• 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.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.45-46
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• 1995

Alzheimer's disease is believed to be associated with the loss of cholinergic activity in the cortex and hippocampus. In addition, it has been reported that the monoaminergic systems which also controls brain functions are disturbed in Alzheimer's patients. Based on these neurochemical background, a number of cholinesterase inhibitors including tacrine and its analogues and some monoamine oxidase inhibitors such as L-deprenyl and monoamine reuptake inhibitors have been developed for the treatment of dementia, but all of the known drugs are not truly effective. We thought that a drug that activates only one neurotransmitter system is not effective enough for the treatment of the symptoms associated with Alzheimer's disease and vascular dementia, and we conceived that an agent enhancing both central cholinergic and monoaminergic functions would be useful for the treatment of dementia

• Korean Journal of Veterinary Research
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• v.33 no.1
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• pp.71-80
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• 1993

The central nervous system depressant effect of xylazine and xylazine-ketamine was studied in chicken and mice. Intraperitoneal injection of xylazine(1~30 mg/kg) and xylazine(1~30 mg/kg)-ketamine(100 mg/kg) induced a loss of the righting reflex in chicken and mice, respectively. These effects of xylazine were dose-dependent. The results obtained were as follows; 1. The effect of xylazine-induced depression was antagonized by adrenergic antagonists having ${\alpha}_2$-blocking activity(yohimbine, tolazoline, piperoxan and phentolamine). 2. Yohimbine was most effective in the reduction of the CNS depression by xylazine. 3. Phenoxybenzamine and prazosin did not reduced CNS depression by xylazine in both species. 4. Labetalol (${\alpha}_1$, ${\beta}_1$-adrenergic antagonist) and propranolol(${\beta}$-adrenergic blocking agent) were not effective in reducing xylazine induced depression. 5. Cholinergic blocking agents (atropine and mecamylamine), a dopaminergic antagonist (Haloperidol), a histamine $H_1$-antagonist(chlorpheniramine), a histamine $H_2$-antagonist(cimetidine), a serotonergic-histamine $H_1$ antagonist(cyproheptadine) were not effective in reducing xylazine-induced depression. 6. Xylazine-induced depression is mediated by ${\alpha}_2$-adrenergic receptors and appears not to be involved in cholinergic, dopaminergic, serotonergic or histaminergic pathways.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1151-1156
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• 2002

This research was done to make the effective prescription and cope with various senile dementia. Sprague-Dawley rats were injured by ibotenic acid to make a damage on learning and memory functions of model rats. At first acquisition test and retention rest were done in the Morris water maze. And to evaluate the effects of the sample drug(GSD) on choline acetyltranferase and acetylcholine esterase, immunoreactive measurement and enzymatic activity measuring were carried out. The ibotenic acid were injected to hippocampus CA1 and CA3 area. Conclusion : GSD improved the learning ability in the acquisition test and memory function in the retention test significantly. And GSD increased the level of ChAT which is synthesizing acetylcholine in CA1 area, and at the same time it increased the level of AChE which is resolving acetylcholine. These results show that GSD improved the cholinergic catabolism and anabolism, and the increment of metabolic activity of cholinergic system. In other words, it contributes to the recovery of damaged learning and memory function by ibotenic acid. So it can be concluded that GSD will be helpful to cholinergic brain damage induced by primary or senile reduction of acetylcholine secretive activity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1236-1242
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• 2002

In order to make an efficient prescription and cope with dementia, learning and memory functions of Sprague-Dawley model rats were tested with Morris water maze. And to evaluate the effect of the sample drug(CHM) on choline acetyltranferase and acetylcholine esterase, immunoreactive measurement and enzymatic activity measuring were carried out. Rats were injected with ibotenic acid through hippocampus CA1 and CA3 area. The results are as following. CHM improves the learning ability in the acquisition test and memory function in the retention test significantly. And CHM increases the level of AChE which is resolving acetylcholine. Though it doesn't increase the level of ChAT significantly which is synthesizing acetylcholine, but it shows the tendency of increase. So these results show that CHM improve the cholinergic catabolism and anabolism, and the increment of metabolic activity of cholinergic system. Thus it can be concluded that CHM will be helpful to cholinergic brain disease induced by primary or senile reduction of acetylcholine secretive activity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.2
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• pp.553-559
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• 2003

In order to make the efficient prescription and cope with various senile dementia, learning and memory functions of Sprague-Dawley model rats were tested with Morris water maze at first. And to evaluate the effects of the sample drug(GM) on choline acetyltranferase and acetylcholine esterase, immunoreactive measurement and enzymatic activity measuring were carried out. Rats were injected with ibotenic acid through hippocampus CA1 and CA3 area. The results are as following. GM improves the learning ability in tile acquisition test and memory function in the retention test significantly. And GM increases the level of ChAT which is synthesizing acetylcholine in CA3 area, and at the same time it increases the level of AChE which is resolving acetylcholine. These results show that GM improve the cholinergic catabolism and anabolism, and the increment of metabolic activity of cholinergic system contributes to the recovery of damaged learning and memory function by ibotenic acid. So it can be concluded that GM will be helpful to cholinergic brain disease induced by primary or senile reduction of acetylcholine secretive activity.

• Journal of Life Science
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• v.25 no.10
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• pp.1103-1109
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• 2015

Cholinergic innervation of the hippocampus is known to be correlated with learning and memory. The cholinergic agonist carbachol (CCh) modulate synaptic plasticity and produced long-term synaptic depression (LTD) in the hippocampus. However, the exact mechanisms by which the cholinergic system modifies synaptic functions in the hippocampus have yet to be determined. This study introduces an acetylcholine receptor-mediated LTD that requires internalization of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors on the postsynaptic surface and their intracellular mechanism in the hippocampus. In the present study, we showed that the application of the cholinergic agonist CCh reduced the surface expression of GluA2 on synapses and that this reduction was prevented by the M1 muscarinic acetylcholine receptor antagonist pirenzepine in primary hippocampal neurons. The interaction between GluA2 and the glutamate receptor-interacting protein 1 (GRIP1) was disrupted in a hippocampal slice from a rat upon CCh simulation. Under the same conditions, the binding of GluA2 to adaptin-α, a protein involved in clathrin-mediated endocytosis, was enhanced. The current data suggest that the activation of LTD, mediated by the acetylcholine receptor, requires the internalization of the GluA2 subunits of AMPA receptors and that this may be controlled by the disruption of GRIP1 in the PDZ ligand domain of GluA2. Therefore, we can hypothesize that one mechanism underlying the LTD mediated by the M1 mAChR is the internalization of the GluA2 AMPAR subunits from the plasma membrane in the hippocampal cholinergic system.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.50-56
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• 2003

This research was done to make the effective prescription and cope with various senile dementia. So Sprague-Dawley rats were injected with ibotenate to make a damage on learning and memory functions. At first acquisition test and retention rest were done in the Morris water maze. And to evaluate the effects of the sample drug(TBM) on choline acetyltranferase and acetylcholine esterase, immunoreactive measurement and enzymatic activity measuring were carried out. The ibotenic acid were injected to hippocampus CA1 and CA3 area. The results were as following. TBM improved the learning ability in the acquisition test and memory function in the retention test significantly. And TBM increased the level of ChAT which is synthesizing acetylcholine in CA3 area, and at the same time it increased the level of AChE which is resolving acetylcholine. These results show that T8M improved the cholinergic catabolism and anabolism, and the increment of metabolic activity of cholinergic system. In other words, it contributes to the recovery of damaged learning and memory function by ibotenic acid. So it can be concluded that TBM will be helpful to cholinergic brain damage induced by primary or senile reduction of acetylcholine secretive activity.

• Korean Journal of Veterinary Research
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• v.39 no.3
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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.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.6
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• pp.799-806
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• 2014

The present study was conducted to evaluate the effects of extract from Eriobotrya japonica leaves (EJE) on cognitive impairment induced by scopolamine, a muscarinic antagonist, in rats. Scopolamine injection (1 mg/kg, i.p.) impaired performance in rats in the passive avoidance test as well as in water maze test and severely reduced cholinergic system reactivity, as indicated by reduced acetylcholine levels and increased acetylcholinesterase activity. Daily administration of EJE significantly increased step-through latency in the passive avoidance test, reduced escape latency, and increased time spent in the platform quadrant in the Morris water maze test. EJE protected against scopolamine-induced cholinergic system deficit, including reduced acetylcholine levels and increased acetylcholinesterase activity in whole brain homogenates. These results suggest that EJE provides a significant anti-amnesic effect against scopolamine-induced cholinergic system deficits and cognitive impairment.