Questo lavoro è stato sostenuto dal Ministero degli Affari Esteri e del Commercio internazionale (Governo del Canada), University of Toronto Connaught Fondo, la Fondazione canadese per l&#39;innovazione, NSERC, la Fondazione Krembil and Trust di Parkinson Cure.

<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>

Gli autori non hanno nulla da rivelare.

Questo protocollo descrive un metodo per la generazione di uno stabile unilaterale 6-OHDA lesionato modello murino della malattia di Parkinson, che è estremamente riproducibile, con un&#39;elevata percentuale di successo lesione, e un tasso di mortalità basso. Il successo di 6-OHDA chirurgia lesione può essere facilmente stimata misurando spontaneo comportamento a rotazione con rotazioni ipsiversive&gt; 70 sulla indicativi di&gt; deplezione dopamina 95% in lesionato striato 27. Quantificazione dei livelli ...

<table border="1" &gt;<tbody&gt;<tr &gt;<td<strongNome&gt; del reagente</strong</td&gt;<td<strong&gt; Azienda</strong</td&gt;<td<strong&gt; Numero di catalogo</strong</td&gt;<td<strong&gt; Commenti (opzionale)</strong</td&gt;</tr&gt;<tr &gt;<td&gt; Desipramina HCl</td&gt;<td&gt; Sigma-Aldrich, Oakville, ON, Canada</td&gt;<td&gt; D125</td&gt;<td&gt; 25mg/kg</td&gt;</tr&gt;<tr&gt;<td&gt; Pargilina HCl</td&gt;<td&gt; Sigma-Aldrich, Oakville, ON, Canada</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; Sigma-Aldrich, Oakville, ON, Canada</td&gt;<td&gt; H116</td&gt;<td&gt; 3 mg / mouse</td&gt;</tr&gt;<tr&gt;<td&gt; Frame stereotassico</td&gt;<td&gt; Kopf Instruments, Tujunga, CA, USA</td&gt;<td&gt; Modello 900</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Il mouse orecchio tazze</td&gt;<td&gt; Kopf Instruments, Tujunga, CA, USA</td&gt;<td&gt; Modello 921 coppe Zygoma</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Il mouse incisivo bar</td&gt;<td&gt; Kopf Instruments, Tujunga, CA, USA</td&gt;<td&gt; Modello 923B</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Il mouse anestesia maschera</td&gt;<td&gt; Kopf Instruments, Tujunga, CA, USA</td&gt;<td&gt; Modello 923B</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Kit di adescamento (siringa contenente 250 ml)</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; PRMKIT 81120</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; RN raccordo a compressione kit (1 mm)</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; 55750-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Tubi PEEK dalla RN kit raccordo a compressione<
 (1/16<sup&gt; °</sup&gt; Pollici)</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; 55751-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Dual piccolo hub RN Coupler</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; 55752-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Luer ai piccoli hub RN adattatore</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; 55753-01</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; 1 ml siringa modello 25S 7001KH</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; 80.100</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; * 33G ago fisso (RN) confezione da 6. . Custom 1 pollice con 45 &lt;° smusso</td&gt;<td&gt; Hamilton Company, Reno, NV, USA</td&gt;<td&gt; 7803-05</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Forbici</td&gt;<td&gt; Strumenti Scienza Belle, Vancouver, BC, Canada.</td&gt;<td&gt; 14084-08</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Scalpel</td&gt;<td&gt; Strumenti Scienza Arti, Vancouver, BC, Canada</td&gt;<td&gt; 10003-12</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Lame di bisturi</td&gt;<td&gt; Strumenti Scienza Arti, Vancouver, BC, Canada</td&gt;<td&gt; 10035-20</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Pinza</td&gt;<td&gt; Strumenti Scienza Arti, Vancouver, BC, Canada</td&gt;<td&gt; 11608-15</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Hemostats</td&gt;<td&gt; Strumenti Scienza Belle, Vancouver, BC, Canada.</td&gt;<td&gt; 13004-14</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Isoflurano</td&gt;<td&gt; Abbot</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; Sterilizzatore</td&gt;<td&gt; Strumenti Scienza Arti, Vancouver, BC, Canada</td&gt;<td&gt; 18000-45</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Infusion Pump</td&gt;<td&gt; Harvard Apparatus</td&gt;<td&gt; Dottorato di Ricerca 22/2000</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Aghi (27G)</td&gt;<td&gt; Becton Dickinson</td&gt;<td&gt; 305.109</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Aghi (25G)</td&gt;<td&gt; Becton Dickinson</td&gt;<td&gt; 305.127</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Siringhe (1 ml)</td&gt;<td&gt; BD siringa</td&gt;<td&gt; 309.692</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Anestesia Carrello</td&gt;<td&gt; LEI medica</td&gt;<td&gt; M2000</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Baytril</td&gt;<td&gt; CDMV, St. Hyacinthe, QC</td&gt;<td&gt; 102.207</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Lidocaina</td&gt;<td&gt; CDMV, St. Hyacinthe, QC</td&gt;<td&gt; 3914</td&gt;<td&gt;</td&gt;</tr&gt;<tr&gt;<td&gt; Betadine soluzione</td&gt;<td&gt; CDMV, St. 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

Il unilateralmente lesionata 6-hyroxydopamine (6-OHDA)-lesionato modello murino della malattia di Parkinson (PD) si è rivelato prezioso per avanzare la nostra comprensione dei meccanismi alla base dei sintomi parkinsoniani, poiché essa ricapitola i cambiamenti nei circuiti dei gangli della base e farmacologia osservata in pazienti parkinsoniani 1-4. Tuttavia, le modifiche precise cellulari e molecolari che si verificano a cortico-striatali sinapsi delle vie di uscita all&#39;interno del corpo striato, che è la zona di ingresso principale dei gangli basali rimanere sfuggente, e questo è ritenuto sito dove alterazioni patologiche sottostanti presentano sintomi parkinsoniani 3 , 5. Nel PD, la comprensione dei meccanismi alla base di cambiamenti nella degenerazione dei gangli basali circuito seguente del nigro-striatale è stata notevolmente migliorata con lo sviluppo del cromosoma batterico artificiale (BAC) in topi che esprimono proteine ​​fluorescenti verdi guidati da promuovere8, consentendo loro di essere valutati singolarmente:;: specifico per le due vie di uscita striatali (eGFP-D2 e eGFP-A2a via indiretta EGFP-D1 diretta via) rs. Ad esempio, studi recenti hanno suggerito che ci sono cambiamenti patologici nella plasticità sinaptica in topi parkinsoniani 9,10. Tuttavia, questi studi hanno utilizzato topi giovani e modelli acuti di parkinsonismo. Non è chiaro se le modifiche descritte in ratti adulti con stabili 6-OHDA lesioni si verificano anche in questi modelli. Altri gruppi hanno tentato di generare una stabile lesionato unilateralmente-6-OHDA modello di topo adulto del PD da parte la lesione del fascio mediale del proencefalo (MFB), purtroppo, il tasso di mortalità in questo studio è estremamente elevata, con solo il 14% sopravvive l&#39;intervento chirurgico per il 21 11 giorni o più. Studi più recenti hanno generato intra-nigral lesioni sia con un tasso di mortalità bassa perdita&gt; 80% dei neuroni dopaminergici, ma espressione di L-DOPA discinesia indotta da 11,12,13,14 era variabilein questi studi. Un altro modello di topo ben definito del PD è l&#39;MPTP-leso il mouse 15. Anche se questo modello si è dimostrato utile nella valutazione dei potenziali agenti neuroprotettivi 16, è meno adatto per la comprensione dei meccanismi alla base dei sintomi del morbo di Parkinson, in quanto questo modello spesso non riesce a indurre deficit motori, e mostra una grande variabilità nella misura di lesione 17, 18 . Qui abbiamo sviluppato una stabile unilaterale 6-OHDA lesionato modello murino di PD mediante somministrazione diretta di 6-OHDA nella MFB, che causa la perdita costante&gt; 95% della dopamina striatale (come misurato mediante HPLC), oltre a produrre il comportamento squilibri osservati nel ben caratterizzati unilaterale 6-OHDA-lesionato modello di ratto PD. Questo modello murino di recente sviluppo del PD si rivelerà un prezioso strumento per la comprensione dei meccanismi alla base della generazione dei sintomi parkinsoniani.

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's Disease

Un protocollo per l&#39;esecuzione unilaterale 6-OHDA lesioni del fascio proencefalo mediale è descritto nei topi. Questo metodo ha un basso tasso di mortalità (13,3%) con l&#39;89% degli animali sopravvissuti mostrano una perdita&gt; 95% della dopamina striatale e di 90,63 ± -4,02% pregiudizi ipsiversive rotazione verso il lato della lesione.

Sviluppo di un unilateralmente lesionata 6-OHDA modello murino della malattia di Parkinson

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

development-unilaterally-lesioned-6-ohda-mouse-model-parkinson-s

Research

JoVE Journal

Medicine

50.9K Views.  University of Toronto at Scarborough. Un protocollo per l'esecuzione unilaterale 6-OHDA lesioni del fascio proencefalo mediale è descritto nei topi. Questo metodo ha un basso tasso di mortalità (13,3%) con l'89% degli animali sopravvissuti mostrano una perdita> 95% della dopamina striatale e di 90,63 ± -4,02% pregiudizi ipsiversive rotazione verso il lato della lesione.

Video: 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.

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.

MALDI Imaging Mass Spectrometry dei neuropeptidi nella malattia di Parkinson

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

Ricerca

Medicina

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.

Pelle Punch Biopsia Espianto Cultura per la derivazione di fibroblasti umani primari

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.

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.

L&#39;uso di fibroblasti umani primari per il monitoraggio fenotipi mitocondriali nel campo della malattia di Parkinson

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.

Un metodo semplice di intubazione mouse polmone

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.

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.

Modelli di interazione gene-ambiente per smascherare i meccanismi di suscettibilità nel morbo di Parkinson

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.

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.

Controllo della Malattia di Parkinson con Adaptive stimolazione cerebrale profonda

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.

Istituzione e caratterizzazione di UTI e CAUTI in un modello murino

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.

Un Sistema di punteggio rapida fenotipica neurologica per la valutazione di progressione della malattia nel SOD1-G93A modello murino della SLA

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.

Un neonatale mouse Spinal Cord Injury compressione Modello

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.

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.

Sviluppo di un Rat modello Alfa-sinucleina per la malattia di Parkinson mediante iniezione stereotassica di un ricombinante vettore virale adeno-associato

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