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- 1. 遅発性ジスキネジア：予防および治療 tardive dyskinesia prevention and treatment
- 2. ハンチントン病：管理 huntington disease management
- 3. 統合失調症に対する薬物療法：副作用マネージメント pharmacotherapy for schizophrenia side effect management
- 4. 米国外の緩和ケアとホスピス palliative care and hospice outside of the united states
- 5. レット症候群 rett syndrome
- Overexpression of the dopamine D3 receptor in the rat dorsal striatum induces dyskinetic behaviors.
- Cote SR1, Chitravanshi VC2, Bleickardt C1, Sapru HN2, Kuzhikandathil EV3.Author information 1Department of Pharmacology and Physiology, Rutgers-New Jersey Medical School, Newark, NJ 07101, USA.2Department of Neurological Surgery, Rutgers-New Jersey Medical School, Newark, NJ 07101, USA.3Department of Pharmacology and Physiology, Rutgers-New Jersey Medical School, Newark, NJ 07101, USA. Electronic address: firstname.lastname@example.org.Abstractl-DOPA-induced dyskinesias (LID) are motor side effects associated with treatment of Parkinson's disease (PD). The etiology of LID is not clear; however, studies have shown that the dopamine D3 receptor is upregulated in the basal ganglia of mice, rats and non-human primate models of LID. It is not known if the upregulation of D3 receptor is a cause or result of LID. In this paper we tested the hypothesis that overexpression of the dopamine D3 receptor in dorsal striatum, in the absence of dopamine depletion, will elicit LID. Replication-deficient recombinant adeno-associated virus-2 expressing the D3 receptor or enhanced green fluorescent protein (EGFP) were stereotaxically injected, unilaterally, into the dorsal striatum of adult rats. Post-hoc immunohistochemical analysis revealed that ectopic expression of the D3 receptor was limited to neurons near the injection sites in the dorsal striatum. Following a 3-week recovery period, rats were administered saline, 6mg/kg l-DOPA, 0.1mg/kg PD128907 or 10mg/kg ES609, i.p., and motor behaviors scored. Rats overexpressing the D3 receptor specifically exhibited contralateral axial abnormal involuntary movements (AIMs) following administration of l-DOPA and PD128907 but not saline or the novel agonist ES609. Daily injection of 6mg/kg l-DOPA to the rats overexpressing the D3 receptor also caused increased vacuous chewing behavior. These results suggest that overexpression of the D3 receptor in the dorsal striatum results in the acute expression of agonist-induced axial AIMs and chronic l-DOPA-induced vacuous chewing behavior. Agonists such as ES609 might provide a novel therapeutic approach to treat dyskinesia.
- Behavioural brain research.Behav Brain Res.2014 Apr 15;263:46-50. doi: 10.1016/j.bbr.2014.01.011. Epub 2014 Jan 23.
- l-DOPA-induced dyskinesias (LID) are motor side effects associated with treatment of Parkinson's disease (PD). The etiology of LID is not clear; however, studies have shown that the dopamine D3 receptor is upregulated in the basal ganglia of mice, rats and non-human primate models of LID. It is not
- PMID 24462727
- Sustained Increase of PKA Activity in the Postcommissural Putamen of Dyskinetic Monkeys.
- Azkona G1, Marcilla I, López de Maturana R, Sousa A, Pérez-Navarro E, Luquin MR, Sanchez-Pernaute R.Author information 1Animal Model Unit, Inbiomed, San Sebastian, Spain.AbstractLevodopa-induced dyskinesias (LID) are a frequent complication of Parkinson's disease pharmacotherapy that causes significant disability and narrows the therapeutic window. Pharmacological management of LID is challenging partly because the precise molecular mechanisms are not completely understood. Here, our aim was to determine molecular changes that could unveil targetable mechanisms underlying this drug complication. We examined the expression and downstream activity of dopamine receptors (DR) in the striatum of 1-methyl-4-phenyl-1,2,3,6 tetrahydropiridine (MPTP)-lesioned monkeys with and without L-DOPA treatment. Four monkeys were made dyskinetic and other four received a shorter course of L-DOPA and did not develop LID. Our results show that L-DOPA treatment induces an increase in DRD2 and DRD3 expression in the postcommissural putamen, but only DRD3 is correlated with the severity of LID. Dyskinetic monkeys show a hyperactivation of the canonical DRD1-signaling pathway, measured by an increased phosphorylation of protein kinase A (PKA) and its substrates, particularly DARPP32. In contrast, activation of the DRD2-signaling pathway, visible in the levels of Akt phosphorylated on Thr308 and GSK3β on Ser9, is associated with L-DOPA treatment, independently of the presence of dyskinesias. Our data clearly demonstrate that dyskinetic monkeys present a dysregulation of the DRD3 receptor and the DRD1 pathway with a sustained increase of PKA activity in the postcommissural putamen. Importantly, we found that all signaling changes related to long-term L-DOPA administration are exquisitely restricted to the postcommissural putamen, which may be related to the recurrent failure of pharmacological approaches.
- Molecular neurobiology.Mol Neurobiol.2014 Apr 5. [Epub ahead of print]
- Levodopa-induced dyskinesias (LID) are a frequent complication of Parkinson's disease pharmacotherapy that causes significant disability and narrows the therapeutic window. Pharmacological management of LID is challenging partly because the precise molecular mechanisms are not completely understood.
- PMID 24705818
- Quadruple deep brain stimulation in Huntington's disease, targeting pallidum and subthalamic nucleus: case report and review of the literature.
- Gruber D1, Kuhn AA, Schoenecker T, Kopp UA, Kivi A, Huebl J, Lobsien E, Mueller B, Schneider GH, Kupsch A.Author information 1Department of Neurology, Charité-University Medicine Berlin, Campus Virchow Klinikum, Augustenburger Platz 1, 13353, Berlin, Germany, email@example.com.AbstractDeep brain stimulation (DBS) represents an established treatment option in a growing number of movement disorders. Recent case reports suggest beneficial effect of globus pallidus internus (GPi)-DBS in selected patients suffering from Huntington's disease with marked disabling chorea. We present a 41-year-old man with genetically confirmed HD following quadruple GPi- and subthalamic nucleus (STN)-DBS. Motor function was assessed by Abnormal Involuntary Movement Scale (AIMS) and by Unified Huntington Disease Rating Scale (UHDRS) presurgery and postsurgery for up to 4 years. Furthermore, cognitive, neuropsychiatric state and quality of life (QoL) including life satisfaction (QLS) were annually evaluated. Chorea assessed by AIMS and UHDRS subscores improved by 52 and 55 %, 45 and 60 %, 35 and 45 % and 55-66 % at 1-4 years, respectively, compared to presurgical state following GPi-STN-DBS. During these time periods bradykinesia did not increase following separate STN- and combined GPi-STN-DBS compared to presurgical state. Mood, QoL and QLS were ameliorated. However, dysexecutive symptoms increased at 4 years postsurgery. The present case report suggests that bilateral GPi- and STN-DBS may represent a new treatment avenue in selected HD patients. Clinically, GPi-DBS attenuated chorea and was associated with a larger effect-adverse effect window compared to STN-DBS. However, GPi-DBS-induced bradykinesia may emerge as one main limitation of GPi-DBS in HD. Thus, quadruple GPi-STN-DBS may be indicated, if separate GPi-DBS does not result in sufficient control of motor symptoms. Future controlled studies need to confirm if the present anecdotal observation of additive beneficial effects of GPi- and STN-DBS in a HD patient with severe generalized chorea and relatively intact cognitive and affective functions indeed represents a new therapeutic option.
- Journal of neural transmission (Vienna, Austria : 1996).J Neural Transm.2014 Apr 4. [Epub ahead of print]
- Deep brain stimulation (DBS) represents an established treatment option in a growing number of movement disorders. Recent case reports suggest beneficial effect of globus pallidus internus (GPi)-DBS in selected patients suffering from Huntington's disease with marked disabling chorea. We present a 4
- PMID 24699718
- Cortical activities associated with voluntary movements and involuntary movements.
- Shibasaki Hiroshi
- Clinical neurophysiology 123(2), 229-243, 2012-02
- … Recent advance in non-invasive techniques including electrophysiology and functional neuroimaging has enabled investigation of control mechanism of voluntary movements and pathophysiology of involuntary movements in human. …
- NAID 120003824943
- 大石 誠也,浅井 信吉,蔡 東生
- 情報処理学会研究報告. グラフィクスとCAD研究会報告 2011-CG-145(16), 1-6, 2011-11-10
- UNESCO 世界遺産にも登録されている龍安寺の石庭は枯山水庭園の代表的庭園と言われ,年間に多くの参観者が訪れる.龍安寺石庭は 15 個の石が白い砂の上に抽象的にちりばめられたシンプルな庭園である.本稿では龍安寺にて行われたアイ・トラッキング実験のデータから,二種類の眼球運動に注目した 2 通りの解析を行う.1 つ目は跳躍運動に注目した解析で,石 (もしくは石群) から石 (もしくは石群) への視 …
- NAID 110008682569
- This failure is particularly glaring given that some European countries, by participating in NATO operations in Libya, have been party to the very conflict that has been one of the main causes of the involuntary movement of people.
- Involuntary movement is movement that is not under the control of the brain. ... Name Phone number with area code * Email address Was your baby breathing after birth? Yes No Did your baby have seizures after birth? Yes No ...
- abnormal movement、asterixis、ballismus、dyskinesia、hemiballismus、involuntary movement
- 体外成熟培養法 in vitro maturation
- 生体顕微鏡 biomicroscopy、in vivo microscope、in vivo microscopy
- 不随意運動 involuntary movement
- social movement, front
- nonvoluntary, unvoluntary