapancreatic neurons were activated by electrical field stimulation (EFS: 15 V, 2 msec and 8 Hz). Pancreatic exocrine secretion, including volume flow and amylase output, and release of somatostatin from the pancreas were respectively determined. Somatostatin cells in the islet were stained with an immunoperoxidase method. EFS significantly increased pancreatic volume flow and amylase output, which were reduced by atropine by 59% and 78%, respectively. Intraarterial infusion of either pertussis toxin or a somatostatin antagonist resulted in a further increase in the EFS-evoked pancreatic secretion. EFS also further elevated exocrine secretion in the pancreas treated with cysteamine, which was completely restored by intraarterial infusion of somatostatin. EFS significantly increased not only the number of immunoreactive somatostatin cells in the islet but also the concentration of immunoreactive somatostatin in portal effluent. It is concluded from the above results that intrapancreatic cholinergic activation elevates pancreatic exocrine secretion as well as release of endogenous somatostatin. Endogenous somatostatin exerts an inhibitory influence on exocrine secretion induced by intrapancreatic cholinergic activation via the islet-acinar portal system in the isolated pancreas of the rat.

• 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.

• Anatomy and Cell Biology
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• v.51 no.4
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• pp.266-273
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• 2018

The ganglion cardiacum or juxtaductal body is situated along the left recurrent laryngeal nerve in the aortic window and is an extremely large component of the cardiac nerve plexus. This study was performed to describe the morphologies of the ganglion cardiacum or juxtaductal body in human fetuses and to compare characteristics with intracardiac ganglion. Ganglia were immunostained in specimens from five fetuses of gestational age 12-16 weeks and seven fetuses of gestational age 28-34 weeks. Many ganglion cells in the ganglia were positive for tyrosine hydroxylase (TH; sympathetic nerve marker) and chromogranin A, while a few neurons were positive for neuronal nitric oxide synthase (NOS; parasympathetic nerve marker) or calretinin. Another ganglion at the base of the ascending aorta carried almost the same neuronal populations, whereas a ganglion along the left common cardinal vein contained neurons positive for chromogranin A and NOS but no or few TH-positive neurons, suggesting a site-dependent difference in composite neurons. Mixtures of sympathetic and parasympathetic neurons within a single ganglion are consistent with the morphology of the cranial base and pelvic ganglia. Most of the intracardiac neurons are likely to have a non-adrenergic non-cholinergic phenotype, whereas fewer neurons have a dual cholinergic/noradrenergic phenotype. However, there was no evidence showing that chromogranin A- and/or calretinin-positive cardiac neurons corresponded to these specific phenotypes. The present study suggested that the ganglion cardiacum was composed of a mixture of sympathetic and parasympathetic neurons, which were characterized the site-dependent differences in and near the heart.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.5
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• pp.317-328
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• 2019

It is known that top-down associative inputs terminate on distal apical dendrites in layer 1 while bottom-up sensory inputs terminate on perisomatic dendrites of layer 2/3 pyramidal neurons (L2/3 PyNs) in primary sensory cortex. Since studies on synaptic transmission in layer 1 are sparse, we investigated the basic properties and cholinergic modulation of synaptic transmission in layer 1 and compared them to those in perisomatic dendrites of L2/3 PyNs of rat primary visual cortex. Using extracellular stimulations of layer 1 and layer 4, we evoked excitatory postsynaptic current/potential in synapses in distal apical dendrites (L1-EPSC/L1-EPSP) and those in perisomatic dendrites (L4-EPSC/L4-EPSP), respectively. Kinetics of L1-EPSC was slower than that of L4-EPSC. L1-EPSC showed presynaptic depression while L4-EPSC was facilitating. In contrast, inhibitory postsynaptic currents showed similar paired-pulse ratio between layer 1 and layer 4 stimulations with depression only at 100 Hz. Cholinergic stimulation induced presynaptic depression by activating muscarinic receptors in excitatory and inhibitory synapses to similar extents in both inputs. However, nicotinic stimulation enhanced excitatory synaptic transmission by ~20% in L4-EPSC. Rectification index of AMPA receptors and AMPA/NMDA ratio were similar between synapses in distal apical and perisomatic dendrites. These results provide basic properties and cholinergic modulation of synaptic transmission between distal apical and perisomatic dendrites in L2/3 PyNs of the visual cortex, which might be important for controlling information processing balance depending on attentional state.

• Journal of Microbiology and Biotechnology
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• v.21 no.8
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• pp.874-883
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• 2011

Many studies have shown that the steamed root of Rehmannia glutinosa (SRG), which is widely used in the treatment of various neurodegenerative diseases in the context of Korean traditional medicine, is effective for improving cognitive and memory impairments. The purpose of this study was to examine whether SRG extracts improved memory defects caused by administering scopolamine (SCO) into the brains of rats. The effects of SRG on the acetylcholinergic system and proinflammatory cytokines in the hippocampus were also investigated. Male rats were administered daily doses of SRG (50, 100, and 200 mg/kg, i.p.) for 14 days, 1 h before scopolamine injection (2 mg/kg, i.p.). After inducing cognitive impairment via scopolamine administration, we conducted a passive avoidance test (PAT) and the Morris water maze (MWM) test as behavioral assessments. Changes in cholinergic system reactivity were also examined by measuring the immunoreactive neurons of choline acetyltransferase (ChAT) and the reactivity of acetylcholinesterase (AchE) in the hippocampus. Daily administration of SRG improved memory impairment according to the PAT, and reduced the escape latency for finding the platform in the MWM. The administration of SRG consistently significantly alleviated memory-associated decreases in cholinergic immunoreactivity and decreased interleukin-$1{\beta}$ (IL-$1{\beta}$) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) mRNA expression in the hippocampus. The results demonstrated that SRG had a significant neuroprotective effect against the neuronal impairment and memory dysfunction caused by scopolamine in rats. These results suggest that SRG may be useful for improving cognitive functioning by stimulating cholinergic enzyme activities and alleviating inflammatory responses.

• Journal of Nutrition and Health
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• v.32 no.8
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• pp.864-869
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• 1999

To investigate the effect of dietary phosphatidylcholine(PPC) supplement on memory improvement, biochemical study on the brain, and morphometric studies on the cholinergic neurons in the rat basal forebrain were undertaken. The pregnancy rats were divided into the normal control, the choline deficient and the PPC supplemental groups according to quantity of the PPC in diet. According to choline deficiency and PPC supplement after birth, the neonate rate of the normal control group were subdivided into the control diet(N-N) and the PPC supplied (N-S) groups, the choline deficient group were subdivided into the continually deficient (D-D), the control diet(D-N) and the PPC supplied groups(D-S), and the PPC supplemental group were subdivided into the control diet (S-N)and the continually supplied (S-S)group. The PPC supplemented diet was added 2% egg PPC in AIN 76 formula diet. PPC concentrations and cholinesterase(CE) activities were measured in the serum, the liver and the brain, respectively. Immunohistochemical stains for choline acetyltransferase(ChAT) was employed for the morphological and morphometric studies. The maze test was undertaken to evaluate memory improvement. PPC concentration and CE activities in the serum, liver and the brain were high in the PPC supplemental groups and low in the choline deficient groups. ChAT immunoreactivity neurons at the medial septal diagonal bond complex and the basal forebrain nucleus of Meynert were reduced in the choline deficient groups. Average failure rate for the maze test was the lowest in the S-S group and the highest in the D-D group. Insufficient choline suppley during the neuronal development would result in cholinergic neuronal damage, which could be prevented by adequate PPC supplement. It is consequently suggested that PPC supplement may be effective on memory improvement by maintaining the cholinergic neuronal activity in the basal forebrain of the rats.