• Biomolecules & Therapeutics
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• 제26권4호
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• pp.368-373
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• 2018

Rapid eye movement (REM) sleep has an essential role in the process of learning and memory in the hippocampus. It has been reported that linalool, a major component of Lavandula angustifolia, has antioxidant, anti-inflammatory, and neuroprotective effects, along with other effects. However, the effect of linalool on the cognitive impairment and behavioral alterations that are induced by REM-sleep deprivation has not yet been elucidated. Several studies have reported that REM-sleep deprivation-induced memory deficits provide a well-known model of behavioral alterations. In the present study, we examined whether linalool elicited an anti-stress effect, reversing the behavioral alterations observed following REM-sleep deprivation in mice. Furthermore, we investigated the underlying mechanism of the effect of linalool. Spatial memory and learning memory were assessed through Y maze and passive avoidance tests, respectively, and the forced swimming test was used to evaluate anti-stress activity. The mechanisms through which linalool improves memory loss and behavioral alterations in sleep-deprived mice appeared to be through an increase in the serotonin levels. Linalool significantly ameliorated the spatial and learning memory deficits, and stress activity observed in sleep-deprived animals. Moreover, linalool led to serotonin release, and cortisol level reduction. Our findings suggest that linalool has beneficial effects on the memory loss and behavioral alterations induced by REM-sleep deprivation through the regulation of serotonin levels.

• The Korean Journal of Physiology and Pharmacology
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• 제4권5호
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• pp.355-359
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• 2000

Cocaine induces immediate early gene expression and behavioral changes by blocking dopamine transporters in the terminals of nigrostriatal neurons in the striatum. The pharmacological role of serotonin 2/1C (5HT2/1C) receptors in cocaine-induced expression of zif268 (NGFI-A, egr1 and Krox-24) mRNA, a member of the zinc finger, was investigated using quantitative in situ hybridization histochemistry in vivo. Behavioral alterations induced by cocaine were also monitored in relation with blockade of the receptors. Systemic injection of ritanserin (1 mg/kg, s.c.), a 5HT2/1C receptor antagonist, did not reverse behavioral alterations and zif268 mRNA gene expression induced by 15 mg/kg cocaine, i.p., in the dorsal and ventral striatum. These data indicate that ritanserin-sensitive 5HT2/1C receptors are not necessary for cocaine-induced behavioral alterations and zif268 mRNA gene expression in the striatum.

• The Korean Journal of Physiology and Pharmacology
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• 제4권5호
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• pp.361-367
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• 2000

Cocaine functions as indirect dopamine and serotonin (5-hydroxytryptamine, 5HT) agonists and induces genomic and behavioral alterations in the striatum. Previously we demonstrated that ritanserin, a 5HT2/1C receptor antagonist, is not responsible for cocaine-induced behavioral alterations and zif268 mRNA gene expression in the striatum (see the previous paper in this issue). In this study, it was hypothesized that dopamine and 5HT2/1C receptors are required for cocaine-induced behavioral alterations and c-fos and zif268 mRNA expression. This hypothesis was addressed by infusing amperozide which antagonizes both 5HT2/1C and dopamine receptors and was analyzed using the quantitative in situ hybridization histochemistry in vivo. Systemic injection of amperozide (5 mg/kg, s.c.) significantly blocked increase in behavior, c-fos and zif268 mRNA expression induced by 15 mg/kg cocaine, i.p., in the dorsal striatum. These data suggest that dopamine and 5HT2/1C receptors are necessary for cocaine-induced behavioral alterations and immediate early gene expression in the dorsal striatum.

• 약학회지
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• 제58권5호
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• pp.300-306
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• 2014

Ethanol consumption causes psychomotor alterations. Hovenia Semen seu Fructus (HS), widely distributed in Korea, China, and Japan, has been reported to have beneficial effects on acute alcohol-induced liver injury. The present study sought to assess the effects of HS extract on ethanol-induced psychomotor alterations in rats. Sprague-Dawley rats were orally (p.o.) given ethanol (4 g/kg) (ethanol group) to induce psychomotor alterations. A separate group (HS-treated groups), were treated with different dosages of HS (50, 100, and 200 mg/kg, p.o.), 30 minutes before ethanol treatment. The control group received only the vehicle (saline). Ethanol-induced psychomotor alterations were evaluated in the open-field, rota-rod, hanging wire, and cold swimming test. In addition, blood ethanol and acetaldehyde concentrations were also measured. Behavioral evaluations and blood analysis were carried out 0.5, 1, 2, 4, and 8 hours after ethanol administration. Pre-treatment of HS ameliorated ethanol-induced alterations in the open-field, rota-rod, and cold swimming test, significantly evident in 2 and 4 hours after ethanol treatment. These improvements coincided with decrease in blood ethanol and acetaldehyde concentration. Based on these results, the present study suggests that HS may have ameliorating effects against ethanol-induced psychomotor alterations.

• Archives of Pharmacal Research
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• 제18권3호
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• pp.146-152
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• 1995

To achieve a better understanding of the effects on behavioral safety caused by possible neuroprotective doses (50 mg/kg, p.o.) of dextromethorphan HBr (DM), several motor activity measures were monitored in two generations of mice through a long-term period of ten months. Adult male mice (G1), in the presence of DM, developed behavioral tolerance after an initial suppression period. Prenatally exposed, second generation (G2) mice formed two groups, prenatal exposure alone (G2C) and prenatally exposed with additional postnatal exposure (G2T). In the presence of DM, group G2T was characterized by significant behavioral impairment; while G2C exhibited behavioral activation. These results suggest that more attention should be given to the prenatal effects of DM on a developing organism.

• 대한약리학회지
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• 제31권2호
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• pp.179-194
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• 1995

This study aimed to determine whether exposure to stress during developmental period causes permanent behavioral and/or neurochemical alterations. Alterations of behavior were studied in young and aged rats which have been exposed to uncontrollable and unpredictable electric shocks on postnatal day(PND) 14 or PND 14 and 21. The concentrations of monoaminergic neurotransmitters were also measured to determine whether the behavioral alterations were accompanied by neurochemical changes. The results obtained are as follows: 1) The rate of increase in body weight was reduced at one day after exposure to the 1st series of shocks on PND14. However, these findings could not be observed after exposure to the 2nd series of shocks on PND 21. 2) Explorative activity decreased at one day after exposure to the 1st series of shocks on PND14. However this findings could not be observed after exposure to the 2nd series of shocks on PND 21. 3) At 100 days of age, there were little changes in the spontaneous locomotor activities measured for consecutive 23 hrs. However, there was positive correlation between the shock number showing the 1st helplessness during receiving the 1st series of shocks and the night time ambulatory activity of females, and was negative correlation between the shock number showing the 1st helplessness during receiving the 1st or 2nd series of shocks on PND 14 or 21 and the night time ambulatory activity of females. 4) At $360{\sim}390$ days of age, night time ambulatory activity decreased in female rats which have been exposed to shocks on PND 14 and 21, but not in males. 5) In the aged female rats, the concentrations of 5-HT, dopamine and their metabolites were not different among groups. However, the ratio of 5-HIAA/5-HT increased in the frontal cortices of rats exposed to shocks on PND 14 and 21. These results demonstrate that the early experience of serious stress results in persistent alterations of behavior accompanying altered neurochemistry, and aging may unmask a subtle neuronal deficit causes by the early experience of serious stress.

• Natural Product Sciences
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• 제20권1호
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• pp.44-50
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• 2014

Laurus nobilis (L. nobilis) is traditionally used as an herbal medicine to treat various diseases. Ethanol (EtOH) consumption entails physiological, mental and psychomotor alterations. The aim of the present study was to assess the effects of L. nobilis in attenuating the EtOH-induced psychomotor alterations. L. nobilis was administered to SD rats, 30 minutes before EtOH administration (4 g/kg), at doses of 25, 50 and 100 mg/kg. Evaluations of psychomotor activity in the open-field, accelerating rota-rod, wire, and swimming ability were done at 1, 2, 4 and 8 hours after EtOH administration. In addition, blood ethanol and acetaldehyde levels were also measured. Pre-treatment of L. nobilis significantly improved EtOH-induced psychomotor alterations and decreased blood ethanol and acetaldehyde levels. These findings suggest that L. nobilis might be an effective substance to attenuate the harmful effects of EtOH, particularly psychomotor alterations, and can potentially be considered as a functional food.

• 약학회지
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• 제58권6호
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• pp.364-370
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• 2014

The aim of this study was to find optimal ratio of herbal extracts to ameliorate ethanol-induced psychomotor alterations. Four mixtures of Laurus nobilis (L. nobilis), Rosa roxburghii (R.R.) and Opuntia ficus indica (OFI) were pretreated 30 minutes before ethanol administration in rats. Behavioral activities were evaluated. Blood ethanol and acetaldehyde levels were also measured. These effects of mixture of R.R (50 mg/kg)+OFI (100 mg/kg)+L.nobilis (100 mg/kg) were better than those of other mixtures. This mixture could be used as an effective substance to develop a functional food.

• Biomolecules & Therapeutics
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• 제31권2호
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• pp.148-160
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• 2023

Depression is a neuropsychiatric disorder associated with persistent stress and disruption of neuronal function. Persistent stress causes neuronal atrophy, including loss of synapses and reduced size of the hippocampus and prefrontal cortex. These alterations are associated with neural dysfunction, including mood disturbances, cognitive impairment, and behavioral changes. Synaptic plasticity is the fundamental function of neural networks in response to various stimuli and acts by reorganizing neuronal structure, function, and connections from the molecular to the behavioral level. In this review, we describe the alterations in synaptic plasticity as underlying pathological mechanisms for depression in animal models and humans. We further elaborate on the significance of phytochemicals as bioactive agents that can positively modulate stress-induced, aberrant synaptic activity. Bioactive agents, including flavonoids, terpenes, saponins, and lignans, have been reported to upregulate brain-derived neurotrophic factor expression and release, suppress neuronal loss, and activate the relevant signaling pathways, including TrkB, ERK, Akt, and mTOR pathways, resulting in increased spine maturation and synaptic numbers in the neuronal cells and in the brains of stressed animals. In clinical trials, phytochemical usage is regarded as safe and well-tolerated for suppressing stress-related parameters in patients with depression. Thus, intake of phytochemicals with safe and active effects on synaptic plasticity may be a strategy for preventing neuronal damage and alleviating depression in a stressful life.

• Molecules and Cells
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• 제40권6호
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• pp.379-385
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• 2017

Drug addiction is a severe psychiatric disorder characterized by the compulsive pursuit of drugs of abuse despite potential adverse consequences. Although several decades of studies have revealed that psychostimulant use can result in extensive alterations of neural circuits and physiology, no effective therapeutic strategies or medicines for drug addiction currently exist. Changes in neuronal connectivity and regulation occurring after repeated drug exposure contribute to addiction-like behaviors in animal models. Among the involved brain areas, including those of the reward system, the striatum is the major area of convergence for glutamate, GABA, and dopamine transmission, and this brain region potentially determines stereotyped behaviors. Although the physiological consequences of striatal neurons after drug exposure have been relatively well documented, it remains to be clarified how changes in striatal connectivity underlie and modulate the expression of addiction-like behaviors. Understanding how striatal circuits contribute to addiction-like behaviors may lead to the development of strategies that successfully attenuate drug-induced behavioral changes. In this review, we summarize the results of recent studies that have examined striatal circuitry and pathway-specific alterations leading to addiction-like behaviors to provide an updated framework for future investigations.