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- 저자 : Yamamoto Tsuneyuki (검색결과 3 건)
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중추도파민신경활성에 미치는 뇌기능개선 후보약물의 행동약리학적 연구
이순철,유관희,山本經之 충남대학교 약학대학 의약품개발연구소 1995 藥學論文集 Vol.11 No.-
The present study was undertaken to elucidate the behavioral characteristics of nootropic candidates, centrophenoxine, N-methyl-D-glucamine, piracetam and red ginseng saponin components on stereotyped sniffing behavior induced by apomorphine in rats. Apomorphine, a direct dopaminergic receptor agonist, induced stereotyped behaviors including sniffing, licking, gnowing and biting in a dose dependent manner, and that behaviors were completely inhibited when measured at 1 week after 6-hydroxydopamine(6-OHDA) treatment. Centrophenoxine, N-methyl-D-glucamine, red ginseng total sapomin (TS), panaxatriol (PT), and Rg_1 enhanced but panaxadiol (PD) inhibited, whereas priacetam and Rb1 were not effective of the stereotyped sniffing behavior induced by apomorphine (1 ㎎/㎏). The enhanced stereotyped behavior by centrophenoxine, N-methyl-D-glucamine, red ginseng total saponin, panaxatriol(PT), and Rg_1 was blocked by pretreatment of 6-OHDA. These results suggest that dopaminergic neuronal activity plays an important role in the action of some nootropic candidates. Red ginseng total saponin, panaxatriol and Rg_1 seems to have a similiarity to centrophenoxine, N-methyl-D-glucamate in modulating of dopaminergic neuronal activity and also may be useful for the nootropic candidates.
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Pharmacological Studies on Aggressive Behavior Induced by Three Different Regional Brain Lesions
이순철,T. 야마모토,S.우에끼,Lee, Soon-Chul,Yamamoto, Tsuneyuki,Ueki, Showa The Korean Society of Pharmacology 1987 대한약리학잡지 Vol.23 No.2
본 연구는 측좌각, 봉선핵 및 후구 등 서로 다른 뇌 부위의 손상으로 야기된 공격성에 대한 약물의 효과를 비교 검토하여 다음과 같은 결과를 얻었다. 1. 측좌각, 봉선핵 및 후구 손상으로 야기된 muricide는 atropine으로 억제되었으나 hyperirritability는 억제되지 않았다. 2. 측좌각, 봉선핵 손상으로 인한 muricide는 L-DOPA, L-5-HTP에 의하여 현저히 억제되었으나 후구 손상으로 인한 muricide는 거의 억제되지 않았다. 3. 측좌각, 봉선핵 및 후구 손상으로 인한 muricide는 항우울제에 의하여 현저히 억제되었다. 특히 측좌각 및 봉선핵 손상으로 인한 muricide 억제에는 nomifensine과 clomipramine이 효과적이었으며 후구 손상으로 인한 muricide 억제에는 imipramine이 가장 효과적이었다. 그러나 hyperirritability는 항우울제에 의하여 거의 억제되지 않았다. 이상의 결과에서 측좌각 손상으로 인한 공격성의 약물학적 특징은 후구보다는 봉선핵 손상으로 인한 공격성과 유사하였으며 muricide 억제에 대한 항우울제의 효과가 서로 다른 것을 이용하여 항우울제의 작용평가에 도움이 될 것으로 사료된다. The effects of various drugs on muricide and hyperirritability induced by bilateral lesions of the nucleus accumbens septi (NAB) were investigated in comparison with those on aggression induced by midbrain raphe nuclei-lesioned rats (raphe) and olfactory bulbectomized rats (OB). Muricide in NAB, raphe and OB rats were markedly suppressed by atropine. Muricide in NAB and raphe rats were significantly suppressed by L-DOPA, L-5-HTP, but muricide in OB rats was scarcely suppressed by L-DOPA and L-5-HTP. Hyperirritability in NAB, raphe and OB rats were significantly reduced by L-DOPA and haloperidol but not suppressed by atropine. On the other hand, muricide in NAB rats was markedly suppressed by antidepressants, particularily, nomifensine, clomipramine and desipramine. Muricide in raphe rats was markedly inhibited by nomifensine and clomipramine but only slightly inhibited by desipramine. Muricide in OB rats was markedly suppressed by imipramine. Hyperirritability in NAB, raphe and OB rats were slightly suppressed by antidepressants. These results suggested that the pharmacological characteristics of aggression induced by NAB rats resembles that induced by raphe rats, but differs from that induced by OB rats. It is also suggested that employment of different types of experimentally induced muricide in rats can be useful for the evaluation of antidepressants.
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Dang, Duy-Khanh,Shin, Eun-Joo,Mai, Anh-Thu,Jang, Choon-Gon,Nah, Seung-Yeol,Jeong, Ji Hoon,Ledent, Catherine,Yamamoto, Tsuneyuki,Nabeshima, Toshitaka,Onaivi, Emmanuel S.,Kim, Hyoung-Chun Elsevier 2017 FREE RADICAL BIOLOGY AND MEDICINE Vol.108 No.-
<P><B>Abstract</B></P> <P>Accumulating evidence suggests that cannabinoid ligands play delicate roles in cell survival and apoptosis decisions, and that cannabinoid CB1 receptors (CB1R) modulate dopaminergic function. However, the role of CB1R in methamphetamine (MA)-induced dopaminergic neurotoxicity in vivo remains elusive. Multiple high doses of MA increased phospho-ERK and CB1R mRNA expressions in the striatum of CB1R (+/+) mice. These increases were attenuated by CB1R antagonists (i.e., AM251 and rimonabant), an ERK inhibitor (U0126), or dopamine D2R antagonist (sulpiride). In addition, treatment with MA resulted in dopaminergic impairments, which were attenuated by CB1R knockout or CB1R antagonists (i.e., AM251 and rimonabant). Consistently, MA-induced oxidative stresses (i.e., protein oxidation, lipid peroxidation and reactive oxygen species) and pro-apoptotic changes (i.e., increases in Bax, cleaved PKCδ- and cleaved caspase 3-expression and decrease in Bcl-2 expression) were observed in the striatum of CB1R (+/+) mice. These toxic effects were attenuated by CB1R knockout or CB1R antagonists. Consistently, treatment with four high doses of CB1R agonists (i.e., WIN 55,212-2 36mg/kg and ACEA 16mg/kg) also resulted in significant oxidative stresses, pro-apoptotic changes, and dopaminergic impairments. Since CB1R co-immunoprecipitates PKCδ in the presence of MA or CB1R agonists, we applied PKCδ knockout mice to clarify the role of PKCδ in the neurotoxicity elicited by CB1Rs. CB1R agonist-induced toxic effects were significantly attenuated by CB1R knockout, CB1R antagonists or PKCδ knockout. Therefore, our results suggest that interaction between D2R, ERK and CB1R is critical for MA-induced dopaminergic neurotoxicity and that PKCδ mediates dopaminergic damage induced by high-doses of CB1R agonist.</P> <P><B>Highlights</B></P> <P> <UL> <LI> MA or CB1R agonists increased CB1R mRNA level in the striatum of wild type mice. </LI> <LI> Inhibition of CB1R attenuated dopaminergic degeneration induced by MA. </LI> <LI> CB1R co-immunoprecipitated PKCδ in the presence of MA or CB1R agonists. </LI> <LI> Oxidative burdens contributed to PKCδ cleavage and apoptotic activity. </LI> <LI> CB1R agonists-induced dopaminergic degeneration was protected by PKCδ inhibition. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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