이 작품은 외교 계열과 국제 무역 (캐나다 정부), 토론토 Connaught 펀드, 혁신, NSERC, Krembil 재단과 치료 파킨슨병 Trust와 캐나다 재단의 대학에 의해 지원되었다.

<ol>
	<li>Costall, B., Naylor, R. J., Pycock, C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Non-specific+supersensitivity+of+striatal+dopamine+receptors+after+6-hydroxydopamine+lesion+of+the+nigrostriatal+pathway.">Non-specific supersensitivity of striatal dopamine receptors after 6-hydroxydopamine lesion of the nigrostriatal pathway.</a> Eur. J. Pharmacol. 35, 276-283 (1976).</li><li>Maneuf, Y. P., Mitchell, I. J., Crossman, A. R., Brotchie, J. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=On+the+role+of+enkephalin+cotransmission+in+the+GABAergic+striatal+efferents+to+the+globus+pallidus.">On the role of enkephalin cotransmission in the GABAergic striatal efferents to the globus pallidus.</a> Exp. Neurol. 125, 65-71 (1994).</li><li>Robertson, G. S., Robertson, H. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Evidence+that+L-dopa-induced+rotational+behavior+is+dependent+on+both+striatal+and+nigral+mechanisms.">Evidence that L-dopa-induced rotational behavior is dependent on both striatal and nigral mechanisms.</a> J. Neurosci. 9, 3326-3331 (1989).</li><li>Ungerstedt, U., Arbuthnott, G. W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Quantitative+recording+of+rotational+behavior+in+rats+after+6-hydroxy-dopamine+lesions+of+the+nigrostriatal+dopamine+system.">Quantitative recording of rotational behavior in rats after 6-hydroxy-dopamine lesions of the nigrostriatal dopamine system.</a> Brain Res. 24, 485-493 (1970).</li><li>Brotchie, J. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Novel+approaches+to+the+symptomatic+treatment+of+parkinsonian+syndromes:+alternatives+and+adjuncts+to+dopamine-replacement.">Novel approaches to the symptomatic treatment of parkinsonian syndromes: alternatives and adjuncts to dopamine-replacement.</a> Curr. Opin. Neurol. 10, 340-345 (1997).</li><li>Besson, M. J., Graybiel, A. M., Nastuk, M. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=[3H]SCH+23390+binding+to+D1+dopamine+receptors+in+the+basal+ganglia+of+the+cat+and+primate:+delineation+of+striosomal+compartments+and+pallidal+and+nigral+subdivisions.">[3H]SCH 23390 binding to D1 dopamine receptors in the basal ganglia of the cat and primate: delineation of striosomal compartments and pallidal and nigral subdivisions.</a> Neuroscience. 26, 101-119 (1988).</li><li>Gerfen, C. R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=D1+and+D2+dopamine+receptor-regulated+gene+expression+of+striatonigral+and+striatopallidal+neurons.">D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons.</a> Science. 250, 1429-1432 (1990).</li><li>Schiffmann, S. N., Jacobs, O., Vanderhaeghen, J. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Striatal+restricted+adenosine+A2+receptor+(RDC8)+is+expressed+by+enkephalin+but+not+by+substance+P+neurons:+an+in+situ+hybridization+histochemistry+study.">Striatal restricted adenosine A2 receptor (RDC8) is expressed by enkephalin but not by substance P neurons: an in situ hybridization histochemistry study.</a> J. Neurochem. 57, 1062-1067 (1991).</li><li>Hutchison, W. D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Differential+neuronal+activity+in+segments+of+globus+pallidus+in+Parkinson's+disease+patients.">Differential neuronal activity in segments of globus pallidus in Parkinson's disease patients.</a> Neuroreport. 5, 1533-1537 (1994).</li><li>Pan, H. S., Penney, J. B., Young, A. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Gamma-aminobutyric+acid+and+benzodiazepine+receptor+changes+induced+by+unilateral+6-hydroxydopamine+lesions+of+the+medial+forebrain+bundle.">Gamma-aminobutyric acid and benzodiazepine receptor changes induced by unilateral 6-hydroxydopamine lesions of the medial forebrain bundle.</a> J. Neurochem. 45, 1396-1404 (1985).</li><li>Pan, H. S., Walters, J. R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Unilateral+lesion+of+the+nigrostriatal+pathway+decreases+the+firing+rate+and+alters+the+firing+pattern+of+globus+pallidus+neurons+in+the+rat.">Unilateral lesion of the nigrostriatal pathway decreases the firing rate and alters the firing pattern of globus pallidus neurons in the rat.</a> Synapse. 2, 650-656 (1988).</li><li>Gong, S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=A+gene+expression+atlas+of+the+central+nervous+system+based+on+bacterial+artificial+chromosomes.">A gene expression atlas of the central nervous system based on bacterial artificial chromosomes.</a> Nature. 425, 917-925 (2003).</li><li>Kreitzer, A. C., Malenka, R. C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Endocannabinoid-mediated+rescue+of+striatal+LTD+and+motor+deficits+in+Parkinson's+disease+models.">Endocannabinoid-mediated rescue of striatal LTD and motor deficits in Parkinson's disease models.</a> Nature. 445, 643-647 (2007).</li><li>Shen, W., Flajolet, M., Greengard, P., Surmeier, D. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Dichotomous+dopaminergic+control+of+striatal+synaptic+plasticity.">Dichotomous dopaminergic control of striatal synaptic plasticity.</a> Science. 321, 848-851 (2008).</li><li>Lundblad, M., Picconi, B., Lindgren, H., Cenci, M. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=A+model+of+L-DOPA-induced+dyskinesia+in+6-hydroxydopamine+lesioned+mice:+relation+to+motor+and+cellular+parameters+of+nigrostriatal+function.">A model of L-DOPA-induced dyskinesia in 6-hydroxydopamine lesioned mice: relation to motor and cellular parameters of nigrostriatal function.</a> Neurobiol. Dis. 16, 110-123 (2004).</li><li>Grealish, S., Mattsson, B., Draxler, P., Bjorklund, A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Characterisation+of+behavioural+and+neurodegenerative+changes+induced+by+intranigral+6-hydroxydopamine+lesions+in+a+mouse+model+of+Parkinson's+disease.">Characterisation of behavioural and neurodegenerative changes induced by intranigral 6-hydroxydopamine lesions in a mouse model of Parkinson's disease.</a> Eur. J. Neurosci. 31, 2266-2278 (2010).</li><li>Dauer, W., Przedborski, S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Parkinson's+disease:+mechanisms+and+models.">Parkinson's disease: mechanisms and models.</a> Neuron. 39, 889-909 (2003).</li><li>Francardo, V. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Impact+of+the+lesion+procedure+on+the+profiles+of+motor+impairment+and+molecular+responsiveness+to+L-DOPA+in+the+6-hydroxydopamine+mouse+model+of+Parkinson's+disease.">Impact of the lesion procedure on the profiles of motor impairment and molecular responsiveness to L-DOPA in the 6-hydroxydopamine mouse model of Parkinson's disease.</a> Neurobiol. Dis. 42, 327-340 (2011).</li><li>Jakowec, M. W., Petzinger, G. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned+model+of+parkinson's+disease,+with+emphasis+on+mice+and+nonhuman+primates.">1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned model of parkinson's disease, with emphasis on mice and nonhuman primates.</a> Comp. Med. 54, 497-513 (2004).</li><li>Visanji, N. P., Brotchie, J. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=MPTP-Induced+Models+of+Parkinson's+Disease+in+Mice+and+Non-Human+Primates.">MPTP-Induced Models of Parkinson's Disease in Mice and Non-Human Primates.</a> Curr. Protoc. Pharmacol. Chapter 5, 42-42 (2005).</li><li>Sedelis, M., Schwarting, R. K., Huston, J. P. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Behavioral+phenotyping+of+the+MPTP+mouse+model+of+Parkinson's+disease.">Behavioral phenotyping of the MPTP mouse model of Parkinson's disease.</a> Behav. Brain Res. 125, 109-125 (2001).</li><li>Schallert, T., Fleming, S. M., Leasure, J. L., Tillerson, J. L., Bland, S. T. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=CNS+plasticity+and+assessment+of+forelimb+sensorimotor+outcome+in+unilateral+rat+models+of+stroke,+cortical+ablation,+parkinsonism+and+spinal+cord+injury.">CNS plasticity and assessment of forelimb sensorimotor outcome in unilateral rat models of stroke, cortical ablation, parkinsonism and spinal cord injury.</a> Neuropharmacology. 39, 777-787 (2000).</li><li>Paul, M. L., Currie, R. W., Robertson, H. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Priming+of+a+D1+dopamine+receptor+behavioural+response+is+dissociated+from+striatal+immediate-early+gene+activity.">Priming of a D1 dopamine receptor behavioural response is dissociated from striatal immediate-early gene activity.</a> Neuroscience. 66, 347-359 (1995).</li><li>Breese, G. R., Traylor, T. D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Effect+of+6-hydroxydopamine+on+brain+norepinephrine+and+dopamine+evidence+for+selective+degeneration+of+catecholamine+neurons.">Effect of 6-hydroxydopamine on brain norepinephrine and dopamine evidence for selective degeneration of catecholamine neurons.</a> J. Pharmacol Exp. Ther. 174, 413-420 (1970).</li><li>Breese, G. R., Chase, T. N., Kopin, I. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Metabolism+of+tyramine-3H+and+octopamine-3H+by+rat+brain.">Metabolism of tyramine-3H and octopamine-3H by rat brain.</a> Biochem. Pharmacol. 18, 863-869 (1969).</li><li>Frankin, K. B. J., Paxinos, G. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=.">.</a> The Mouse Brain in Stereotaxic Coordinates. , (2008).</li><li>Cornell-Bell, A. H., Finkbeiner, S. M., Cooper, M. S., Smith, S. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Glutamate+induces+calcium+waves+in+cultured+astrocytes:+long-range+glial+signaling.">Glutamate induces calcium waves in cultured astrocytes: long-range glial signaling.</a> Science. 247, 470-473 (1990).</li><li>Iancu, R., Mohapel, P., Brundin, P., Paul, G. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Behavioral+characterization+of+a+unilateral+6-OHDA-lesion+model+of+Parkinson's+disease+in+mice.">Behavioral characterization of a unilateral 6-OHDA-lesion model of Parkinson's disease in mice.</a> Behav. Brain Res. 162, 1-10 (2005).</li><li>Tan, Y., Williams, E. A., Lancia, A. J., Zahm, D. S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=On+the+altered+expression+of+tyrosine+hydroxylase+and+calbindin-D+28kD+immunoreactivities+and+viability+of+neurons+in+the+ventral+tegmental+area+of+Tsai+following+injections+of+6-hydroxydopamine+in+the+medial+forebrain+bundle+in+the+rat.">On the altered expression of tyrosine hydroxylase and calbindin-D 28kD immunoreactivities and viability of neurons in the ventral tegmental area of Tsai following injections of 6-hydroxydopamine in the medial forebrain bundle in the rat.</a> Brain Res. 869, 56-68 (2000).</li><li>Thiele, S. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Generation+of+a+model+of+L-DOPA-induced+dyskinesia+in+two+different+mouse+strains.">Generation of a model of L-DOPA-induced dyskinesia in two different mouse strains.</a> J. Neurosci. Methods. 197, 193-208 (2011).</li><li>Henry, B., Crossman, A. R., Brotchie, J. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Characterization+of+a+rodent+model+in+which+to+investigate+the+molecular+and+cellular+mechanisms+underlying+the+pathophysiology+of+L-dopa-induced+dyskinesia.">Characterization of a rodent model in which to investigate the molecular and cellular mechanisms underlying the pathophysiology of L-dopa-induced dyskinesia.</a> Adv. Neurol. 78, 53-61 (1998).</li></ol>

저자가 공개하는 게 없다.

이 프로토콜은 높은 병변 성공률과 낮은 사망률로, 극단적으로 재현할 수있다 파킨슨병의 안정 일방적 6-OHDA-lesioned 마우스 모델의 생성을위한 방법을 설명합니다. 6-OHDA 병변 수술의 성공은 쉽게 lesioned striatum 27&gt; 95 %의 도파민 고갈 지표&gt; 70 % ipsiversive의 회전과 함께 자발적인 회전 동작의 측정에 의해 추정 할 수 있습니다. 그것이 striatal 도파민 레벨 28 직접 측정을 제공으로 str...

<table border="1" &gt;<tbody&gt;<tr &gt;<td<strong시약의&gt; 이름</strong</td&gt;<td<strong&gt; 회사 소개</strong</td&gt;<td<strong&gt; 카탈로그 번호</strong</td&gt;<td<strong&gt; 댓글 (옵션)</strong</td&gt;</tr&gt;<tr &gt;<td&gt; desipramine HCL</td&gt;<td&gt; 시그마 - 올드 리치, 옥빌, ON, 캐나다</td&gt;<td&gt; D125</td&gt;<td&gt; 25mg/kg</td&gt;</tr&gt;<tr&gt;<td&gt; pargyline HCL</td&gt;<td&gt; 시그마 - 올드 리치, 옥빌, ON, 캐나다</td&gt;<td&gt; P8013</td&gt;<td&gt; 5mg/kg</td&gt;</tr&gt;<tr&gt;<td&gt; 6-OHDA HBR</td&gt;<td&gt; 시그마 - 올드 리치, 옥빌, ON, 캐나다</td&gt;<td&gt; H116</td&gt;<td&gt; 3mg / 마우스</td&gt;</tr&gt;<tr&gt;<td&gt; stereotaxic 프레임</td&gt;<td&gt; Kopf 인 스트 루먼트, Tujunga, CA, 미국</td&gt;<td&gt; 모델 900</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 마우스 귀 컵</td&gt;<td&gt; Kopf 인 스트 루먼트, Tujunga, CA, 미국</td&gt;<td&gt; 모델 921 관골의 귀 컵</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 마우스 앞니 바</td&gt;<td&gt; Kopf 인 스트 루먼트, Tujunga, CA, 미국</td&gt;<td&gt; 모델 923B</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 마우스 마취 마스크</td&gt;<td&gt; Kopf 인 스트 루먼트, Tujunga, CA, 미국</td&gt;<td&gt; 모델 923B</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 마중물 키트 (250ml 주사기를 포함)</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; PRMKIT 81,120</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; RN 압축 피팅 키트 (1 ㎜)</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; 55750-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<tdRN 압축 피팅 킷에서&gt; 픽 튜빙<
 (1/16<sup&gt; 일</sup&gt; 인치)</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; 55751-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 듀얼 작은 허브 RN 커플러</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; 55752-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td로&gt; luer 작은 허브 RN 어댑터</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; 55753-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 1ml 초 주사기 모델 7001KH</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; 80,100</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; * 6의 33G 이동식 바늘 (RN) 갑. . 45 &lt;° 베벨과 정의 1 인치</td&gt;<td&gt; 해밀턴 회사, 리노, 네바다, 미국</td&gt;<td&gt; 7803-05</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 가위</td&gt;<td&gt; 파인 과학 도구, 밴쿠버, 브리티시 컬럼비아, 캐나다.</td&gt;<td&gt; 14084-08</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 메스</td&gt;<td&gt; 파인 과학 도구, 밴쿠버, BC, 캐나다</td&gt;<td&gt; 10003-12</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 메스 블레이드</td&gt;<td&gt; 파인 과학 도구, 밴쿠버, BC, 캐나다</td&gt;<td&gt; 10035-20</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Forcep</td&gt;<td&gt; 파인 과학 도구, 밴쿠버, BC, 캐나다</td&gt;<td&gt; 11608-15</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Hemostats</td&gt;<td&gt; 파인 과학 도구, 밴쿠버, 브리티시 컬럼비아, 캐나다.</td&gt;<td&gt; 13004-14</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Isoflurane</td&gt;<td&gt; 원장</td&gt;<td&gt; 02241315</td&gt;<td&gt; 2~3%</td&gt;</tr&gt;<tr&gt;<td&gt; Suters (Vicryl 4.0)</td&gt;<td&gt; Syneture</td&gt;<td&gt; SS-683</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Steriliser</td&gt;<td&gt; 파인 과학 도구, 밴쿠버, BC, 캐나다</td&gt;<td&gt; 18000-45</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 주입 펌프</td&gt;<td&gt; 하버드 장치</td&gt;<td&gt; 박사 2,000분의 22</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 바늘 (27G)</td&gt;<td&gt; Becton 디킨슨</td&gt;<td&gt; 305,109</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 바늘 (25G)</td&gt;<td&gt; Becton 디킨슨</td&gt;<td&gt; 305,127</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 주사기 (1ml)</td&gt;<td&gt; BD 주사기</td&gt;<td&gt; 309,692</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Anaesthesia 트롤리</td&gt;<td&gt; 레이 의학</td&gt;<td&gt; M2000</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Baytril</td&gt;<td&gt; CDMV, 세인트 hyacinthe, QC</td&gt;<td&gt; 102,207</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Lidocaine</td&gt;<td&gt; CDMV, 세인트 hyacinthe, QC</td&gt;<td&gt; 3914</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Betadine 용액</td&gt;<td&gt; CDMV, 세인트 hyacinthe, QC</td&gt;<td&gt; 19,955</td&gt;<td&gt;</td&gt;</tr&gt;</tbody&gt;</table

development of a unilaterally-lesioned 6-ohda mouse model of parkinson's disease

그것이 recapitulates 기저 신경 회로의 변화와 약리학가 관찰한 이후 일방적으로 lesioned 6 hyroxydopamine (6-OHDA) lesioned 파킨슨병의 쥐 모델 (PD)는 parkinsonian 증상의 기초 메커니즘에 대한 우리의 이해를 발전에 귀중한 것으로 판명되었습니다 parkinsonian 환자 1-4. 다만, 기저 신경의 주요 입력 영역입니다 striatum, 내의 출력 경로의 cortico-striatal 시냅스에서 발생하는 정확한 세포와 분자 변화는 애매 남아 있으며 이것은 parkinsonian 증상을 밑에있는 병적인 이상이 3 발생할 사이트로 여겨지고 5. 경찰서에서 nigro-striatal 경로의 기저 신경 회로를 다음과 변성 변화의 기본 메커니즘을 이해하는 것은 크게 촉진에 의한 지나친 표현 녹색 형광 단백질은 세균 인공 염색체의 개발 (BAC) 생쥐하여 고급되었습니다그들은 고립에서 공부 수 있도록 8, :; : 두 striatal 출력 경로 (eGFP-D2와 eGFP-A2a 간접 경로 eGFP-D1 직접 경로)에 대한 구체적인 RS. 예를 들어, 최근의 연구 parkinsonian 마우스 9,10의 시냅스 소성의 병리 학적 변화가있다는 것을 제안했습니다. 그러나 이러한 연구는 청소년 생쥐와 parkinsonism의 급성 모델을 활용. 그것은 안정적인 6-OHDA의 병변과 성인 쥐에 설명된 변경 사항은 또한 이러한 모델에서 발생하는지 불분명하다. 다른 그룹은 중간 forebrain 번들 (MFB)을 lesioning하여 경찰의 안정 일방적-lesioned 6-OHDA 성인 마우스 모델을 생성하기 위해 시도했습니다 .. 안타깝게도,이 연구에서 사망률이 겨우 14 %가 21 수술을 이겨낸과 함께 매우 높은였다 일 이상 11. 더 많은 최근 연구에서 낮은 사망률 모두 함께 내부 nigral 병변을 올렸습니다 dopaminergic 뉴런의&gt; 80 % 감소, L-DOPA 유도 운동 이상증 11,12,13,14 중 단 표현이 변수였다이러한 연구 인치 경찰의 또 다른 잘 확립 마우스 모델은 MPTP-lesioned 마우스 15입니다. 이 모델은 잠재 neuroprotective 요원 16 평가에서 유용하게 입증되었습니다하는 동안, 그것은이 모델은 종종 모터 적자를 유도하는 데 실패로 경찰의 메카니즘 밑에 증상을 이해하는 데 덜 적합하고, 병변 17 정도, 18의 넓은 다양성을 보여줍니다 . 여기에서 우리는 지속&gt; 95 % striatal 도파민의 손실 (등 HPLC로 측정)뿐만 아니라 행동을 생산의 원인이 MFB,에 6-OHDA를 직접 관리하여 경찰의 안정 일방적 6-OHDA-lesioned 마우스 모델을 개발 불균형은 경찰의 잘 특성화 일방적 6-OHDA-lesioned 쥐 모델에서 관찰했다. 경찰이 새롭게 개발한 마우스 모델 parkinsonian 증상 세대의 기본 메커니즘을 이해하는 데 유용한 도구를 새삼 느끼게 될 것이다.

Watch this Scientific Journal Video about Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease at JoVE.com

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson&#039;s Disease

생쥐의 중간 forebrain 번들의 일방적 6-OHDA의 병변을 수행하기위한 프로토콜이 설명되어 있습니다. 이 방법은 striatal 도파민과 90.63의&gt; 95 %의 손실을 보여주는 살아남은 동물의 89 %를 낮은 사망률 (13.3 %) ± -4.02 % 병변의 측면을 향해 ipsiversive 회전 편견을 가지고 있습니다.

파킨슨병의 일방적-6-OHDA lesioned 마우스 모델의 개발

The unilaterally lesioned 6-hyroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease (PD) has proved to be invaluable in advancing our ...

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Medicine

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease

50.8K 조회수.  University of Toronto at Scarborough. 생쥐의 중간 forebrain 번들의 일방적 6-OHDA의 병변을 수행하기위한 프로토콜이 설명되어 있습니다. 이 방법은 striatal 도파민과 90.63의> 95 %의 손실을 보여주는 살아남은 동물의 89 %를 낮은 사망률 (13.3 %) ± -4.02 % 병변의 측면을 향해 ipsiversive 회전 편견을 가지고 있습니다.

비디오: Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease

MALDI Imaging Mass Spectrometry of Neuropeptides in Parkinson's Disease

MALDI imaging mass spectrometry (IMS) is a powerful approach that facilitates the spatial analysis of molecular species in biological tissue samples2 (Fig.1). A 12 &mu;m thin tissue section is covered with a MALDI matrix, which facilitates desorption and ionization of intact peptides and proteins that can be detected with a mass analyzer, typically using a MALDI TOF/TOF mass spectrometer. Generally hundreds of peaks can be assessed in a single rat brain tissue section. In contrast to commonly used imaging techniques, this approach does not require prior knowledge of the molecules of interest and allows for unsupervised and comprehensive analysis of multiple molecular species while maintaining high molecular specificity and sensitivity2. Here we describe a MALDI IMS based approach for elucidating region-specific distribution profiles of neuropeptides in the rat brain of an animal model Parkinson's disease (PD). 
PD is a common neurodegenerative disease with a prevalence of 1% for people over 65 of age3,4. The most common symptomatic treatment is based on dopamine replacement using L-DOPA5. However this is accompanied by severe side effects including involuntary abnormal movements, termed L-DOPA-induced dyskinesias (LID)1,3,6. One of the most prominent molecular change in LID is an upregulation of the opioid precursor prodynorphin mRNA7. The dynorphin peptides modulate neurotransmission in brain areas that are essentially involved in movement control7,8. However, to date the exact opioid peptides that originate from processing of the neuropeptide precursor have not been characterized. Therefore, we utilized MALDI IMS in an animal model of experimental Parkinson's disease and L-DOPA induced dyskinesia. 
MALDI imaging mass spectrometry proved to be particularly advantageous with respect to neuropeptide characterization, since commonly used antibody based approaches targets known peptide sequences and previously observed post-translational modifications. By contrast MALDI IMS can unravel novel peptide processing products and thus reveal new molecular mechanisms of neuropeptide modulation of neuronal transmission. While the absolute amount of neuropeptides cannot be determined by MALDI IMS, the relative abundance of peptide ions can be delineated from the mass spectra, giving insights about changing levels in health and disease. In the examples presented here, the peak intensities of dynorphin B, alpha-neoendorphin and substance P were found to be significantly increased in the dorsolateral, but not the dorsomedial, striatum of animals with severe dyskinesia involving facial, trunk and orolingual muscles (Fig. 5). Furthermore, MALDI IMS revealed a correlation between dyskinesia severity and levels of des-tyrosine alpha-neoendorphin, representing a previously unknown mechanism of functional inactivation of dynorphins in the striatum as the removal of N-terminal tyrosine reduces the dynorphin's opioid-receptor binding capacity9. This is the first study on neuropeptide characterization in LID using MALDI IMS and the results highlight the potential of the technique for application in all fields of biomedical research.

MALDI Imaging Mass Spectrometry of Neuropeptides in Parkinson&#039;s Disease

Dopamine replacement pharmacotherapy using L-DOPA is the most commonly used symptomatic treatment of Parkinson&#x2019;s disease, but is accompanied by side effects including involuntary abnormal movements, termed dyskinesia 1. Here, a protocol for MALDI imaging mass spectrometry is presented that detects changes in rat brain neuropeptide levels related to dyskinesia.

파킨슨병의 Neuropeptides의 든 이미징 질량 분광법

MALDI imaging mass spectrometry (IMS) is a powerful approach that facilitates the spatial analysis of molecular species in biological tissue samples2 ...

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의학

Skin Punch Biopsy Explant Culture for Derivation of Primary Human Fibroblasts

Tissues and cell lines derived from an individual with disease are ideal sources to study disease-related cellular phenotypes. Patient-derived fibroblasts in this protocol have been successfully used in the derivation of induced pluripotent stem cells to model disease1. Early passages of these fibroblasts can also be used for cell-based functional assays to study specific disease pathways, mechanisms2 and subsequent drug screening approaches. The advantage of the presented protocol over enzymatic procedures are 1) the reproducibility of the technique from small amounts of tissue derived from older patients, e.g. patients affected with Parkinson's disease, 2) the technically simple approach over more challenging methodologies using enzymatic treatments, and 3) the time consideration: this protocol takes 15-20 min and can be performed immediately after biopsy arrival. Enzymatic treatments can take up to 4 hr and have the problems of overdigestion, reduction of cell viability and subsequent attachment of cells when not handled properly. This protocol describes the dissection and preparation of a 4-mm human skin biopsy for derivation of a fibroblast culture and has a very high success rate which is important when dealing with patient-derived tissue samples. In this culture, keratinocytes migrate out of the biopsy tissue within the first week after preparation. Fibroblasts appear 7-10 days after the first outgrowth of keratinocytes. DMEM high glucose media supplemented with 20% FBS favors the growth of fibroblasts over keratinocytes and fibroblasts will overgrow the keratinocytes. After 2 passages keratinocytes have been diluted out resulting in relatively homogenous fibroblast cultures which expresses the fibroblast marker SERPINH1 (HSP-47). Using this approach, 15-20 million fibroblasts can be derived in 4-8 weeks for cell banking. The skin dissection takes about 15-20 min, cells are then monitored once a day under the microscope, and media is changed every 2-3 days after attachment and outgrowth of cells.

The fibroblast explant culture protocol from human skin punch biopsies is a technically robust and simple way to derive skin cells within 4-8 weeks for banking of about 15-20 million cells at a low passage number.

인간의 기본 섬유 아세포의 유도를위한 피부 펀치 생검 절편 문화

Tissues and cell lines derived from an individual with disease are ideal sources to study disease-related cellular phenotypes. Patient-derived fibroblasts ...

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Parkinson's disease (PD) is the second most common movement disorder and affects 1% of people over the age of 60 1. Because ageing is the most important risk factor, cases of PD will increase during the next decades 2. Next to pathological protein folding and impaired protein degradation pathways, alterations of mitochondrial function and morphology were pointed out as further hallmark of neurodegeneration in PD 3-11.
After years of research in murine and human cancer cells as in vitro models to dissect molecular pathways of Parkinsonism, the use of human fibroblasts from patients and appropriate controls as ex vivo models has become a valuable research tool, if potential caveats are considered. Other than immortalized, rather artificial cell models, primary fibroblasts from patients carrying disease-associated mutations apparently reflect important pathological features of the human disease.
Here we delineate the procedure of taking skin biopsies, culturing human fibroblasts and using detailed protocols for essential microscopic techniques to define mitochondrial phenotypes. These were used to investigate different features associated with PD that are relevant to mitochondrial function and dynamics. Ex vivo, mitochondria can be analyzed in terms of their function, morphology, colocalization with lysosomes (the organelles degrading dysfunctional mitochondria) and degradation via the lysosomal pathway. These phenotypes are highly relevant for the identification of early signs of PD and may precede clinical motor symptoms in human disease-gene carriers. Hence, the assays presented here can be utilized as valuable tools to identify pathological features of neurodegeneration and help to define new therapeutic strategies in PD.

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson&#039;s Disease

Fibroblasts from patients carrying mutations in Parkinson's disease-causing genes represent an easily accessible ex vivo model to study disease-associated phenotypes. Live cell imaging gives the opportunity to study morphological and functional parameters in living cells. Here we describe the preparation of human fibroblasts and subsequent monitoring of mitochondrial phenotypes.

파킨슨 병 분야에서 Mitochondrial Phenotypes을 모니터링하기위한 기본 인간 섬유 아세포의 사용

Parkinson's disease (PD) is the second most  common movement disorder and affects 1% of people over the age of 60 1. Because ageing is  the most important ...

A Simple Method of Mouse Lung Intubation

A simple procedure to intubate mice for pulmonary function measurements would have several advantages in longitudinal studies with limited numbers or expensive animal. One of the reasons that this is not done more routinely is that it is relatively difficult, despite there being several published studies that describe ways to achieve it. In this paper we demonstrate a procedure that eliminates one of the major hurdles associated with this intubation, that of visualizing the trachea during the entire time of intubation. The approach uses a 0.5 mm fiberoptic light source that serves as an introducer to direct the intubation cannula into the mouse trachea. We show that it is possible to use this procedure to measure lung mechanics in individual mice over a time course of at least several weeks. The technique can be set up with relatively little expense and expertise, and it can be routinely accomplished with relatively little training. This should make it possible for any laboratory to routinely carry out this intubation, thereby allowing longitudinal studies in individual mice, thereby minimizing the number of mice needed and increasing the statistical power by using each mouse as its own control.

This paper describes a striaghforward and efficient method of intubating mice for pulmonary function measurements or pulmonary instillation, that allows the mice to recover and be studied at later times. The procedure involves an inexpensive fiberoptic light source that directly illuminates the trachea.

마우스 폐 삽관 법의 간단한 방법

A  simple procedure to intubate mice for pulmonary function measurements would  have several advantages in longitudinal studies with limited numbers or  ...

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Lipoxygenase (LOX) activity has been implicated in neurodegenerative disorders such as Alzheimer&#39;s disease, but its effects in Parkinson&#39;s disease (PD) pathogenesis are less understood. Gene-environment interaction models have utility in unmasking the impact of specific cellular pathways in toxicity that may not be observed using a solely genetic or toxicant disease model alone.&#160;To evaluate if distinct LOX isozymes selectively contribute to PD-related neurodegeneration, transgenic (i.e. 5-LOX and 12/15-LOX deficient) mice can be challenged with a toxin that mimics cell injury and death in the disorder.&#160;Here we describe the use of a neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which produces a nigrostriatal lesion to elucidate the distinct contributions of LOX isozymes to neurodegeneration related to PD. The use of MPTP in mouse, and nonhuman primate, is well-established to recapitulate the nigrostriatal damage in PD.&#160;The extent of MPTP-induced lesioning is measured by HPLC analysis of dopamine and its metabolites and semi-quantitative Western blot analysis of striatum for tyrosine hydroxylase (TH), the rate-limiting enzyme for the synthesis of dopamine. To assess inflammatory markers, which may demonstrate LOX isozyme-selective sensitivity, glial fibrillary acidic protein (GFAP) and Iba-1 immunohistochemistry are performed on brain sections containing substantia nigra, and GFAP Western blot analysis is performed on striatal homogenates.&#160;This experimental approach can provide novel insights into gene-environment interactions underlying nigrostriatal degeneration and PD.

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson&#039;s Disease

Lipoxygenase (LOX) isozymes can generate products that may increase or decrease neuroinflammation and neurodegeneration.&#160;A gene-environment interaction study could identify LOX isozyme-specific effects. Using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of nigrostriatal damage in two LOX isozyme-deficient transgenic lines allows for comparison of the contribution of LOX isozymes on dopaminergic integrity and inflammation.

파킨슨 병에서 감수성 메커니즘을 마스크를 해제하는 유전자 환경 상호 작용 모델

Lipoxygenase (LOX) activity has been implicated in neurodegenerative disorders such as Alzheimer&#39;s disease, but its effects in Parkinson&#39;s disease ...

Controlling Parkinson's Disease With Adaptive Deep Brain Stimulation

Adaptive deep brain stimulation (aDBS) has the potential to improve the treatment of Parkinson&#39;s disease by optimizing stimulation in real time according to fluctuating disease and medication state. In the present realization of adaptive DBS we record and stimulate from the DBS electrodes implanted in the subthalamic nucleus of patients with Parkinson&#39;s disease in the early post-operative period. Local field potentials are analogue filtered between 3 and 47 Hz before being passed to a data acquisition unit where they are digitally filtered again around the patient specific beta peak, rectified and smoothed to give an online reading of the beta amplitude. A threshold for beta amplitude is set heuristically, which, if crossed, passes a trigger signal to the stimulator. The stimulator then ramps up stimulation to a pre-determined clinically effective voltage over 250 msec and continues to stimulate until the beta amplitude again falls down below threshold. Stimulation continues in this manner with brief episodes of ramped DBS during periods of heightened beta power.
Clinical efficacy is assessed after a minimum period of stabilization (5 min) through the unblinded and blinded video assessment of motor function using a selection of scores from the Unified Parkinson&#39;s Rating Scale (UPDRS). Recent work has demonstrated a reduction in power consumption with aDBS as well as an improvement in clinical scores compared to conventional DBS. Chronic aDBS could now be trialed in Parkinsonism.

Controlling Parkinson&#039;s Disease With Adaptive Deep Brain Stimulation

Adaptive deep brain stimulation (aDBS) is effective for Parkinson&#8217;s disease, improving symptoms and reducing power consumption compared to conventional deep brain stimulation (cDBS). In aDBS we track a local field potential biomarker (beta oscillatory amplitude) in real time and use this to control the timing of stimulation.

적응 깊은 뇌 자극으로 파킨슨 병을 제어

Adaptive deep brain stimulation (aDBS) has the potential to improve the treatment of Parkinson&#39;s disease by optimizing stimulation in real time ...

Establishment and Characterization of UTI and CAUTI in a Mouse Model

Urinary tract infections (UTI) are highly prevalent, a significant cause of morbidity and are increasingly resistant to treatment with antibiotics. Females are disproportionately afflicted by UTI: 50% of all women will have a UTI in their lifetime. Additionally, 20-40% of these women who have an initial UTI will suffer a recurrence with some suffering frequent recurrences with serious deterioration in the quality of life, pain and discomfort, disruption of daily activities, increased healthcare costs, and few treatment options other than long-term antibiotic prophylaxis. Uropathogenic Escherichia coli (UPEC) is the primary causative agent of community acquired UTI. Catheter-associated UTI (CAUTI) is the most common hospital acquired infection accounting for a million occurrences in the US annually and dramatic healthcare costs. While UPEC is also the primary cause of CAUTI, other causative agents are of increased significance including Enterococcus faecalis. Here we utilize two well-established mouse models that recapitulate many of the clinical characteristics of these human diseases. For UTI, a C3H/HeN model recapitulates many of the features of UPEC virulence observed in humans including host responses, IBC formation and filamentation. For CAUTI, a model using C57BL/6 mice, which retain catheter bladder implants, has been shown to be susceptible to E. faecalis bladder infection. These representative models are being used to gain striking new insights into the pathogenesis of UTI disease, which is leading to the development of novel therapeutics and management or prevention strategies.

The ability to model urinary tract infections (UTI) is crucial in order to be able to understand bacterial pathogenesis and spawn the development of novel therapeutics. This work&#8217;s goal is to demonstrate mouse models of experimental UTI and catheter associated UTI that recapitulate and predict findings seen in humans.

마우스 모델의 설립 및 요로 감염 및 CAUTI의 특성

Urinary tract infections (UTI) are highly prevalent, a significant cause of morbidity and are increasingly resistant to treatment with antibiotics. ...

A Quick Phenotypic Neurological Scoring System for Evaluating Disease Progression in the SOD1-G93A Mouse Model of ALS

The SOD1-G93A transgenic mouse is the most widely used animal model of amyotrophic lateral sclerosis (ALS). At ALS TDI we developed a phenotypic screening protocol, demonstrated in video herein, which reliably assesses the neuromuscular function of SOD1-G93A mice in a quick manner. This protocol encompasses a simple neurological scoring system (NeuroScore) designed to assess hindlimb function. NeuroScore is focused on hindlimb function because hindlimb deficits are the earliest reported neurological sign of disease in SOD1-G93A mice. The protocol developed by ALS TDI provides an unbiased assessment of onset of paresis (slight or partial paralysis), progression and severity of paralysis and it is sensitive enough to identify drug-induced changes in disease progression. In this report, the combination of a detailed manuscript with video minimizes scoring ambiguities and inter-experimenter variability thus allowing for the protocol to be adopted by other laboratories and enabling comparisons between studies taking place at different settings. We believe that this video protocol can serve as an excellent training tool for present and future ALS researchers.

This video protocol describes a sensitive, reliable, and quick method for evaluating the neuromuscular deficits in a transgenic mouse model of amyotrophic lateral sclerosis.

ALS의 SOD1-G93A 마우스 모델에서 질병의 진행을 평가하기위한 빠른 표현형 신경 채점 시스템

The SOD1-G93A transgenic mouse is the most widely used animal model of amyotrophic lateral sclerosis (ALS). At ALS TDI we developed a phenotypic screening ...

A Neonatal Mouse Spinal Cord Compression Injury Model

Spinal cord injury (SCI) typically causes devastating neurological deficits, particularly through damage to fibers descending from the brain to the spinal cord. A major current area of research is focused on the mechanisms of adaptive plasticity that underlie spontaneous or induced functional recovery following SCI. Spontaneous functional recovery is reported to be greater early in life, raising interesting questions about how adaptive plasticity changes as the spinal cord develops. To facilitate investigation of this dynamic, we have developed a SCI model in the neonatal mouse. The model has relevance for pediatric SCI, which is too little studied. Because neural plasticity in the adult involves some of the same mechanisms as neural plasticity in early life1, this model may potentially have some relevance also for adult SCI. Here we describe the entire procedure for generating a reproducible spinal cord compression (SCC) injury in the neonatal mouse as early as postnatal (P) day 1. SCC is achieved by performing a laminectomy at a given spinal level (here described at thoracic levels 9-11) and then using a modified Yasargil aneurysm mini-clip to rapidly compress and decompress the spinal cord. As previously described, the injured neonatal mice can be tested for behavioral deficits or sacrificed for ex vivo physiological analysis of synaptic connectivity using electrophysiological and high-throughput optical recording techniques1. Earlier and ongoing studies using behavioral and physiological assessment have demonstrated a dramatic, acute impairment of hindlimb motility followed by a complete functional recovery within 2 weeks, and the first evidence of changes in functional circuitry at the level of identified descending synaptic connections1.

This article describes a method for generating a reproducible spinal cord compression injury (SCI) in the neonatal mouse. The model provides an advantageous platform for studying mechanisms of adaptive plasticity that underlie spontaneous functional recovery.

신생아 마우스 척수 압축 부상 모델

Spinal cord injury (SCI) typically causes devastating neurological deficits, particularly through damage to fibers descending from the brain to the spinal ...

Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector

In order to study the molecular pathways of Parkinson&#39;s disease (PD) and to develop novel therapeutic strategies, scientific investigators rely on animal models. The identification of PD-associated genes has led to the development of genetic PD models. Most transgenic &#945;-SYN mouse models develop gradual &#945;-SYN pathology but fail to display clear dopaminergic cell loss and dopamine-dependent behavioral deficits. This hurdle was overcome by direct targeting of the substantia nigra with viral vectors overexpressing PD-associated genes. Local gene delivery using viral vectors provides an attractive way to express transgenes in the central nervous system. Specific brain regions can be targeted (e.g. the substantia nigra), expression can be induced in the adult setting and high expression levels can be achieved. Further, different vector systems based on various viruses can be used. The protocol outlines all crucial steps to perform a viral vector injection in the substantia nigra of the rat to develop a viral vector-based alpha-synuclein animal model for Parkinson&#39;s disease.

Development of an Alpha-synuclein Based Rat Model for Parkinson&#039;s Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector

This manuscript describes how viral vector-mediated local gene delivery provides an attractive way to express transgenes in the central nervous system. The protocol outlines all crucial steps to perform a viral vector injection in the substantia nigra of the rat to develop a viral vector-based animal model for Parkinson's disease.

재조합 아데노 - 관련 바이러스 성 벡터의 정위 주사를 통해 파킨슨 병에 대한 알파 - 시누 클레인 기반 쥐 모델 개발

In order to study the molecular pathways of Parkinson&#39;s disease (PD) and to develop novel therapeutic strategies, scientific investigators rely on ...